Search Criteria: Strain Type is "Mutant Stock"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 003008 | B6;129S-Tnftm1Gkl/J | Level 4 |
| Mice homozygous for the Tnftm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does ..... For more information please see the full phenotype on the strain data sheet | ||
| 003243 | B6;129S-Tnfrsf1atm1Imx Tnfrsf1btm1Imx/J | Level 4 |
| Mice homozygous for both the Tnfrsf1atm1Imx and Tnfrsf1btm1Imx targeted mutations (p55 and p75 deficient) are viable and fertile. Double homozygous mutant mice fail to bind TNF. Thymus, spleen, and other lymphoid tissue are normal, indicating that TNF is not required for normal development of these organs. | ||
| 002633 | B6;129S4-Nos1tm1Plh/J | Level 4 |
| Mice homozygous for the Nos1tm1Plh targeted mutation are viable and fertile; however, they have enlarged stomachs and reduced stroke size. Hyperglycemic-euglycemic clamp studies demonstrate that homozygotes exhibit insulin resistance at the level of peripheral tissues. Homozygous males are reported to be more aggressive than normal wildtype siblings although this has not been confirmed in The Jackson Laboratory colony. These mice may be useful model for stroke research. | ||
| 006494 | B6CBA-Tg(HDexon1)62Gpb/3J | Level 4 |
| This line is transgenic for the 5' end of the human HD gene carrying approximately 120 +/- 5 (CAG)repeat expansions. The transgene is ubiquitously expressed. Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. They urinate frequently and exhibit loss of body weight and muscle bulk through the course of the disease. Neurologically they develop Neuronal Intranuclear Inclusions (NII) which contain both the huntingtin and ubiquitin proteins. Previously unknown, these NII have subsequently been identified in human HD patients. The age of onset of HD symptoms is reported to occur between 9 and 11 weeks. Commonly known as the "R6/2" strain. Transgenic mice develop hyperglycemia by 12 weeks of age with a corresponding decrease in insulin levels. Pancreatic beta cel ..... | ||
| 007850 | J:NU | Level 4 |
| Outbred homozygous nude (Foxn1nu/Foxn1nu) mice are the standard in vivo model for drug efficacy testing in oncology. Nude mice are athymic and hairless as a result of the recessive nu mutation. T cell precursors exist but development is blocked in the absence of a thymus, resulting in an immunodeficiency that permits transplantation of tumor cell xenografts. Homozygous females are poor breeders and fail to lactate. Heterozygous males and females breed well and have normal immune function. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. | ||
| 100410 | WBB6F1/J-KitW/KitW-v | Level 4 |
| Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. KitW/KitW-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. KitW/KitW-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment. | ||
| 012755 | 129-Sirt3tm1.1Fwa/J | Repository- Live |
| The targeted mutation deletes exon 2-3 of the mouse sirtuin (silent information regulator 2 (Sir2)) homolog 3, Sirt3, gene, abolishing gene function. Homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Sirt3-/- mice exhibit hyperacetylation of mitochondrial enzymes, including glutamate dehydrogenase (GDH) and long-chain acyl co-enzyme A dehydrogenase (LCAD), leading to a decrease in the modulation of mitochondrial metabolism and fatty acid oxidation. They show reduced ATP production, cold intolerance, and hypoglycemia. These mice may be useful in studying the role of fatty acid oxidation in diabetes, cardiovascular disease, steatosis, fasting, cold exposure, and life span. | ||
| 006050 | 129-Sirt6tm1Fwa/J | Repository- Live |
| Homozygous neonates are smaller than their wildtype and heterozygous littermates. They develop normally until approximately 21 days of age, when they develop an acute and rapid, aging-like degenerative pathology resulting in death by postnatal day 24. Homozygous mutant mice exhibit subcutaneous fat loss, lordokyphosis (hunchbacked spine) with osteopenia (30% loss of bone mineral density), colitis, and severe lymphopenia due to increased lymphocyte apoptosis. At day 12, mice have reduced insulin-like growth factor I (IGF-1) levels in serum, and develop severe hypoglycemia. Mouse embryonic fibroblasts (MEFs) prepared from homozygous embryos exhibit reduced proliferation, defective base excision repair function, as indicated by increased sensitivity to alkylating agents and ionizing radiation, and increased chromosomal aberrations. The donating investigators report that no gene product (mRNA or protein) is detected by RT-PCR or immuoblot analysis of tissues, MEFs or embryonic stem cells f ..... For more information please see the full phenotype on the strain data sheet | ||
| 012888 | 129-Wlstm1.1Lan/J | Repository- Live |
| These Wls floxed mutant mice possess loxP site before the ATG start site in the 5' untranslated region of exon 1 and another upstream of exon 2 of the wntless homolog (Drosophila) (Wls) gene. Mice that are homozygous for this allele are viable, fertile, and normal in size. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 1 deleted in cre-expressing tissues, abolishing gene function. When bred to a strain expressing Cre recombinase in the germline, homozygotes fail to develop mesoderm and are embryonic lethal by E8.5. When bred to a strain expressing Cre recombinase in pancreatic precursors, the mutant mice develop pancreatic hypoplasia. When bred to a strain expressing Cre recombinase in neural crest cells, the mutant mouse strain has severe brain malformations and exhibit postnatal lethality. This mutant mouse strain is useful to study Wnt signaling in any organ or tissue that can be targeted ..... For more information please see the full phenotype on the strain data sheet | ||
| 014103 | 129;FVB-Tmem79m1J/GrsrJ | Repository- Live |
| Homozygotes can be identified by 7 to 8 days of age. They have a slightly shiny, off-white coat color with sparse hair, and some adults develop an irritation around the eyes. The zigzag hairs are abnormal, having extra kinks. | ||
| 012856 | A;C-Relbshep/GrsrJ | Repository- Live |
| 007750 | B6(C)-Mir150tm1Rsky/J | Repository- Live |
| Mice homozygous for this targeted allele (miR150-/- or MiR-150-/-) are viable and fertile with normal development of T cells, follicular B cells, and MZ B cells. No miR-150 is expressed in spleen, mesenteric lymph node, and thymus of homozygotes. Homozygous mice exhibit B cell expansion (CD19+B220loCD5+CD43+CD23-; B1a subset) in spleen and peritoneal cavity (with reciprocal reduction in B2 cells) and enhanced humoral immune response (increased serum immunoglobulins of various classes both at steady-state and following T cell-dependent antigen exposure). Homozygous miR-150 deficiency also leads to enhanced induction of the miR-150 target protein c-Myb in activated B and T cells, but no reported change in expression of the miR-150 target genes Foxp1 or ZFP91 in resting or activated B cells. These miR150-/- mice may be useful in mircoRNA biology, specifically to study the role of miR-150 and its target genes (inc ..... For more information please see the full phenotype on the strain data sheet | ||
| 012704 | B6(Cg)-Crhtm1(cre)Zjh/J | Repository- Live |
| The CRH-ires-CRE allele harbors an internal ribosome entry site and Cre recombinase in the 3' UTR of the corticotropin releasing hormone locus (Crh). As such, cre expression is directed by the endogenous Crh promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When CRH-ires-CRE mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Crh-expressing cells in the offspring.
The donating investigator reports Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Crh expression pattern with highly efficient recombination). They report Cre recombinase activity is observed in CRH positive neurons (some interneurons), and may not have examined cre expression in tissues other than brain.
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| 013593 | B6.129S-Atoh1tm4.1Hzo/J | Repository- Live |
| These Math1M1GFP/M1GFP mice contain an enhanced green fluorescent protein (eGFP) fused to the 3' end of the atonal homolog 1 (Atoh1) gene. Homozygous mice are viable and fertile. GFP is expressed all Math1-expressing neurons including hindbrain neurons such as the suparafacial respiratory group/retrotrapezoid nucleus (pFRG/ RTN). These neurons are involved in respiratory rhythm generation and defects in these are associated with congenital central hypoventilation syndrome (CCHS). These mice may be useful for tracing the development, migration, and differentiation of Math1-expressing pFRG/RTN and paratrigeminal neurons. | ||
| 013595 | B6.129S-Atoh1tm6.1Hzo/J | Repository- Live |
| These Atoh1FLAG mice contain three c-terminal FLAG tags fused to the 3' end of the atonal homolog 1 (Atoh1) gene. Homozygous mice are viable and fertile. Atoh1FLAG expression is evident evident in all Atoh1 expressing cells including cerebellar granule neuron precursors (GNPs) where it binds the active transcriptional enhancer region of the GLI-Kruppel family member GLI2 (Gli2) gene. These mice may be useful for studying postnatal cerebellar development and regulation of Sonic Hedgehog-induced medulloblastoma. | ||
| 013786 | B6.129S1(Cg)-Lama2tm1Eeng/J | Repository- Live |
| A targeting vector was designed to insert a β-galactosidase (lacZ) gene and a neomycin (neo) resistance cassette downstream of the start codon of the laminin, alpha 2 (Lama2) gene, abolishing gene function. Heterozygous dyW mice are viable, fertile and normal in size, while homozygous mice exhibit growth retardation and most die between 2-4 weeks of age. Laminin2, or Merosin, is expressed in striated muscle, peripheral and central nervous systems, thymus, thyroid, intestine, and testis and has been associated with merosin-deficient congenital muscular dystrophy (MCMD). Homozygous dyW mice are passive, small, and emaciated, and demonstrate partial hindleg lameness and clasping. Their muscles contain necrotic fibers with occasional areas of regeneration, and they exhibit pronounced fibrosis and increased creatine kinase (CK) activity. When heterozygous dyW mice are bred with transgenic mice expressing the mouse m ..... For more information please see the full phenotype on the strain data sheet | ||
| 006600 | B6.129S1-Mnx1tm4(cre)Tmj/J | Repository- Live |
| Mice heterozygous for this HB9cre targeted mutation are viable and fertile, with cre expression replacing HB9 (Hlxb9 or Mnx1) expression. Under control of the endogenous upstream elements, cre expression is directed to motor neurons. In heterozygotes, cre expression coincides with HB9 expression. Homozygous HB9cre mice die at or soon after birth, with expression of Cre recombinase likewise directed to motor neurons but no expression of endogenous HB9. When these HB9cre mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination in the resulting offspring leads to deletion of the flanked sequences in Mnx1/HB9 expressing cells; making them useful in neurodevelopmental studies of homeobox genes, motor neuron function and differentiation, and the central nervous system. | ||
| 015828 | B6.129S2(FVB)-Pak4tm2.1Amin/J | Repository- Live |
| These Pak4 floxed mutant mice possess loxP sites flanking exons 2-4 of the p21 protein (Cdc42/Rac)-activated kinase 4 (Pak4) gene. Homozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Pak4 is a member of the group B family of PAK serine/threonine kinases and is expressed early in development in a variety of tissues. It is involved in the formation of filopodia in response to Cdc42, promoting neuronal growth. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2-4 deleted in cre-expressing tissues. This strain may be useful for studying the role of Pak4 in the development of extraembryonic tissue, embryonic vasculature, and the placenta. | ||
| 014648 | B6.Cg-Gt(ROSA)26Sortm37(H1/tetO-RNAi:Taz)Arte/ZkhuJ | Repository- Live |
| These mutant mice have a tetracycline inducible Taz specific short hair pin RNA (shRNA) driven by the endogenous mouse Gt(ROSA)26Sor promoter.
Expression of the shRNA is controlled by the transcription of the H1 RNA polymerase III promoter, which is coupled to a tet-operator (tetO) sequence. Expression of the shRNA is blocked by codon-optimized version of the tet repressor itetR, which is part of the allelic construct found in this mouse. Doxycycline (dox--a tetracycline analog) treatment decreases the affinity of the itetR for the tetO sequence, allowing transcription of the shRNA.
Dox-induced Taz gene silencing is detected in heart (to ~3.7% of wildtype), skeletal muscle (to ~11.2%), liver (to ~8.9%) and brain (to ~3.4%) by RT-PCR analysis. Gene product (mRNA) in transgenic mice without dox induction is reduced by 35% of wildtype control levels. Withdrawal of dox at 4 weeks partially reverses the reduction of Taz expression. Protein product ..... For more information please see the full phenotype on the strain data sheet | ||
| 006368 | B6.Cg-Tg(Cr2-cre)3Cgn/J | Repository- Live |
| Mice homozygous for this "CD21-cre3a" transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Cre recombinase under the control of the mouse complement receptor 2 (CR2) promoter. Cre recombinase expression is detected specifically in mature transitional B cells. When CD21-cre3a mice were crossed to a lacZ-expressing Cre reporter strain, Cre recombinase activity is detected in 65-70% of mature B cells (as determined by FACS analysis of bone marrow cells). When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in deletion of the targeted gene in mature B lymphocytes and follicular dendritic cells. This strain represents an effective tool for generating tissue specific-targeted mutants that would be useful to study B lymphocyte development. | ||
| 007606 | B6.Cg-Tg(Thy1-cre/ERT2,-EYFP)AGfng/J | Repository- Live |
| These transgenic mice ("SLICK" for single-neuron labeling with inducible Cre-mediated knock-out) have a tamoxifen inducible Cre-mediated recombination system and Enhanced Yellow Fluorescent Protein driven by 2 bidirectional copies of the mouse thymus cell antigen 1 promoter. Hemizygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make the strain homozygous. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted neuron-specific deletions only in neurons where the Thy1 promoter is active. These cells will be evident by the expression of Yellow Fluorescent Protein. Transgenic mice express YFP constitutively in neurons. The Donating Investigator reports that founder line A mice express the transgene in small subsets of motor neurons and dorsal root ganglion neurons.
..... For more information please see the full phenotype on the strain data sheet | ||
| 013128 | B6129S-Del(7Slx1b-Sept1)4Aam/J | Repository- Live |
| These mutant mice possess an engineered deletion spanning approximately 0.39 Mb on mouse Chromosome 7. The region involved encompasses a chromosomal segment, between the GIY-YIG domain containing 2 (Giyd2) gene and the septin 1(Sept1) loci, that shares conserved synteny with the Autism spectrum disorders critical interval on human Chromosome 16 (the 16p11.2 region). Mice carrying one copy of the deletion prove to be viable while mice homozygous for the deletion are embryonic lethal. These mice exhibit neuroanatomical and behavioral phenotypes reminiscent of human autism. This mutant mouse may be useful in studying Autism and other associated disorders.
(Mice bearing the reciprocal duplication are also available (see Stock No. 013129)) | ||
| 010801 | B6129S-Tc(Hsa21)1TybEmcf/J | Repository- Live |
| Mice carrying a human fragment of Chromosome 21 (Hsa21) are viable, fertile, and normal in size, only the female carriers consistently transmits the mutation to the germline. When maintained on a background other than (C57BL/6 X 129S8/SvEv) germline transmission is completely abolished. These Tc1 mice contain 42Mb (approximately 83%) of a freely segregating Hsa21 containing 269 genes, including most of the gene orthologues located on mouse Chromosome 10 (Mmu10), Mm16, and Mmu17, which have been found to contribute to human Down Syndrome (DS). This mouse strain represents the most complete model of DS, exhibiting alterations in behavior, learning, memory, synaptic plasticity, cerebellar neuronal number, heart development, mandible size, defects in motor coordination, perturbed haematopoiesis, and reduced tumour angiogenesis. These mice may be useful for studying the genes involved in human chromosome aneuploidy and its role in DS. | ||
| 010687 | B6;129-Adora2atm1Dyj/J | Repository- Live |
| These mice possess loxP sites on either side of exon 2 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have the critical exon deleted in the cre-expressing tissues. When bred to a strain expressing Cre recombinase in the forebrain (see Stock No. 005359 for example), this mutant mouse strain may be useful in studies of locomoter activity response to addictive substances. | ||
| 010531 | B6;129-Bmi1tm1(cre/ERT)Mrc/J | Repository- Live |
| These targeted mutant mice carry tamoxifen-inducible Cre under the transcriptional control of the mouse Bmi1 (Bmi1 polycomb ring finger oncogene) promoter specifically expressed in discrete cells located near the bottom of crypts in the small intestine (predominantly four cells above the base of the crypt). When crossed with a strain containing a loxP-flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions. When crossed with a floxed reporter strain, lineage tracing of Bmi1-expressing cells is possible. | ||
| 008364 | B6;129-Chattm1(cre/ERT)Nat/J | Repository- Live |
| These targeted mutation mice carry a tamoxifen-inducible Cre cassette knocked into the 3' UTR of the gene. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating 4-hydroxytamoxifen-induced, Cre-mediated targeted deletions specifically in cholinergic neurons. Heterozygotes and homozygotes are normal in size, viability and fertility. | ||
| 014125 | B6;129-Flnctm1Lmk/J | Repository- Live |
| The Flnc Δ41-48 mutant allele has the last eight exons (exons 41-48) of the filamin C (FLNc) locus deleted. The deleted region encodes the last five filamin-like repeats (including the dimerization domain) and the Hinge 2 domain of FLNc. As such, the Flnc Δ41-48 allele expresses a truncated mRNA at reduced levels compared to the wildtype allele in limb muscle and heart tissues. Western blot analysis on limb muscle protein lysates shows that the Flnc Δ41-48 allele expresses a truncated protein at very low levels. Heterozygous mice are viable and fertile with no reported abnormalities. Mice homozygous for the Flnc Δ41-48 allele die at birth. At embryonic day (E)18.5, homozygous mice born via Cesarean section are able to take several short breaths but exhibit respiratory distress (failure to inflate lungs) and die shortly thereafter. While the hearts of the homozygotes appear normal and unaffected, skeletal muscles exhibit severe abnor ..... For more information please see the full phenotype on the strain data sheet | ||
| 012824 | B6;129-Fzd6tm1Nat/J | Repository- Live |
| Homozygoos Fzd6 (frizzled homolog 6 (Drosophila)) targeted mutant mice have altered hair patterning. Instead of a parallel orientation of hair follicles on the body surface, these mice have a variety of whorls or tufts indicating a global mis-orientation of follicle patterning. The phenotype strongly resembles the wing-hair and bristle patterning defects observed in Drosophila frizzled. LacZ expression replaces that of the targeted gene in skin and hair follicles. | ||
| 012825 | B6;129-Fzd7tm1.1Nat/J | Repository- Live |
| Homozygous Fzd7 (frizzled homolog 7 (Drosophila)) targeted mutation mice have a small kink in the tail, most commonly found at the tip. Nuclear-localized lacZ expression replaces that of the targeted gene. This strain may be useful in further characterization of this receptor. | ||
| 010527 | B6;129-Gt(ROSA)26Sortm1(DTA)Mrc/J | Repository- Live |
| These R26RDTA (or ROSA26-DTA176) mice carry a loxP-flanked stop cassette associated with an attentuated diptheria toxin. When crossed with a Cre recombinase-expressing strain, tissue/cell-specific ablation of cells can be achieved. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 016262 | B6;129-Gt(ROSA)26Sortm1(Foxo1/GFP)Jke/J | Repository- Live |
| The FOXO1/GFP allele contains a loxP-flanked transcriptional STOP cassette (PGK-Neo-polyA) upstream of a forkhead box O1 (Foxo1)-green fluorescent protein (GFP) fusion protein. Homozygotes are viable and fertile. In the absence of Cre, reporter gene expression is prevented by the STOP sequence. When bred to mice that express Cre recombinase, offspring will have the floxed-STOP cassette deleted in the cre-expressing tissue(s), resulting in FOXO1/GFP expression in Cre-recombinase-expressing cells. FOXO1 is a component of the phosphoinositide 3-kinase (PI3K)-AKT pathway, and shuttles between the nucleus and the cytoplasm upon activation/inhibition by AKT. The PI3K-AKT signaling pathway is activated after administration of insulin and leptin. Exclusion of FoxO1 from the nucleus upon AKT phosphorylation allows visualization of activated/inactivated AKT by monitoring sub-cellular localization of the FOXO1-GFP fusion protein. These mice may be useful for ..... For more information please see the full phenotype on the strain data sheet | ||
| 004847 | B6;129-Gt(ROSA)26Sortm1(cre/ERT)Nat/J | Repository- Live |
| These R26CreER mutant mice have a tamoxifen-inducible Cre-mediated recombination system driven by the endogenous mouse Gt(ROSA)26Sor promoter. The mutant allele consists of a fusion product involving Cre recombinase and an altered version of the mouse estrogen receptor ligand binding domain. The mutant ligand binding domain does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the CRE/ESR1 protein can only gain access to the nuclear compartment to mediate recombination after exposure to tamoxifen. Tamoxifen administration will also induce Cre recombination in the developing embryos of treated mothers. When crossed with a strain containing a loxP site-flanked sequence of interest, this mutant is useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Homozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnor ..... For more information please see the full phenotype on the strain data sheet | ||
| 006911 | B6;129-Gt(ROSA)26Sortm1(rtTA*M2)Jae Col1a1tm2(tetO-Pou5f1)Jae/J | Repository- Live |
| Mice heterozygous for both targeted mutations (R26-rtTA and Cola1a::tetO-Oct4) are viable and fertile. These "Oct-4/rtTA" mice express rtTA-M2, an optimized form of reverse tetracycline-controlled transactivator (rtTA) protein, in multiple tissues. In the absence of the tetracycline analog doxycycline (dox), Oct4 (Pou5f1) expression from the Col1a1 locus is not detected. Following dox administration, high Oct4 expression is induced in liver, bone marrow, stomach, intestine, and skin, with lower levels in the heart, lungs, kidney, spleen, and thymus; no expression was detected in the brain and testes. Dox-inducd activation of Oct4 results in dysplasia in epithelial tissues. These mutant mice may be useful for studies of tumorigenesis and pluripotent cells. | ||
| 008516 | B6;129-Gt(ROSA)26Sortm1Joe/J | Repository- Live |
| Homozygous ROSA26 GNZ knock-in mice are viable and fertile, with a nuclear-localized green fluorescent protein/beta-galactosidase fusion protein (GFP-NLS-lacZ or GNZ) inserted into the Gt(ROSA)26Sor (ROSA26) locus. Widespread expression of GNZ is blocked by an upstream loxP-flanked STOP sequence (in the absence of Cre recombinase, no expressed GFP or beta-galactosidase activity is observed in GNZ embryos(E9.5-18.5)). When bred to cre expressing mice, offspring will have the STOP sequence deleted in tissues where Cre recombinase is present. The resulting GNZ fusion protein expression allows for enhanced (single cell level) visualization / resolution. The donating investigator reports that Cre recombinase activity can be visualized by direct GFP fluorescence, but the high resolution nuclear staining of GNZ may be best visualized by immunostaining for either GFP or beta-galactosidase. These ROSA26 GNZ mice are useful as a Cre reporter strain; expressing both G ..... For more information please see the full phenotype on the strain data sheet | ||
| 004077 | B6;129-Gt(ROSA)26Sortm2Sho/J | Repository- Live |
| These mice contain an Enhanced Green Fluorescent Protein (EGFP) gene inserted into the Gt(ROSA)26Sor locus. Expression of the EGFP gene is blocked by a loxP-flanked STOP fragment placed between the EGFP sequence and the Gt(ROSA)26Sor promoter. This strain serves as a reporter strain, with successful Cre excision being indicated by EGFP expression in cre-expressing tissues. Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The donating investigator indicates that the EGFP expression level in this reporter strain is suitable for applications involving FACS but is too low for histological applications. | ||
| 010557 | B6;129-Gt(ROSA)26Sortm3(rtTA,tetO-cre/ERT)Nat/J | Repository- Live |
| These R26rtTACreER mice have a CreERT, reverse tetracycline trans-activator (rtTA), and Tet-responsive element (TRE) targeted to the mouse Gt(ROSA)26Sor gene to create a gene expression tool with two independent layers of pharmacologic control and a widespread pattern of activity. In this construct, expression of tamoxifen-sensitive CreERT is under the control of rtTA, a sequence-specific DNA-binding protein that activates transcription upon binding tetracycline derivatives such as doxycycline. Upon administration of doxycycline, rtTA activates transcription of the CreER coding region by binding to the Tet operator located immediately 5' of a minimal promoter. This enhances the dynamic range of CreER and enables sparse labeling in situations where reduced recombination efficiency facilitates behavioral, morphological or functional studies of modified cells among populations of unmodified neighbors. | ||
| 013071 | B6;129-Hbatm1(HBA)Tow Hbbtm2(HBG1,HBB*)Tow/Hbbtm3(HBG1,HBB)Tow/J | Repository- Live |
| These mice may harbor several knockin mutations: 1) the Hbatm1(HBA)Tow mutation (also called hα ; designed with the human hemoglobin α gene replacing the endogenous mouse α-globin), as well as 2) the Hbbtm2(HBG1,HBB*)Tow mutation (also called -1400 γ-βS ; designed with the human hemoglobin gamma (Aγ) gene and the human sickle hemoglobin beta (βS) gene replacing the endogenous mouse major and minor β-globin), and/or 3) the Hbbtm3(HBG1,HBB)Tow mutation (also called -383 γ-βA ; designed with the human hemoglobin gamma (Aγ) gene and the human wildtype hemoglobin beta (βA) gene replacing the endogenous mouse major and minor β-globin). --Of note, these mice should not harbor any wildtype allele at the Hbb locus.--
Mice homozygous at the ..... | ||
| 005034 | B6;129-Hcn1tm2Kndl/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No mRNA encoding the pore/S6 transmembrane domain is detected by in situ hybridization. No HCN1 protein is detected by Western blot analysis of membrane extracts from cerebellum, hippocampus or cortex. Mutant mice exhibit impaired learning capacity in visible platform swimming water maze task and rotorod test, and abnormal eye blink conditioning response. Purkinje cell electrophysiology is abnormal. This mutant mouse strain may be useful in studies of learning, memory and neurophysiology. | ||
| 012251 | B6;129-Igf1rtm2Arge/J | Repository- Live |
| These mice possess loxP sites on either side of exon 3 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 3 deleted in the cre-expressing tissue(s).
When crossed with a mouse overexpressing constitutively active Kras and expressing mammary gland specific Cre recombinase, this IGF1RLox mutant mouse strain may be useful in studies of mammary tumorigenesis (Proc Natl Acad Sci U S A 2009 Feb 17;106(7):2359-64).
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| 016221 | B6;129-Ip6k2tm1Dlin/J | Repository- Live |
| In this strain, a floxed-neo cassette replaces the first 202 nucleotides of exon 2 of the inositol hexaphosphate kinase 2 (Ip6k2) gene, abolishing gene expression. Homozygotes are viable, fertile, and normal in size. IP6K2 suppresses growth and increases apoptosis during cell stress by catalyzing the synthesis of inositol polyphosphates. These compounds are involved in the regulation of telomere length, protein phosphorylation, and cell growth and movement. After chronic exposure to the carcinogen 4-nitroquinoline 1-oxide (4-NQO) these mice exhibit a four-fold increase in the incidence of invasive squamous cell carcinoma (SCC) formation in the tongue, oral cavity, and esophagus. They also display relative resistance to ionizing radiation and exhibit increased survival following total body irradiation. Cells from these mice are relatively resistant to growth-suppression by interferon-β (IFN-β). These mice may be useful for studying the mechanisms of IP6K2-dependent ..... For more information please see the full phenotype on the strain data sheet | ||
| 004605 | B6;129-Itgb1tm1Efu/J | Repository- Live |
| These mice possess loxP sites on either side of exon 3 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
When bred to a strain expressing Cre recombinase in the epithelial cells of the intestine (see Stock No. 004586 for example), this mutant mouse strain may be useful in studies of intestinal hyperplasia. When bred to a strain expressing Cre recombinase in the podocytes of the kidney glomeruli (see Stock No. 008205 for example), this mutant mouse strain may be useful in studies of glomerular structural integrity. | ||
| 016209 | B6;129-Lrrk2tm2.1Shn/J | Repository- Live |
| Mice homozygous for the LRRK2 KO1 mutation are viable and fertile, with the promoter and exon 1 of the Lrrk2 (leucine-rich repeat kinase 2) gene deleted. No mRNA or protein expression from the targeted allele is observed in brain tissues, however and truncated mRNA signal is observed in kidney tissue. Homozygous mice do not exhibit neurodegeneration or neuropathological changes in the brain. In the kidneys, a tissue where LRRK2 is normally expressed at ~6-fold greater levels than brain, homozygous loss of LRRK2 results in renal atrophy by 20 months of age. This is accompanied by significant (~60-fold) age-dependent accumulation of aggregated α-synuclein and ubiquitinated proteins in the kidney. Specifically, homozygous KO kidneys show widely distributed cytosolic α-synuclein-immunoreactive granular aggregates (some amy also contain phospho-Ser-129 α-synuclein) or inclusions in boxy cells of renal tubules in the cortical area by 20 months of age. Other kidney ..... For more information please see the full phenotype on the strain data sheet | ||
| 016210 | B6;129-Lrrk2tm3.1Shn/J | Repository- Live |
| Mice homozygous for the LRRK2 KO2 mutation are viable and fertile, with exons 29-30 (encoding the first half of the Ras-like small GTPase domain) of the Lrrk2 (leucine-rich repeat kinase 2) gene deleted. No mRNA or protein expression from the targeted allele is observed in brain tissue, however some truncated mRNA is observed in kidney tissues. Homozygous mice do not exhibit neurodegeneration or neuropathological changes in the brain. In the kidneys, a tissue where LRRK2 is normally expressed at ~6-fold greater levels than brain, homozygous loss of LRRK2 results in renal atrophy by 20 months of age. This is accompanied by significant (~60-fold) age-dependent accumulation of aggregated α-synuclein and ubiquitinated proteins in the kidney. Specifically, homozygous KO kidneys show widely distributed cytosolic α-synuclein-immunoreactive granular aggregates (some of them may also contain phospho-Ser-129 α-synuclein) or inclusions in boxy cells of renal tubules in ..... For more information please see the full phenotype on the strain data sheet | ||
| 008634 | B6;129-Mavstm1Zjc/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Loss of MAVS (mitochondrial antiviral signaling) protein expression abolishes viral induction of interferons and prevents the activation of NFΚB (Rela, v-rel reticuloendotheliosis viral oncogene homolog A (avian)) and IRF3 (interferon regulatory factor 3) in multiple cell types, except plasmacytoid dendritic cells (pDCs). The protein is not required for interferon induction by cytosolic DNA or by Listeria monocytogenes. Mice lacking the protein fail to induce interferons in response to poly(I:C) stimulation and are severely compromised in immune defense against viral infection. Experimental results provide in vivo evidence that the cytosolic viral signaling pathway through the targeted gene is specifically required for innate immune responses against viral infection. | ||
| 011122 | B6;129-Mertktm1Grl/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. In response to endotoxin, homozygotes exhibit an increase in spleen size and a decrease in monocyte response. Retinal photoreceptor epithelial cells fail to phagocytose outer segment membranes resulting in complete photoreceptor degeneration and blindness.
When combined with the mutations Tyro3tm1Grl (Stock No. 007937) and Axltm1Grl (Stock No. 011121) mice exhibit a lymphoproliferative disorder, autoimmunity, increased apoptosis in multiple tissues, abnormal spermatogenesis and reduced (in females) fertility or infertility (in males). This mutant mouse strain may be useful in studies of autoimmunity, germ cell development homeostatic regulation and apoptosis. | ||
| 010528 | B6;129-Myf6tm2(cre)Mrc/J | Repository- Live |
| In this strain, the mouse myogenic factor 6 (Myf6) promoter drives expression of both the targeted gene and cre in differentiated myocytes of skeletal muscle lineage. When crossed with a strain carrying a loxP-flanked genomic segment of interest, tissue-specific excision of that segment may be achieved in the offspring. | ||
| 008475 | B6;129-Nlgn3tm1Sud/J | Repository- Live |
| These mice carry an R451C mutation in exon 7 of the gene. mRNA is detected by real-time PCR analysis of brain from homozygous animals. Mutant mice exhibit enhancements in inhibitory synaptic transmission as well as spacial learning and memory, but show deficits in social interaction. This mutant mouse strain may be useful in studies of the pathophysiology of autism. Exon 7 is additionally flanked by loxP sites. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical abnormalities. | ||
| 006377 | B6;129-Nrxn3tm1Sud Nrxn1tm1Sud Nrxn2tm1Sud/J | Repository- Live |
| Mice that are homozygous for all three targeted mutations die within 24 hours of birth. Although newborn mice are initially capable of directed movements and react to tactile stimuli, the integrative brain functions required for breathing are impaired. At birth, the body and brain weights of triple targeted mutation mice are indistinguishable. Assymetric type I and symmetric type II synapses in triple homozygotes are ultrastructurally normal. The density of symmetric (presumptive inhibitory) synapses are reduced whereas the density of asymmetric (presumptive excitatory) synapses are not. Neurotransmitter release is generally impaired due to reduced Ca2+ channel function. No protein product from any of the targeted genes is detected in brain tissue. Quantification of the levels of 22 other neuronal proteins detected no major changes. This mutant mouse strain represents a model that may be useful in studies of synaptic vesicle exocytosis mechanisms in neurons. | ||
| 015825 | B6;129-Pak6tm1Amin Pak7tm1Amin/J | Repository- Live |
| In this strain, exons in the p21 protein (Cdc42/Rac)-activated kinase 6 (Pak6) and 7 (Pak7) genes are disrupted with neomycin resistance (neo) cassettes, abolishing expression of both genes. Homozygotes are viable, fertile, and normal in size. Pak6 and Pak7 are members of the group B family of PAK serine/threonine kinases and are coexpressed in the cortex, striatum, and hippocampus. Both genes alos play a role in neuronal growth and cell survival. These mice have impaired cognitive function and deficits in learning and memory retention. They display a lower level of activity and decreased level of aggression compared to wildtype littermates. These mice may be useful for studying learning, memory, and locomotion. | ||
| 005549 | B6;129-Pax3tm1(cre)Joe/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Pax3 locus. Expression of the targeted gene product (mRNA and protein) mimics endogenous gene expression as detected by in situ hybridization and immunohistochemistry of homozygous embryos aged E12.5. No endogenous Pax3 gene product (protein) is detected in homozygotes and approximately one half of the endogenous gene product (protein) is detected in heterozygotes by Western blot analysis. Cre recombinase expression is detected in the dorsal neural tube and somites of E9 to 11.5 embryos and in the cardiac neural crest cells and colonic epithelia of E11.5 embryos. Recombination occurs in neural crest and somite derivatives of later gestation embryos. Homozygous mice have an embryonic lethal phenotype, failing to develop past embryonic day 18.5. At age E13.5 homozygous embryos display severe cardiac and neural tube defects (exencephaly), absent limb musculature and reduced or absent dorsal root ganglia. Heterozygous ..... For more information please see the full phenotype on the strain data sheet | ||
| 012653 | B6;129-Pax7tm1.1Fan/J | Repository- Live |
| These mice possess loxP sites on either side of exon 2 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 deleted in the cre-expressing tissue(s).
For example, when crossed to a strain expressing tamoxifen-inducible Cre recombinase in myogenic progenitor cells (see Stock No. 012476), this mutant mouse strain may be useful in studies muscle stem cells. | ||
| 012476 | B6;129-Pax7tm2.1(cre/ERT2)Fan/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Only approximately 10% of homozygotes live to adulthood. Surviving adult homozygotes are approximately half the size of heterozygote animals. The fertility of homozygotes has not been tested. In contrast to B6.129S-Pax7tm1(cre/ERT2)Gaka/J mice, which express a functional PAX7 gene product, no PAX7 protein is detected in 10 day old homozygotes. The Ds-Red is not detectable by immunostaining or FACS. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions in tissues such as myogenic progenitor cells and adult myogenic satellite cells. | ||
| 009067 | B6;129-Postntm1Jmol/J | Repository- Live |
| Homozyous targeted mutation mice are more prone to ventricular rupture in the first 10 days after a myocardial infarction, but surviving mice show less fibrosis and better ventricular performance. They also show less fibrosis and hypertrophy following long-term pressure overload. The developing feet and hearts of 1-day-old mice show no expression of protein. No significant protein is found in the extracellular matrix of the heart after postnatal development, although the valves show persistent expression within fibroblasts. Homozygotes are slightly smaller than wild-type and heterozygous animals. This strain may be useful in studies of cardiac remodeling and hypertrophy. | ||
| 014168 | B6;129-Pot1atm1.1Tdl/J | Repository- Live |
| These targeted mutant mice possess loxP sites on either side of the third coding exon of the Pot1a (protection of telomeres 1A) gene. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice that express Cre recombinase, resulting offspring will not express the targeted gene in cre-expressing tissues. | ||
| 014169 | B6;129-Pot1btm1.1Tdl/J | Repository- Live |
| These targeted mutant mice possess loxP sites on either side of the third coding exon of the Pot1b (protection of telomeres 1B) gene. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the gene. This strain may be useful in studies of telomere biology. | ||
| 009071 | B6;129-Ppiftm1Jmol/J | Repository- Live |
| Mitochondria isolated from the livers, hearts, and brains of homozygous targeted mutant mice are resistant to swelling and permeability transition in vitro. Hepatocytes and fibroblasts are largely protected from Ca2+-overload and oxidative stress-induced cell death. Mice are protected from ischaemia/reperfusion-induced cell death in vivo. This strain may be useful in studies of mitochondrial-driven cell death. | ||
| 006375 | B6;129-Rab3btm1Sud Rab3atm1Sud Rab3dtm1Rja Rab3ctm1Sud/J | Repository- Live |
| Mice homozygous for all four targeted mutations die shortly after birth due to respiratory problems. No protein products from the targeted genes are detected in brain or pituitary tissue. Mutant mice display no apparent changes in synapse structure or brain composition except for the loss of rabphilin. Analysis of cultures of hippocampal neurons uncovered no significant change in spontaneous or sucrose-evoked release of presynaptic vesicles. The size of the excitatory postsynaptic current (EPSC) induced by action potentials is ~30% smaller in mutant mice as compared to controls. This mutant mouse strain may be useful in studies of synaptic vesicle exocytosis mechanisms in neurons. | ||
| 010673 | B6;129-Runx1tm3.1Spe/J | Repository- Live |
| These mice possess loxP sites on either side of exon 4 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 4 deleted in the cre-expressing tissues. When bred to a strain with inducible Cre recombinase during development (see Stock No. 003556 for example), this mutant mouse strain may be useful in studies of hematopoiesis and development. | ||
| 004293 | B6;129-Shhtm2Amc/J | Repository- Live |
| Mice that are homozygous for the Shhtm2Amc targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This conditional mutant contains two loxP sites flanking exon 2 of the targeted allele. Cre-mediated recombination excises exon 2 and some surrounding intronic sequence, generating a null allele. When the conditional mutant is crossed with a ubiquitously-expressing Cre recombinase carrier to remove Shh activity in the early embryo, the resulting phenotype resembles the Shh null mutation. These conditional mutant mice may be mated to strains expressing Cre recombinase to study the effects of temporal and tissue-specific ablation of the targeted allele. This mutant mouse strain represents a model that may be useful in studies of developmental defects resulting from disruption of Shh-dependent pathways.
When bred to a strain expressing Cre recombinase under the control of a tet ..... | ||
| 008041 | B6;129-Sirt1tm1Ygu/J | Repository- Live |
| Mice homozygous for this targeted allele (SirT1co/co) are viable and fertile. A loxP-flanked neomycin cassette just upstream of exon 4 and a third loxP site downstream of exon 4 were inserted to create this targeted mutant Sirt1 allele. The floxed mutation does not affect SIRT1 protein expression in MEFs or mammary gland tissue in homozygotes. When bred to mice that express Cre recombinase, the resulting offspring have exon 4 (encoding an evolutionarily conserved Sir2 motif) deleted in cre-expressing tissue(s); (the donating investigator reports only one recombination event: complete removal of the neomycin cassette and exon 4, leaving a single loxp). These SirT1co/co mice may be useful in generating conditional mutants for studying transcriptional regulation and the role of estrogen, insulin growth factor-1 (IGF-1), and transcription factors (including NF-kappaB) in mammary gland development, mammary cancer, apoptosis, and metabolic di ..... For more information please see the full phenotype on the strain data sheet | ||
| 009600 | B6;129-Six2tm3(EGFP/cre/ERT2)Amc/J | Repository- Live |
| While heterozygous mice are viable and fertile with no reported abnormalities, homozygous mice die shortly after birth. The Six2GCE "knock-in" allele both abolishes Six2 gene function and expresses an eGFPCreERT2 fusion protein (EGFP and creERT2 fusion protein) from the Six2 promoter/enhancer elements. While EGFP immunofluorescence is observed in nephron progenitor population cap mesenchyme from the onset of metanephric kidney development, Cre-ERT2 fusion gene activity is inducible; observed in the same cells only following tamoxifen administration. As such, when Six2GCE mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequences in the Six2-expressing cells of the offspring.
The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor which does not bind its natural ligand ..... | ||
| 013074 | B6;129-Synj1tm1Pdc/J | Repository- Live |
| Homozygous Synj1 (synaptojanin 1) targeted mutation mice exhibit neurological defects and die within approximately 24 hours of birth due to an inability to feed. Phosphatidylinositol-4,5-bisphosphate (PI(4,5)P2) levels are increased, and clathrin-coated vesicles accumulate in the area that surrounds the synaptic vesicle cluster in nerve endings. Western blot analysis demonstrates that protein is not expressed in knockout mice. This strain may be useful in studies of synaptic vesicle recycling. | ||
| 013064 | B6;129-Tas1r1tm1Csz/J | Repository- Live |
| This strain carries a targeted mutation of the Tas1r1 (taste receptor, type 1, member 1) gene which encodes a component of the heterodimeric G-protein coupled umami (monosodium L-glutamate, MSG) taste sensor. Homozygous mice lack expression of the gene and have normal viability, body weight, overall anatomy and general behavior. Taste receptor cells appear normal morphologically and numerically. Although the mice show robust neural responses to sour (citric acid), salty (NaCl), bitter (6-n-propylthiouracil, PROP), and sweet (D-amino acids, sucrose, maltose, glucose, saccharin) tastants, responses to umami L-amino acid tastants are lost. This strain may be useful in studies of taste and nutrient sensing. | ||
| 013066 | B6;129-Tas1r3tm1Csz/J | Repository- Live |
| This strain carries a targeted mutation of the Tas1r3 (taste receptor, type 1, member 3) gene which encodes a component of the heterodimeric G-protein coupled sweet receptor and umami (monosodium L-gluamate, MSG) sensor. Homozygous mice lack expression of the gene and have normal viability, body weight, overall anatomy and general behavior. Taste receptor cells appear normal morphologically and numerically. Although the mice show robust neural responses to sour (citric acid), salty (NaCl), and bitter (6-n-propylthiouracil, PROP) tastants, umami (L-amino acid) taste responses are completely lost and sweet (D-amino acids, sucrose, maltose, glucose, saccharin) tastant responses are severely defective. This strain may be useful in studies of taste and nutrient sensing. | ||
| 013067 | B6;129-Tas2r105tm2Csz/J | Repository- Live |
| This strain carries a targeted mutation of the Tas2r105 (taste receptor, type 2, member 105; also known as T2R5) gene which encodes a cycloheximide-specific G-protein coupled receptor associated with bitter taste sensing. Homozygotes selectively lack electrophysiological responses to the taste of cycloheximide, but not to other bitter substances tested. Responses to sweet, umami, salty and sour tastants are not affected. Homozygous mice lack expression of the targeted gene and have normal viability, body weight, overall anatomy and general behavior. Taste receptor cells appear normal morphologically and numerically. This strain may be useful in studies of taste and chemosensation. | ||
| 013598 | B6;129-Tcf4tm1Zhu/J | Repository- Live |
| A targeting vector was designed to replace the C-terminus DNA-binding domain of transcription factor 4 (Tcf4 or E2-2) gene with a neomycin (neo) selection cassette. Homozygotes are born at a low frequency and die within the first week of life. E2-2 is a widely expressed E2A-related helix-loop-helix (HLH) protein required for the generation of normal numbers of pro-B cells in mouse embryos. While homozygous E2-2 mutant embryos are capable of making B cells, they produce only half as many as wildtype. When crossed to mice containing a (Atoh1)-lacZ transgene, β-galactosidase staining is evident in anterior extramural migratory stream (AES) cells which accumulate in the region lateral to the pontine nucleus. The resulting mice exhibit a reduction in size of the pontine nucleus and a lack of migration of neuronal precursors to the region of the pontine nucleus. Mice heterozygous for the mutation are viable, fertile, and normal in size. This strain may be ..... For more information please see the full phenotype on the strain data sheet | ||
| 012603 | B6;129-Tgfbr2tm1Karl/J | Repository- Live |
| These TβRII floxed mutant mice possess loxP sites flanking exon 4 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 4 deleted in cre-expressing tissues. This strain may be useful for studying the cellular and mechanical role of TGF-β in regulating development, hematopoiesis, wound healing, and immune function.
For example, when crossed to a strain expressing Cre recombinase in the neural tube, midbrain and dorsal spinal cord (see Stock No. 007807), this mutant mouse strain may be useful in studies of DiGeorge syndrome. For example, when crossed to a strain expressing interferon inducible Cre recombinase (see Stock No. > ..... | ||
| 008045 | B6;129-Trp53tm2Holl/J | Repository- Live |
| In this mutant strain, exons 4-9 of the endogenous mouse Trp53 gene have been replaced with the homologous human TRP53 region. Transcription of the human sequence is under the control of the endogenous mouse promoter. The inserted human sequence segment encodes the DNA binding domain and the TRP53 polyproline domain. This latter domain contains a polymorphism at codon 72 that encodes either arginine or proline in human populations. This mutant strain expresses the proline variant at codon 72 and the related strain, 129-Trp53tm1Holl/J (Stock No. 004301) expresses the arginine variant. Mice that are homozygous for this mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Immortalized cell lines derived from primary embryonic fibroblasts harvested from these mice frequently harbor a TRP53 (p53) mutation in the DNA binding domain t ..... For more information please see the full phenotype on the strain data sheet | ||
| 012587 | B6;129-Ubbtm3Nat/J | Repository- Live |
| A CMV/beta actin (Z/AP) promoter located 2 kb 5' of the Ubb (ubiquitin B) gene drives constitutive expression of a nuclear-localized beta-galactosidase/neomycin resistance protein reporter (NLS-beta-geo) in the absence of Cre-mediated recombination. Following Cre-mediated recombination, the NLS-beta-geo coding region is excised and a downstream open reading frame is expressed. The downstream open reading frame codes for a single large protein (tdTomato/Tobacco etch virus protease (TEVP), a 6xMyc epitope, a TEVP cleavage site, post-synaptic density protein (PSD95) fused to green fluorescence protein (GFP) with a 3xHA epitope) which cleaves itself into two pieces shortly after translation. When Cre-mediated recombination occurs in neurons, the amino terminal piece (tdTomato/TEVP, a 6xMyc epitope, a TEVP cleavage site) labels all axon and dendrites, and the carboxy-terminal portion (PSD95, GFP, 3xHA epitope) labels presynaptic structures. | ||
| 010563 | B6;129-Xpctm1Ecf/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, and normal in size. No gene product (mRNA) is detected by Northern blot analysis using an exon 11-15 probe of MEFs from homozygotes. A truncated transcript is detected when an exon 7-10 probe is used. MEFs from homozygotes are more sensitive to UV radiation cytotoxicity and exhibit impaired DNA repair. Homozygous mice are more susceptible to skin cancer after UVB radiation exposure and to liver and lung cancer after chemical carcinogen (acetylaminofluorene) exposure. Homozygotes develop lung tumors as early as 6 months of age. By 16-17 months of age all homozygotes have lung tumors. Most classified as adenomas, some as adenocarcinomas and all were Non-small Cell Lung Cancers (NSCLCs). A few tumors progress to malignant metatstatic adenocarcinoma. Heterozygotes exhibit an increased predisposition to skin cancer after exposure to UVB radiation when compared to wild-type controls. This mutant mouse strain may be usefu ..... For more information please see the full phenotype on the strain data sheet | ||
| 006401 | B6;129P-Trpa1tm1Kykw/J | Repository- Live |
| Homozygous mice are viable and fertile. The donating investigator reports a dramatic loss of fecundity after 5-6 months of age. The targeting vector contains an endoplasmic reticulum (ER) retention signal (KDEL), which is reported to sequester the potential truncated mRNA product in the ER. The vector also contains an IRES-PLAP reporter gene, allowing extracellular antibody staining/chromogenic development tracking of cells normally expressing the endogenous gene. Homozygous mice display behavioral deficits in response to mustard oil, cold, and punctate mechanical stimuli. These mice have a normal startle reflex to loud noise, a normal sense of balance, a normal auditory brainstem response, and normal transduction currents in vestibular hair cells. These mutants may be useful in neurobiological studies involving dorsal root ganglion neurons and cells of the inner ear, as well as for auditory, temperature, or chemical irritant trials. | ||
| 008529 | B6;129P-Tg(Neurog1-cre/ERT2)1Good/J | Repository- Live |
| These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the mouse neurogenin 1, Neurog1, promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain. The mutant mouse estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the Cre/ESR1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Tamoxifen administration induces Cre recombination in the cortex, hippocampus, thalamus, hypothalamus and cochlear-vestibular ganglion. Hemizygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnorma ..... For more information please see the full phenotype on the strain data sheet | ||
| 015854 | B6;129P2-Foxl2tm1(GFP/cre/ERT2)Pzg/J | Repository- Live |
| These Fox L2-GCE knock in mice utilize a tamoxifen inducible Cre-mediated recombination system. A GFP-Cre/ERT2 cassette (GCE) was inserted into the Foxl2, forkhead box L2, locus. No green fluorescence was detected by direct fluorescence microscopy, however, immunohistochemical analysis revealed GFP expression in embryos, 15.5 embronic days of age. Tamoxifen administration induces Cre recombination in a small population of granulosa precursor cells in the medulla of the developing ovary of embryos, 15.5 embronic days of age. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make the strain homozygous. This strain was transferred from the collection of the GenitoUrinary Development Molecular Anatomy Project (GUDMAP). | ||
| 012601 | B6;129P2-Lyve1tm1.1(EGFP/cre)Cys/J | Repository- Live |
| These Lyve-1 EGFP-hCre mice have the Lyve1 (lymphatic vessel endothelial hyaluronan receptor 1) promoter driving expression of Cre recombinase and enhanced green fluorescent protein (EGFP) in lymphatic endothelial cells (LECs). Gene expression from the targeted gene is not blocked. Immunofluorescence analysis of tissue shows selective EGFP staining in the nuclei of cells expressing Lyve1. In the absence of antibody staining, however, the EGFP fluorescence is not readily detected. When crossed with a strain carrying a loxP-flanked genomic segment of interest, tissue-specific excision of that segment may be achieved. Greater than 90% excision efficiency has been reported in LECs with lower excision rates in some hematopoietic precursor cells (e.g. CD45+ lymphocytes and myeloid cells) and blood endothelial cells. This strain is useful for conditional ablation of genes in the lymphatic endothelium and studies of lymphatic development, function and lymphang ..... For more information please see the full phenotype on the strain data sheet | ||
| 009336 | B6;129P2-Map1lc3btm1Mrab/J | Repository- Live |
| Homozygous (LC3β-/-) mice are viable and fertile, harboring an IRES Tau-lacZ/floxed PGK-neo allele that disrupts exons III-IV of the targeted gene. No LC3β protein expression from the targeted locus is detected in developing head and trunk tissues at embryonic day (E)14.5 or E18.5. No lacZ expression is reported. While homozygotes have a mild survival advantage in the absence of feeding (suggesting compensatory increase(s) in other autophagy proteins), no other overt phenotype is reported. LC3β-/- mouse embryonic fibroblasts (MEFs) exhibit reduced fibronectin synthesis but retain normal levels of fibronectin protein. These LC3β-mutant mice may be useful in studying the role of murine light chain RNA-binding proteins in fibronectin regulation as well as starvation and autophagy. | ||
| 006847 | B6;129P2-Mecp2tm1Bird/J | Repository- Live |
| These mice possess two functional loxP sites flanking exons 3-4 of the targeted gene on the X chromosome. Homozygous females and hemizygous males are viable and fertile. Northern blot analysis showed the expected mature transcript from the Mecp2lox locus. Also detected was an unspliced beta-globin transcript that was introduced into the locus as part of the targeting vector. When these mutant mice are bred to mice that express cre recombinase, resulting offspring will have exons 3-4 deleted in the cre-expressing tissue(s). Mice with this X-linked floxed mutation may be useful in neurological and developmental studies of Rett syndrome. For example, when crossed to a strain expressing Cre recombinase in nervous tissue (see Stock No. 003771), this mutant mouse strain develops a neurological phenotype that mimics Rett syndrome. When bred to a strain expressing Cre recombinase in embryonic fo ..... | ||
| 002596 | B6;129P2-Nos2tm1Lau/J | Repository- Live |
| Mice homozygous for the Nos2tm1Lau targeted mutation resemble wildtype mice in appearance and histology. Homozygotes are viable and fertile. Unlike Nos1 and Nos3, Nos2 is synthesized de novo in response to a variety of inflammatory stimuli. Induction of Nos2 results in the production of large amounts of nitric oxide (NO) over prolonged periods of time. Excessive NO production has been shown to be beneficial through its antitumor and antimicrobial activities. It is also thought to cause tissue damage and contribute to pathology in a variety of inflammatory conditions including rheumatoid arthritis, inflammatory bowel disease, cardiac allograft rejection, hepatoxicity, myocardial ischemia-reperfusion and septic shock. NO has been demonstrated to play a role in the regulation of blood pressure and hemodynamics. In an LPS-induced model of septic shock, Nos2tm1Lau homozygotes had virtually no serum NO response, but were ..... For more information please see the full phenotype on the strain data sheet | ||
| 008069 | B6;129P2-Pvalbtm1(cre)Arbr/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Pvalb, parvalbumin, locus. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in more than 90% of neurons that express parvalbumin, such as interneurons in the brain and proprioceptive afferent sensory neurons in the dorsal root ganglia. This mutant mouse strain represents a model that may be useful in studies of neuronal differentiation. | ||
| 012336 | B6;129P2-Terf1tm2.1Tdl/J | Repository- Live |
| These TRF1F mice harbor loxP sites flanking exon 1 (encoding the translation start site) of the telomeric repeat binding factor 1 locus. Telomeres serve a dual role in protecting the chromosome ends from degradation/repair activities and in intracellular signaling for regulating cell proliferation. Mammalian telomeres are formed by tandem TTAGGG sequence repeats bound by a specialized complex of six telomere-associated proteins called the shelterin complex. As TRF1 is one of the components of shelterin, these TRF1F mutant mice may be useful in generating conditional mutations for studying the shelterin complex of telomeres, telomere maintenance, chromosomal stability, cancer, and aging. | ||
| 008776 | B6;129P2-Zbtb7btm2Litt/J | Repository- Live |
| Exons 2 and 3 of the targeted gene were replaced with enhance green fluorescent protein (EGFP). In the T lymphocytes of heterozygotes, GFP is specifically expressed in CD4+ cells. In homozygotes, CD4+ cells are almost completely absent because of a redirection of MHC class II restricted T cells to the cytotoxic lineage. B220+ cells also express GFP. | ||
| 013193 | B6;129S-Barhl1tm1Xia/J | Repository- Live |
| In this strain, the entire coding region of the endogenous BarH-like 1 (Barhl1) gene is replaced with a lacZ (β-galactosidase) reporter gene and a loxP-flanked neomycin resistance (neo) cassette, abolishing gene function. Homozygous mice are viable, fertile, and normal in size, with β-gal staining in Barhl1 expressing tissues. LacZ expression in embryos and neonates is evident in all hair cells, but is more abundantly observed in the cochlear outer hair cells. LacZ expression in adults is strong in the outer hair cells, and weak in the inner and vestibular hair cells, with persistent expression in hair cells of the organ of Corti. These mice exhibit age-related progressive degeneration of both cochlear outer and cochlear inner hair cells in the organ of Corti, resulting in hearing loss. The progression is apical-to-basal for outer hair cell and basal-to-apical for inner hair cells. Barhl1-/- mice have elevated audit ..... For more information please see the full phenotype on the strain data sheet | ||
| 002848 | B6;129S-Fcgr2btm1Ttk/J | Repository- Live |
| Mice homozygous for the Fcgr2tm1Ttk targeted mutation are viable and fertile. Myeloid and lymphoid development is normal. Immunoglobulin levels are elevated in response to thymus-dependent and thymus-independent antigens. Mice are sensitive to IgG-triggered degranulation and have an enhanced passive cutaneous analphylaxis reaction. | ||
| 002073 | B6;129S-Gt(ROSA)26Sor/J | Repository- Live |
| Mice hemizygous or homozygous for the ROSA26 retroviral insertion display no distinguishing phenotype. lacZ is expressed in all tissues of the developing embryo and in most tissues of the adult mouse. | ||
| 012569 | B6;129S-Gt(ROSA)26Sortm32(CAG-COP4*H134R/EYFP)Hze/J | Repository- Live |
| Ai32 mice heterozygous for the Rosa-CAG-LSL-ChR2(H134R)-EYFP-WPRE conditional allele are viable and fertile. A loxP-flanked STOP cassette prevents transcription of the downstream ChR2(H134R)-EYFP fusion gene. Because this CAG promoter driven reporter construct was targeted for insertion into the Gt(ROSA)26Sor locus, ChR2(H134R)-EYFP expression is determined by which tissue(s) express Cre recombinase. When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissues; resulting in expression of the ChR2(H134R)-EYFP fusion protein. The donating investigator reports that Ai32 mice do not express ChR2(H134R)-EYFP prior to introduction of Cre recombinase. Fusion protein expression following exposure to cre can be detected by EYFP fluorescence (and presumably by mRNA (in situ hybridization) and antibody staining (immunohistochemistry); although this was not tested by the donating investigator). ..... For more information please see the full phenotype on the strain data sheet | ||
| 012570 | B6;129S-Gt(ROSA)26Sortm34.1(CAG-Syp/tdTomato)Hze/J | Repository- Live |
| Ai34D (or Ai34Δneo) mice heterozygous for the Rosa-CAG-LSL-Synaptophysin-tdTomato-WPRE conditional allele are viable and fertile. A loxP-flanked STOP cassette prevents transcription of the downstream Synaptophysin-tdTomato fusion gene. The Synaptophysin-tdTomato fusion protein is composed of near-full-length mouse synaptophysin protein fused in-frame to the amino terminus of the tdTomato fluorescent protein. Because the CAG promoter driven reporter construct was targeted for insertion into the Gt(ROSA)26Sor locus, Synaptophysin-tdTomato expression is determined by which tissue(s) express Cre recombinase. When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissues; resulting in expression of the Synaptophysin-tdTomato fusion protein. The donating investigator reports that Ai34D mice do not express Synaptophysin-tdTomato prior to introduction of Cre recombinase. Following exposure to ..... For more information please see the full phenotype on the strain data sheet | ||
| 012735 | B6;129S-Gt(ROSA)26Sortm35.1(CAG-AOP3/GFP)Hze/J | Repository- Live |
| Ai35D (or Ai35Δneo) mice heterozygous for the Rosa-CAG-LSL-Arch-GFP-WPRE conditional allele are viable and fertile. A loxP-flanked STOP cassette prevents transcription of the downstream Arch-GFP fusion gene (see below for detailed description of Arch-GFP). Because the CAG promoter driven reporter construct was targeted for insertion into the Gt(ROSA)26Sor locus, Arch-GFP expression is determined by which tissue(s) express Cre recombinase. When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissues; resulting in expression of the Arch-GFP fusion protein.
The donating investigator reports that Ai35D mice do not express Arch-GFP prior to introduction of Cre recombinase. Fusion protein expression following exposure to cre can be detected by GFP fluorescence and mRNA (in situ hybridization) [and presumably by antibody staining (immunohistochemistry); although this was not test ..... For more information please see the full phenotype on the strain data sheet | ||
| 014538 | B6;129S-Gt(ROSA)26Sortm38(CAG-GCaMP3)Hze/J | Repository- Live |
| Ai38 mice heterozygous for the Rosa-CAG-LSL-GCaMP3-WPRE conditional allele are viable and fertile. A loxP-flanked STOP cassette prevents transcription of the downstream GCaMP3 fusion gene (see below for detailed description of GCaMP3). Because the CAG promoter driven reporter construct was targeted for insertion into the Gt(ROSA)26Sor locus, GCaMP3 expression is determined by which tissue(s) express Cre recombinase. When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissues; resulting in expression of the fluorescent calcium indicator protein, GCaMP3. The donating investigator reports that Ai38 mice do not express GCaMP3 prior to introduction of Cre recombinase. Following exposure to Cre recombinase, GCaMP3 expression (EGFP fluorescence) is detected in the cre-expressing tissues. In the absence of calcium binding, low EGFP fluorescence is reported. Following calcium binding (s ..... For more information please see the full phenotype on the strain data sheet | ||
| 014539 | B6;129S-Gt(ROSA)26Sortm39(CAG-HOP/EYFP)Hze/J | Repository- Live |
| Ai39 mice heterozygous for the Rosa-CAG-LSL-eNpHR3.0-EYFP-WPRE conditional allele are viable and fertile. A loxP-flanked STOP cassette prevents transcription of the downstream eNpHR3.0-EYFP fusion gene (see below for detailed description of eNpHR3.0-EYFP). Because the CAG promoter driven reporter construct was targeted for insertion into the Gt(ROSA)26Sor locus, eNpHR3.0-EYFP expression is determined by which tissue(s) express Cre recombinase. When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissues; resulting in expression of the eNpHR3.0-EYFP fusion protein. The donating investigator reports that Ai39 mice do not express eNpHR3.0-EYFP prior to introduction of Cre recombinase.
Fusion protein expression following exposure to cre can be detected by EYFP fluorescence and mRNA (in situ hybridization) [and presumably by antibody staining (immunohistochemistry); although this was ..... For more information please see the full phenotype on the strain data sheet | ||
| 010983 | B6;129S-Id3tm1Pzg/J | Repository- Live |
| These mutant mice express Red Fluorescent Protein from the endogenous Id3 (inhibitor of DNA binding 3) locus. Strong red fluorescence is observed in the kidney. Red fluorescence is also detected in the urogenital system of E15.5 heterozygous embryos. Fluorescence mimics the endogenous expression pattern. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make this strain homozygous.
This strain was transferred from the collection of the GenitoUrinary Development Molecular Anatomy Project (GUDMAP). | ||
| 010618 | B6;129S-Jag1tm2Grid/J | Repository- Live |
| These mice possess loxP sites on either side of exon 4, which encodes the DSL (Delta-Serrate-Lag2) domain, of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 4 deleted in the cre-expressing tissue(s). The exon 4-deleted allele produces a nonfunctional JAG1 protein.
When bred to a strain with Cre recombinase expression during development in the telencephalon and discrete head structures, such as the otocyst (see Stock No. 006084 for example), this mutant mouse strain may be useful in studies of developmental inner ear defects. When bred to a strain with Cre recombinase expression in endothelial cells during embryogenesis and adulthood (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 014541 | B6;129S-Nos1tm1.1(cre/ERT2)Zjh/J | Repository- Live |
| The nNOS-CreER-KI (or nNOS-CreERT2-KI) knock-in allele was designed to both abolish neuronal nitric oxide synthase 1 (Nos1) gene function and express CreERT2 fusion protein from the Nos1 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible and can be observed following tamoxifen administration. As such, when nNOS-CreER-KI mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Nos1-expressing cells of the offspring.
Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The donating investigator reports that the phenotype of nNOS-CreER-KI homozygous mice has not been assessed. However, nNOS-CreER-KI homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (abnormal neuron differentiation, increased ..... | ||
| 014635 | B6;129S-Nr1h2tm1Djm/J | Repository- Live |
| In this strain, maintained on a mixed C57BL/6 x 129S6 background, a neomycin (neo) resistance cassette replaces exons 5-6 of the nuclear receptor subfamily 1, group H, member 2 (Nr1h2) gene, abolishing gene function. Homozygous are viable, fertile, and normal in size. Also known as liver X receptor beta (Lxrβ), Nr1h2 binds to retinoid X receptors (RXRα, RXRβ, RXRγ; NR2B1, NR2B2, and NR2B3) and is activated by oxysterols to regulate the expression of genes involved in cholesterol metabolism. Homozygous Lxrβ-/- mice lose their ability to appropriately regulate cholesterol, lipid, and carbohydrate metabolism, and have defects in immune function. These defects are more severe when combined with the knockout of Lxrα (available as Stock No. 013763). These mice may be useful for studying lipid and cholesterol metabolism, and the regulation of the immune r ..... For more information please see the full phenotype on the strain data sheet | ||
| 014181 | B6;129S-Prkd1tm1Eno/J | Repository- Live |
| These mice possess loxP sites flanking exons 12 through 14 of the targeted gene, which encode part of the catalytic domain. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 12 through 14 deleted in the cre-expressing tissue(s).
When bred to a strain with Cre recombinase expression in cardiomyocytes (see Stock No. 011038 for example), this mutant mouse strain may be useful in studies of cardiac response and remodeling due to pathological stress. | ||
| 010686 | B6;129S-Snai1tm2Grid/J | Repository- Live |
| These mice possess loxP sites on either side of exons 2 and 3 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 and 3 deleted in the cre-expressing tissue(s). | ||
| 010987 | B6;129S-Sox18tm1(GFP/cre/ERT2)Pzg/J | Repository- Live |
| These Sox18-GCE mutant mice have a tamoxifen inducible Cre-mediated recombination system. A GFP-Cre/ERT2 cassette (GCE) was inserted into the Sox18, SRY-box containing gene 18, locus. Tamoxifen administration induces Cre recombination. Green fluorescence is detected in the kidneys and ovary of E15.5 heterozygous embryos. Cre recombinase activity is detected in the kidney from E15.5 heterozygous embryos. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygotes are viable and fertile. This strain was transferred from the collection of the GenitoUrinary Development Molecular Anatomy Project (GUDMAP). | ||
| 003244 | B6;129S-Tnfrsf1atm1Imx Il1r1tm1Imx/J | Repository- Live |
| Mice homozygous for both targeted mutations (called TNFRp55(-/-)-IL-1RI(-/-), TNFR1/IL1R1 or IL-1R1/TNFR1 KO) are viable and fertile, lacking both interlekin-1 beta type 1 receptor (IL1R1) and tumor necrosis factor alpha p55 (type 1) receptor (TNFR1). Double homozygotes exhibit characteristics of both the single "knockouts" including reduced inflammatory responses, reduced delayed-type hypersensitivity response, and remain highly susceptible to infection by Listeria monocytogenes. Homozygous mutant mice also have defects in Peyer's patch development, splenic architecture, formation of germinal centers and liver regeneration. Furthermore, IL-1R1/TNFR1 KO mice exhibit alterations in rapid eye movement sleep (REMS) and non-rapid eye movement sleep (NREMS) (a sleep phenotype different from that observed for mice singly homozygous for one or the other of these cytokine receptors), as well as differences in NREMS and REMS following sleep deprivation compared to control mice. | ||
| 014605 | B6;129S-Tg(CMV-BBS1)6Vcs/J | Repository- Live |
| The CMV-BBS1 transgene contains a simian cytomegalovirus (sCMV) IE94 promoter driving expression of the open reading frame of the human Bardet-Biedl syndrome 1 (BBS1) gene, tagged with a 5' 3xFLAG tag and 4xMyc tag. Homozygous mice are viable and fertile. BBS is a pleiotropic disorder characterized by retinal and photoreceptor degeneration, obesity, polydactyly, renal abnormalities, hypogenitalism and cognitive impairment. BBS is associated with an increased incidence of hypertension, diabetes mellitus and heart defects. These mice are phenotypically normal and express the transgene in the eye and testes. | ||
| 007001 | B6;129S-Tg(UBC-cre/ERT2)1Ejb/J | Repository- Live |
| Mice hemizygous for this Cre-ERT2 transgene are viable and fertile. Mice from this founder line have strong tamoxifen-inducible cre activity in all reported tissue types. The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OHT) and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to OHT. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone may be coadministered. When these Cre-ERT2 mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the flanked sequences in widespread cel ..... For more information please see the full phenotype on the strain data sheet | ||
| 013543 | B6;129S1-Dnm3tm1.1Pdc/J | Repository- Live |
| These mice possess loxP sites on either side of exon 2 of the Dnm3 (dynamin 3) gene. Mice that are homozygous for this floxed allele are viable, fertile, and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this floxed strain is useful in eliminating expression of Dnm3 in a tissue-specific fashion. Following germline deletion, complete loss of expression has been documented in brain, lung and testis (sites of major expression) and resultant mice are healthy, viable and fertile. This strain may be useful in further characterizing the role of this gene. | ||
| 003018 | B6;129S1-Il1r1tm1Roml/J | Repository- Live |
| Mice homozygous for the Il1r1tm1Roml targeted mutation exhibit a reduced inflammatory response and no response to interleukin-1 alpha or beta. IL1 receptor type I deficient mice have a reduced delayed type hypersensitivity response and are highly susceptible to infection by Listeria monocytogenes. | ||
| 010619 | B6;129S1-Lfngtm1Grid/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. At birth, homozygotes exhibit shortened trunk and tails. Severely affected homozygotes soon die due to respiratory difficulties related to malformed rib cages. Less severely affected homozygotes survive into adulthood. By age embryonic day 8.5, homozygotes exhibit defective somite formation, with indistinct boundaries and irregular shape and size. Vertebral column formation is disrupted, and ribs are bifurcated and fused. Although sclerotome cells condense, the metameric pattern is not maintained. Fusions in the dorsal root ganglia and axonal patterning defects are revealed by histological analysis. | ||
| 010547 | B6;129S1-Notch3tm1Grid/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern blot analysis of brain, lung and heart tissue or Western blot analysis of lung and brain tissue from homozygotes. Homozygotes exhibit disorganized artery wall morphology, and thin vascular smooth muscle cell coat and processes. | ||
| 010544 | B6;129S1-Notch4tm1Grid/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis of lung and kidney tissue from homozygous adult animals, and in situ hybridization of homozygous embryos. Homozygotes exhibit a slightly elevated systolic blood pressure. | ||
| 013122 | B6;129S1-Smc1atm1Mbk/J | Repository- Live |
| This strain contains mutations in exon 19 of the endogenous structural maintenance of chromosomes 1A, Smc1a, gene. Serine to Alanine mutations in amino acid residues 957 and 966 of exon 19 abolish both of the damage-induced phosphorylation sites of Smc1a. Homozygous Smc1S957AS966A mice are viable, fertile, and normal in size. Cells from these mice show normal aggregation of Nibrin (NBS1) and breast cancer 1 (BRCA1) proteins, and normal activation and migration of Ataxia Telangiectasia, mutated (ATM) at the site of DNA breaks, all of which are required for Smca1 phosphorylation. Smca1 is not phosphorylated in fibroblasts from these mice, they exhibit a defective S-phase checkpoint, decreased survival, and increased chromosomal aberrations and radiosensitivity after DNA damage. These mice may be useful for studying cell survival and chromosomal stability after DNA damage. | ||
| 010722 | B6;129S1-Snai2tm2Grid/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, subfertile, and are smaller in size than wildtype controls. Homozygotes have diluted coat color and areas of depigmentation, sometimes exhibiting white forehead blaze and spots on tails and feet. From birth to weaning age (approximately 3 weeks), homozygotes exhibit slowed growth rate and by 3 weeks of age weigh approximately 70% of wildtype control. After weaning, mutant growth rates are similar to wildtype, but mutants remain small in size. Homozygous adults develop eye infections (suppurative conjunctivitis and blepharitis). Homozygous males have reduced testes size due to reduced seminiferous tubules and are slightly subfertile, producing smaller litters sizes. Approximately 15% of homozygous males are infertile. Spermatogenesis is normal, however, in fertile homozygotes. Homozygotes exhibit macrocytic anemia, decreased hematocrit and leukocyte numbers. T cell differentiation is impaired and thymus size is dimi ..... For more information please see the full phenotype on the strain data sheet | ||
| 005217 | B6;129S1-Tlr3tm1Flv/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Northern blot analysis detects a truncated gene product (mRNA), which is not functional. Unlike wildtype macrophages, macrophages derived from these animals fail to produce inflammatory cytokines, IFN-alpha or IFN-beta when challenged with poly(I:C), polyinosine-polycytidylic acid, a synthetic dsRNA analog. Splenocytes isolated from homozygotes do not respond to viral dsRNA and have diminished IL-6 production. Mice homozygous for the mutation are resistant to poly(I:C) induced shock and produce lower levels of IL-12. This mutant mouse strain may be useful in studies of the toll-like receptor pathway of innate immune response. | ||
| 003263 | B6;129S2-Cdkn1atm1Tyj/J | Repository- Live |
| Homozygotes are viable and fertile. p21, the product of the Cdkn1a gene, belongs to a family of regulators, known as cyclin-dependent kinase inhibitors, which modulate progression through the cell cycle. Following serum restimulation, expression of p21 is superinducible by cycloheximide in wild-type but not in p53-deficient cells. p53 appears to play a critical role in p21 induction following DNA damage. p21 can be regulated independently of p53 during normal tissue development, following serum stimulation, and during cellular differentiation. | ||
| 003374 | B6;129S2-H2dlAb1-Ea/J | Repository- Live |
| Mice that are homozygous null for MHC class II genes H2-Ab1, H2-Aa, H2-Eb1, H2-Eb2, H2-Ea are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. MHC class II gene products (mRNA or protein) are not detected. A dramatic decrease is observed in the number of CD4 positive T cells in thymus, spleen and lymph nodes. This strain should serve as a suitable recipient of xenogenic Class II MHC transgenes allowing the engineering of mouse models of human MHC Class II-associated diseases. | ||
| 002254 | B6;129S2-Il6tm1Kopf/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of lipopolysaccharide (LPS) challenged macrophages. Bioassay and enzyme-linked immunosorbent assay (ELISA) analysis of serum from LPS-challenged homozygotes reveals no detectable protein activity. These interleukin 6 (IL6) mutant mice show defects in responses to various viruses and in inflammatory responses to tissue damage or infection. Of note, IL6-mutant mice may be available on different genetic backgrounds including mixed B6;129S2 (Stock No. 002254), C57BL/6J (Stock No. 002650), and BALB/cByJ (Stock No. 001026). | ||
| 004669 | B6;129S2-Itgb3tm1Hyn/J | Repository- Live |
| Mice that are homozygous for this targeted allele are viable and fertile. No gene product (protein) is detected on the surface of platelets. Significant (50%) embryonic lethality attributed to fetal hemorrhaging and placental defects is observed. Until three weeks of age, additional pup loss may occur due to hemorrhaging in the skin and gastrointestinal tract. Gastrointestinal tract bleeding is commonly observed in adults and is frequently associated with an enlarged spleen. Erythrocyte number, hemoglobin, hematocrits and thrombus formation are all reduced while bleeding time is prolonged. Varying degrees of liver and kidney necrosis are also observed. Although increased numbers of osteoclasts are observed (3.5 fold over that seen in heterozygotes) they appear to be dysfunctional, having a reduced ability to resorb whale dentin in vitro. Mice are osteosclerotic and hypocalcemic. Enhanced tumor angiogenesis and vascular endothelial growth factor-induced blood vessel growth are observed. ..... For more information please see the full phenotype on the strain data sheet | ||
| 009358 | B6;129S2-Lats1tm1Tx/J | Repository- Live |
| Homozygous animals exhibit a lack of mammary gland development, infertility and growth retardation. Accompanying these defects are hyperplastic changes in the pituitary and decreased serum hormone levels. The reproductive hormone defects of homozygotes are reminiscent of isolated luteinizing hormone (LH)-hypogonadotropic hypogonadism and corpus luteum insufficiency in humans. Furthermore, Homozygous mice develop soft tissue sarcomas (some by 4-10 months of age) and ovarian stromal cell tumors (by 3 months of age) and are highly sensitive to carcinogenic treatments. Data demonstrates a role for this gene in mammalian tumorigenesis and specific endocrine dysfunction. | ||
| 003379 | B6;129S2-Scarb1tm1Kri/J | Repository- Live |
| The class B, type I scavenger receptor (Srb1 or Scarb1) is a cell surface HDL receptor that can recognize the apolipoproteins on the surface of the HDL particle. It plays a key role in determining the levels of plasma lipoprotein cholesterol (primarily HDL) and the accumulation of cholesterol stores in the adrenal gland.In this strain plasma cholesterol (primarily HDL) concentrations increase by 31% in heterozygotes and 125% in homozygotes, as compared to wild type controls. Also, cholesterol levels in adrenal tissue in heterozygous and homozygous mutants decrease by 42% and 72% respectively, relative to wild type controls. The plasma concentration of Apoa-I, the major protein in HDL, is unchanged in mutant animals, relative to wild type controls.Homozygous females are infertile; homozygous males are fertile. Please note that the donating investigator reports that the number of homozygotes resulting from a cross between heterozygotes is significantly lower than what the expected Mendel ..... For more information please see the full phenotype on the strain data sheet | ||
| 003641 | B6;129S4-C3tm1Crr/J | Repository- Live |
| Mice homozygous for the C3 (complement component C3) targeted mutation are viable and fertile. Homozygous mutants exhibit an increased susceptibility to lethal infection by Group B streptococci. Reductions in peritoneal mast cell degranulation, production of tumor necrosis factor alpha, neutrophil infiltration and bacterial clearance have also been reported in these mice. Homozygotes also demonstrate a profound defect in antibody response to T cell dependent antigens. They show a diminished level of peanut agglutin+ germinal centers and a failure in isotype switching despite normal B cell signalling in vitro. | ||
| 011001 | B6;129S4-Col1a1tm1(tetO-Pou5f1,-Klf4,-Sox2,-Myc)Hoch/J | Repository- Live |
| Mice homozygous for the Col1a1-tetO-OKSM targeted mutation are viable and fertile, although the donating investigator reports that homozygous mice do not breed as well as expected. Expression of the OKSM cassette (four mouse reprogramming genes Oct4 [Pou5f1], Klf4, Sox2, and c-Myc [Myc]) is controlled by the tet-responsive element (tetO; also called tetracycline operator, tet-operator, or tetracycline-responsive element [TRE]) with CMV minimal enhancer-less promoter. When bred with another mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), expression of the OKSM cassette can be regulated with the tetracycline analog doxycycline (dox) in the resulting double mutant offspring. Somatic expression of the OKSM reprogramming factors allows multiple somatic cell types to be directly reprogrammed to generate induced pluripotent stem cells (iPSCs). Because the reprogram ..... For more information please see the full phenotype on the strain data sheet | ||
| 014592 | B6;129S4-Col1a1tm1(tetO-mCherry)Eggn/J | Repository- Live |
| These Col1a1-tetO-H2B-mcherry mutant mice contain a tet-responsive element (tetO) and a histone H2B-mCherry fusion protein, targeted to the collagen, type I, alpha 1 (Col1a1) locus. Homozygous are viable, fertile, and normal is size. When bred with another mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), expression of mCherry can be regulated with the tetracycline analog doxycycline (dox) in the resulting double mutant offspring.
Specifically, breeding Col1a1-tetO-H2B-mcherry mice with R26-rtTA mice (see Stock No. 006965) results in double mutant mice which express mCherry in embryonic stem (ES) cells, and differentiated trophoblast stem (TS) cells after administration of dox. These mice may be useful for visualizing pluripotent cells. | ||
| 002785 | B6;129S4-E2f1tm1Meg/J | Repository- Live |
| Mice homozygous for defective E2f1 are viable and fertile. They show thymocyte maturation defects due to a failure of apoptosis, eventually resulting in increased proliferation and increased tumorigenesis. As mutant mice age, they show exocrine gland dysplasia and testicular atrophy. Mutant mice develop a broad spectrum of cancers, although mammary carcinomas were not observed on this genetic background. Mutant mice are also protected from experimental autoimmune encephalomyelitis (EAE). These mice may be useful in studies of apoptosis, cancer, thymocyte development/selection, diabetes, autoimmunity, and multiple sclerosis. | ||
| 004424 | B6;129S4-F8tm1Kaz/J | Repository- Live |
| Mice that are homozygous for the targeted, X chromosome-linked mutant allele are viable and fertile. Homozygous females and carrier males have less than 1% of normal factor VIII activity and exhibit prolonged clotting times. Care should be exercise when obtaining tail clippings for the purpose of genotyping. Clipped tails of affected mice must be cauterized immediately or the mouse will succumb to excessive blood loss within several hours. Only mice that have reached the age of 4 weeks or older should have their tails clipped. Published reports indicate that spontaneous bleeding into joints or soft tissues, and that no bleeding difficulties are apparent during birth. These mice recapitulate key features of hemophilia A and provide an excellent model for use in exploring gene therapy strategies.
NOTE: It has been the experience of The Jackson Laboratory, in contrast to the primary publication, and possibly due to genetic background differences as a result of continuous inbreed ..... | ||
| 016168 | B6;129S4-Fbxl3Gt(FHCRC-GT-S13-12G1)Sor/JtJ | Repository- Live |
| In this strain, the insertion of a ROSAFARY gene trap vector creates a null allele in the Fbxl3 (F-box and leucine-rich repeat protein 3) gene. Homozygotes have a free running period of 27 hours as measured by running wheel behavior (23.7 hours in wildtype controls). | ||
| 012463 | B6;129S4-Foxd1tm1(GFP/cre)Amc/J | Repository- Live |
| Heterozygous mice are viable and fertile, normal in size and do not display any gross physical or behavioral abnormalities. The DI states that the strain is homozygous lethal. The FoxD1GC allele expresses an eGFPCre fusion protein (EGFP and cre fusion protein) from the Foxd1 promoter/enhancer elements. When Foxd1 is induced, EGFP immunofluorescence is observed during kidney development in metanephric mesenchyme in cells fated to become stromal cells of the kidney. When FoxD1GC mice are bred with mice containing loxP-flanked sequence, Cre-mediated recombination will result in deletion of the floxed sequences in the Foxd1-expressing cells of the offspring. These mice may be useful for studying therapeutic strategies directly targeting pericyte differentiation in vivo and may productively impact fibrotic kidney disease. | ||
| 012464 | B6;129S4-Foxd1tm2(GFP/cre/ERT2)Amc/J | Repository- Live |
| Heterozygous mice are viable and fertile, normal in size and do not display any gross physical or behavioral abnormalities. The DI states that the strain is homozygous lethal. The Foxd1GCE allele expresses an eGFPCreERT2 fusion protein (EGFP and creERT2 fusion protein) from the Foxd1 promoter/enhancer elements. Foxd1 is induced, and EGFP immunofluorescence is observed, during kidney development in metanephric mesenchyme in cells fated to become stromal cells of the kidney. Cre-ERT2 fusion gene activity is inducible; observed in the same cells only following tamoxifen administration. When Foxd1GCE mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequences in the FoxD1-expressing cells of the offspring. These mice may be useful for studying therapeutic strategies directly targeting pericyte differen ..... For more information please see the full phenotype on the strain data sheet | ||
| 002852 | B6;129S4-Jak3tm1Ljb/J | Repository- Live |
| Mice homozygous for the Jak3tm1Ljb mutation are viable and fertile. B cell development is blocked at pre-B resulting in a significant decrease in peripheral IgM+ B cells. The thymus is small but T cell development is relatively normal. There are increased numbers of CD4+ Cd8- cells in some homozygotes. Proliferative responses to mitogenic signals are defective and Il2 receptor signaling is blocked. The overall phenotype results in a severely immunocompromised mouse. | ||
| 016835 | B6;129S4-L3mbtl1tm1.1Haho/J | Repository- Live |
| The mouse L3mbtl1 gene is the ortholog of the Drosophila tumor suppressor lethal(3)malignant brain tumor (l(3)mbt) gene. Targeting of the Drosophila gene results in embryonic lethality due to a transformation of larval brain cells.
The mouse gene is one of nine mouse genes that carry MBT (malignant brain tumor)-domains (Drosophila has only 3 MBT-domain genes). The protein binds histones in a methylation state-dependent manner and contributes to a higher order chromatin structure and transcriptional repression.
Although non-redundant roles involving oncogene suppression and hematopoiesis regulation were expected with this knockout allele, none have been found. Homozygotes are born at expected frequencies, are fertile, and do not display any obvious physical or behavioral abnormalities. Complete necropsy and histological analysis of all tissues reveal no abnormalities. The gene is normally expressed in brain, but no changes in brain development, spontan ..... | ||
| 012639 | B6;129S4-Mapttm3(HDAC2)Jae/J | Repository- Live |
| Mice homozygous for the HDAC2OE allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Expression of Hdac2 from the microtubule-associated protein tau (Mapt) locus, results in neuron-specific overexpression of Hdac2. This overexpression results in a 2-3 fold expression of Hdac2, increased histone deacetylation, and impaired synaptic plasticity in the hippocampus leading to a negative function in regulating memory formation. This strain may be useful for studying the functional and structural synaptic changes and neuronal adaptive responses implicated in memory formation and storage. | ||
| 006414 | B6;129S4-Mc4rtm1Lowl/J | Repository- Live |
| The mice have a loxp-flanked transcriptional blocking (loxTB) sequence that prevents normal endogenous gene transcription and translation from the endogenous locus. As such, homozygous mice are devoid of functional mRNA in all tested regions of the brain. Homozygous mice exhibit severe early-onset obesity, accompanied by hyperphagia, increased snout-anus length and hyperinsulinemia. The function of this disrupted allele can be restored by the enzymatic activity of Cre-recombinase. These mutant mice may be useful in studies of neurobiology, obesity, diabetes, hunger/appetite, and fat and energy metabolism.
When bred to a strain expressing Cre recombinase in the hypothalamus see Stock No. 006395 for example), this mutant mouse strain exhibits as intermediate phenotype in comparison to homozygous null mice. | ||
| 008752 | B6;129S4-Nhlh2tm1Irk/J | Repository- Live |
| Male mice homozygous for this targeted mutation exhibit bilateral cryptochism, hypogonadism, azoospermia, low testosterone and follicle stimulating hormone levels and lack instinctual male sexual behavior. Homozygous females are hypogondal unless raised in the presence of male mice, have estrous cycle defects, and reduced fertility. No gene product (mRNA) is detected by Northern blot analysis of embryos. Initially, homozygous male mice, 4 to 7 weeks of age, have a reduced weight compared to wildtype controls. By 12 weeks of age, homozygous males are significantly heavier than wildtype, and mutants progressively increase weight with age. Female homozygotes 5 to 6 weeks of age have normal body weight, however by 7 weeks of age they are significantly heavier than wildtype controls. The increased body weight is due to increased adipose tissue, with the exception of female homozygotes more than 52 weeks of age that exhibit increased lean body mass. Male heterozygotes and homozygotes, ..... For more information please see the full phenotype on the strain data sheet | ||
| 008214 | B6;129S4-Pou5f1tm2Jae/J | Repository- Live |
| Mice homozygous for this Oct4-EGFP mutation are viable and fertile. They harbor an IRES-EGFP fusion cassette downstream of the stop codon of the Oct4 (Pou5f1) gene. When treated with specific transcription factors (Oct4, Sox2, c-Myc and Klf4), some Oct4-EGFP murine embryonic fibroblasts (MEFs) have the properties of induced pluripotent stem (iPS) cells. Such iPS cells have the DNA methylation, gene expression and chromatin state of embryonic stem cells and can form viable chimeras, contribute to the germ line, and generate live late-term embryos when injected into tetraploid blastocysts. These Oct4-EGFP mutant mice may be useful for fluorescent labeling of embryonic stem cells, as well as for the selection of iPS cells (i.e. epigenetic reprogramming of somatic cells into pluripotent embryonic stem cells).
Of note, these Oct4-EGFP mutant mice may also be used in conjunction with Oct4-neo mice (Stock No. 008204); a si ..... | ||
| 008154 | B6;129S4-Pparatm1Gonz/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. An altered response to a group of compounds (peroxisome proliferators) that induce peroxisome proliferation and hepatocarcinogenesis is observed. No peroxisome proliferation response is detected when these mice are challenged with classical peroxisome proliferators. Typically, such a response includes hepatomegaly, peroxisome proliferation and transcriptional activation of a set of target enzyme genes. Accumulation of lipid droplets observed in liver tissue suggests that Ppara is involved in maintaining the homeostasis of hepatic lipid metabolism. Homozygotes exhibit increased gonadal adipose tissue stores, abnormal epidermal development and delayed wound healing. This mutant mouse strain may be useful in studies of lipid metabolism, cell proliferation, diabetes, obesity, and wound healing. | ||
| 010944 | B6;129S4-Socs3tm1Ayos/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. This mutant mouse strain may be useful in generating conditional mutations to study cytokine signaling, inflammatory responses, energy homeostasis and diabetes.
For example, when crossed to a strain expressing Cre recombinase in the myeloid cell lineage (see Stock No. 004781), this mutant mouse strain may be useful in studies of cytokine signalling and inflammation. When crossed to a strain expressing Cre recombinase in the central and peripheral nervous system (see Stock No. 003771), this mutant mouse strain may be useful in studies of leptin sensitivity and obesity. When crossed to a strain expressing Cre recombinase ..... | ||
| 014649 | B6;129S4-Yy1tm2Yshi/J | Repository- Live |
| These mice possess loxP sites on either side of exon 1 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 1 deleted in the cre-expressing tissue(s).
When crossed with mice that express Cre recombinase specifically in early B-cell progenitors, this mutant mouse strain may be useful in studies of B-cell maturation. | ||
| 009357 | B6;129S6-Adam10tm1Zhu/J | Repository- Live |
| These mice possess loxP sites on either side of exon 3 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice that express Cre recombinase, the resulting offspring will have this region deleted in the cre-expressing tissues. When bred to a strain expressing Cre recombinase in T cells for example(see Stock No. 003802), this mutant mouse strain may be useful in studies related to thymocyte developmental defects. | ||
| 006410 | B6;129S6-Chattm1(cre)Lowl/J | Repository- Live |
| Homozygous mice maintained at The Jackson Laboratory are viable and fertile. An "IRES-Cre" sequence is inserted downstream of the stop codon such that cre expression is controlled by the endogenous Chat gene promoter. Chat gene expression, however, is unaffected. Cre recombinase activity is reported in all cholinergic neurons. These mice may be useful for "Cre-lox" technology applications in neurobiology, including studies of motor function, learning and memory, Alzheimer's disease, and Down syndrome, and in obesity and diabetes research.
View cre expression characterization. | ||
| 006028 | B6;129S6-Epha2tm1Jrui/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile with no overt developmental or behavioral abnormalities. The Jackson Laboratory is distributing these mice on their original C57BL/6;129S6 mixed background. The published phenotype of these mutant mice is described below. In mutant mice of a mixed BALB/c, C57BL/6, and 129S6 background, murine pulmonary microvascular endothelial cells (MPMEC) isolated from homozygotes express no endogenous protein. MPMEC show impaired ephrin-A1-induced vascular assembly and defective migration both in vitro and in vivo. In addition, MPMEC from homozygous mice exhibit decreased angiogenesis and fail to activate Rac1 in response to ephrin-A1 in vivo. Mutant mice crossed to BALB/c for 7 generations are protected from tumor progression, angiogenesis and metastasis following metastatic mammary adenocarcinoma cell transplantation. These mutant mice may be useful in studies of postnatal angiogenesis (endothelial cell migra ..... | ||
| 013579 | B6;129S6-Fam3btm1Bkht/J | Repository- Live |
| Homozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by RT-PCR and Western blot analysis of pancreatic islets and small intestines from homozygotes. Male mice that are homozygous for the targeted mutation and 4 to 6 months of age exhibit higher blood glucose levels in glucose tolerance tests when compared to wildtype controls. Although, insulin sensitivity is normal in mutant mice, insulin levels are elevated after glucose stimulation (intraperitoneal glucose injection) due to decreased hepatic insulin clearance. Glucose intolerance is not observed in mutant female mice. Isolated pancreatic islets from male homozygotes have impaired glucose-stimulated insulin secretion and calcium signaling. Male homozygotes have reduced hepatic glucose production (HGP) and increased insulin-mediated HGP suppression conditions as determined by hyperinsulinemic-euglycemic clamp assays. Further ..... For more information please see the full phenotype on the strain data sheet | ||
| 013101 | B6;129S6-Gadd45btm1Flv/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Isolated T cells exhibit increased proliferation with activation. Th1 cells from homozygotes are more resistant to activation induced apoptosis. 10 month old homozygotes exhibit mild splenomegaly. Homozygotes are more susceptible to experimental autoimmune encephalomyelitis, with longer duration and severity: 60% of homozygotes die when challenged with a higher dose of heat-inactivated Mycobacterium tuberculosis, compared to no deaths in controls. Immunocomplex deposits develop in the glomeruli of homozygotes. | ||
| 007908 | B6;129S6-Gt(ROSA)26Sortm14(CAG-tdTomato)Hze/J | Repository- Live |
| Ai14 mice hemizygous for this Rosa-CAG-LSL-tdTomato-WPRE::deltaNeo conditional allele are viable and fertile. A loxP-flanked STOP cassette prevents transcription of the downstream red fluorescent protein variant (tdTomato). When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissue(s); resulting in expression of tdTomato. Because this CAG promoter driven reporter construct was targeted for insertion into the Gt(ROSA)26Sor locus, tdTomato expression is determined by which tissue(s) express Cre recombinase. Ai14 mice are not expected to express tdTomato prior to introduction of Cre recombinase and tdTomato expression following exposure to cre is expected to be detectable by fluorescence and mRNA (in situ hybridization). These Ai14 mice are useful as a Cre reporter strain; expressing the red fluorescent protein variant, tdTomato, following Cre-mediated recombination.
The Allen I ..... | ||
| 007905 | B6;129S6-Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/J | Repository- Live |
| Ai9 mice hemizygous for this Rosa-CAG-LSL-tdTomato-WPRE conditional allele are viable and fertile. A loxP-flanked STOP cassette prevents transcription of the downstream red fluorescent protein variant (tdTomato). When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissue(s); resulting in expression of tdTomato. Because this CAG promoter driven reporter construct was targeted for insertion into the Gt(ROSA)26Sor locus, tdTomato expression is determined by which tissue(s) express Cre recombinase. The donating investigator reports that Ai9 mice do not express tdTomato prior to introduction of Cre recombinase and tdTomato expression following exposure to cre can be detected by fluorescence and mRNA (in situ hybridization). Of note, the FRT sites flanking the mutation allow for additional targeted replacement of the reporter sequences through Flp-mediated recombination if ..... For more information please see the full phenotype on the strain data sheet | ||
| 013157 | B6;129S6-Lrp4tm1Her/J | Repository- Live |
| The Lrp4 hypomorphic allele (Lrp4ECD, Lrp4 EC STOP, Lrp4hypo, Megf7-, Lrp4STOP1723) contains a premature stop codon within the exon immediately upstream of the transmembrane segment. Much of the targeted exon and 3' adjacent intron is absent. No functional full-length transcripts are detected in brain tissue. The transcript generated is out of frame beyond the sequences coding for the transmembrane segment, which results in a truncated protein with loss of the transmembrane and intracellular domains of the LRP4 protein. While the LRP4 extracellular domain (ECD) is expressed normally, the lack of a membrane anchor leads to shedding/secretion of the ECD into the extracellular space. This results in diminished, but not completely absent, LRP4 interactions with its extracellular ligands (i.e., hypomorphic phenotype). Mice homozygous for this Lrp4 hypomorphic allele are viable and fertile. Homozygous mice exhibit growth retardation, fully penetrant polysyndactyly wi ..... For more information please see the full phenotype on the strain data sheet | ||
| 013763 | B6;129S6-Nr1h3tm1Djm/J | Repository- Live |
| Homozygous Nr1h3 (nuclear receptor subfamily 1, group H, member 3) targeted mutation mice lose their ability to respond normally to dietary cholesterol. Mice maintained on cholesterol diets fail to induce transcription of the Cyp7a1 (cytochrome P450, family 7, subfamily a, polypeptide 1) gene, a rate-limiting enzyme in bile acid synthesis, and fail to induce expression of ABCG5 (ATP-binding cassette, sub-family G (WHITE), member 5) and ABCG8 (ATP-binding cassette, sub-family G (WHITE), member 8), ATP-binding cassette transporters that are required for cholesterol secretion into bile. Large amounts of cholesterol rapidly accumulate in the liver leading to impaired hepatic function. Impaired reverse cholesterol transport from peripheral tissues is also observed. The ability to regulate lipids and carbohydrates is also lost. Defects in innate immune responses by activated macrophages have also been described. Males are not infertile, but show a significantly higher number ..... For more information please see the full phenotype on the strain data sheet | ||
| 005993 | B6;129S6-Pcsk9tm1Jdh/J | Repository- Live |
| Homozygous mice are viable and fertile with no behavioral abnormalities. No expression of the endogenous RNA or protein is observed in liver. Homozygotes have reduced plasma cholesterol levels; apolipoprotein B (apoB)-containing low-density liproprotein (LDL) is nearly undetectable and apolipoprotein E (apoE)-containing high density liproprotein (HDL) levels are reduced 30%. Homozygotes show increased hepatic LDL-receptor (LDLR) protein (but not RNA) expression. Homogygous mice also have accelerated clearance of circulating cholesterol. Lovastatin addition to the diet of homozygous mice results in further increased hepatic LDLR and LDL clearance from the blood. Heterozygous mice have intermediate plasma cholesterol and LDL clearance. This mouse may be useful in studies of lipid homeostasis, cholesterol metabolism, apolipoprotein function, and statin treatment for hypercholesterolemia. | ||
| 013041 | B6;129S6-Ppp1r14ctm1Uhl/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator reports that the expected number of homozygotes are produced in heterozygous crosses. No gene product (mRNA) is detected by RT-PCR analysis of brain tissue from homozygotes. SNP analysis revealed that the Oprm1 allele variant, which is located close to the targeted gene, is from C57BL/6. Homozygotes exhibit increased phosphatase 1 activity in the thalamus. Homozygotes develop faster morphine tolerance in a hot plate assay ("supraspinal" nociceptive response assessment) and a rightward shift in dose response curve for morphine reward in conditioned place preference when compared to wildtype controls. | ||
| 012716 | B6;129S6-Sun2tm1Mhan/J | Repository- Live |
| Synaptic myonuclear anchorage is not perturbed in Sun2 (Sad1 and UNC84 domain containing 2) homozygous targeted mutation mice. When combined with a Sun1 targeted mutation, however (see Stock No. 012715), defects are seen. Additionally, Sun1/Sun2 compound mutant pups die neonatally and display neuronal migration defects in the brain. Homozygous Sun2 mice are fertile and display no obvious abnormalities in growth and development. This gene does not appear to play a critical role in meiosis. This strain may be useful in neuromuscular research. | ||
| 012362 | B6;129S6-Tg(Camk2a-cre/ERT2)1Aibs/J | Repository- Live |
| Mice hemizygous for the Camk2a-CreERT2 transgene are viable and fertile, with expression of CreERT2 fusion protein (CreERT2 fusion protein) directed to neural populations by the mouse calcium/calmodulin-dependent protein kinase II alpha promoter region. Cre-ERT2 fusion gene activity is inducible; observed at high levels following tamoxifen administration. When Camk2a-CreERT2 transgenic mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Camk2a-expressing cells of the double mutant offspring. Specifically, the donating investigator reports that the Camk2a-CreERT2 transgene directs reporter gene expression in sparse populations of neurons in the cortex, hippocampus, striatum, and other structures in the absence of tamoxifen. Following tamoxifen administration, reporter gene expression is turned on in widespread populations of neurons in the same regions ..... For more information please see the full phenotype on the strain data sheet | ||
| 002385 | B6;129S7-Fyntm1Sor/J | Repository- Live |
| Mice homozygous for the Fyntm1Sor targeted mutation are viable and fertile displaying no overt phenotype. T cell receptor signaling is defective in homozygous mutant mice and are characterized by a reduction in levels of tyrosine-phosphorylated proteins, failure to flux calcium in response to TCR cross-linking, and a reduction in production of calcium-related IL2. THY-1-induced proliferation is also reduced in thymocytes but not in splenic T cells. Neurological defects include blunted long-term potentiation (LTP), impaired special learning, and altered hippocampal development. | ||
| 002077 | B6;129S7-Ldlrtm1Her/J | Repository- Live |
| Mice homozygous for the Ldlrtm1Her mutation have an elevated serum cholesterol level of 200-400 mg/dl and they have very high levels (>2,000 mg/dl) when fed a high fat diet. Normal serum cholesterol in the mouse is 80-100 mg/dl. | ||
| 012604 | B6;129S7-Lrp1tm2Her/J | Repository- Live |
| These LRPflox/flox mutant mice possess a floxed Neo cassette and a single loxP sites downstream of exon 2 of the targeted low-density lipoprotein (LDL) receptor-related protein (LRP) 1 gene, Lrp1. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, the resulting offspring will have exons 1 and 2 deleted in the cre-expressing tissue, resulting in inactivation of Lrp1 gene function. This strain may be useful for studying physiological role of LRP in the uptake of cholesterol-rich lipoproteins from circulation and in maintenance of plasma lipid homeostasis. | ||
| 011039 | B6;129S7-Map3k7tm1Mds/J | Repository- Live |
| These mice carry a floxed allele of Map3k7 (mitogen-activated protein kinase kinase kinase 7). When bred to mice expressing cre recombinase, exon 1 of the targeted gene is deleted in the cre-expressing tissues of the offspring. This strain may be useful in studies of Wolff-Parkinson-White syndrome, electrophysiological and biochemical properties of the heart.
For example, when crossed to a strain expressing Cre recombinase in cardiac muscle cells (see Stock No. 011038), this mutant mouse strain may be useful in studies of cell metabolism. | ||
| 002096 | B6;129S7-Rag1tm1Mom/J | Repository- Live |
| Mice homozygous for the Rag1tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdcscid/Prkdcscid) (Prkdcscid mice produce some B cells and IgM). They have no CD3+ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8-CD4- and most are IL2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings. | ||
| 013038 | B6;129S7-Smad5tm1Zuk/J | Repository- Live |
| In this strain, the allele replaces exon 2 of the endogenous MAD homolog 5 (Smad5) gene with a PGK-hprt selection cassette, abolishing gene function. Mice homozygous for the Smad5 allele have an embryonic lethal phenotype and do not survive past E11.5. Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous embryos lack ectopic vasculogenesis and hematopoiesis in the amnion, lack both a foregut pocket and entrance to the hindgut diverticulum, and are absent of primordial germ cells. The allantois is fused to the chorion and is not elongated. These embryos also exhibit a defect in heart looping and embryonic turning associated with Left-right asymmetry. At later stages, mutant embryos have craniofacial and neural tube abnormalities, are edematous, and after E9.0 the yolk sacs contain red blood cells but still lack well organized vasculature. These mice may be useful for studying ventrolateral morpho ..... For more information please see the full phenotype on the strain data sheet | ||
| 002972 | B6;129S7-Sod1tm1Leb/J | Repository- Live |
| Mice homozygous for the Sod1tm1Leb targeted mutation produce no SOD1 protein. Female homozygous mice are infertile, while male homozygous mice reproduce normally. | ||
| 004758 | B6;129S7-Wnt5atm1Amc/J | Repository- Live |
| Homozygous null mice have a perinatal lethal phenotype and do not survive long after birth due to respiratory failure. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by immunohistochemical analysis in homozygotes. Homozygous 17.5 to 18.5 embryonic day old embryos exhibit severe shortening in all outgrowing axes of the body and limbs with loss of distal structures (absence of tail, limb digits and genital tubercle), and truncated facial features. Newborn homozygous mice succumb to asphyxia due to abnormal lung development and display shortened trachea, overexpansion of the distal airways and impaired capillary/alveolar coupling. This mutant mouse strain may be useful in studies of distal outgrowth of internal organs and organization of morphogenesis in development. | ||
| 008219 | B6;129S7-Zpbptm1Zuk/J | Repository- Live |
| Female mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous males are infertile due to severe abnormal spermatozoa morphology and diminished sperm motility. Heterozygous males exhibit terato-asthenozoospermia (increase in the percentage of abnormal sperm) and globozoospermia, but are fertile with normal fecundity. Electron microscopic examination of sperm reveals ultrastructural abnormalties. No gene product (mRNA or protein) is detected by Northern or Western blot analysis or testicular tissue and sperm. This mutant mouse strain may be useful in studies of acrosomal biogenesis and spermiogenesis. | ||
| 012711 | B6;129X1-Dkkl1tm1.1Mldp/J | Repository- Live |
| In this strain, exons 2-4 of the endogenous mouse Dickkopf-Like 1 (Dkkl1) gene are removed, abolishing gene function. Homozygous mice are viable, normal in size, and do not display any gross physical or behavioral abnormalities. While homozygous females have no fertility problems, homozygous males have reduced fertilization efficiency. In these mice, DKKL1 expression was absent in developing trophectoderm and spermatocytes, and in the acrosome of mature sperm. This absence of expression did not result in infertility as it is not required for development of sperm or fertility in vivo. These mice may be useful for studying spermatogenesis and fertility. | ||
| 009069 | B6;129X1-Dusp6tm1Jmol/J | Repository- Live |
| Homozygous targeted mutant mice have larger hearts than wild-type mice at every age examined. They show greater rates of myocyte proliferation during embryonic development and in the early postnatal period, resulting in cardiac hypercellularity. This lends protection against decompensation and hypertrophic cardiomyopathy following long term pressure overload and myocardial infarction injury in adult mice. Embryonic fibroblasts derived from these mice also show reduced apoptosis rates as compared to wildtype. Homozygotes are viable, fertile and otherwise overtly normal. This strain may be useful in studies of heart function and disease. | ||
| 003723 | B6;129X1-Il15ratm1Ama/J | Repository- Live |
| Il15ra mediates the high-affinity binding of Il15, a pleiotropic cytokine implicated in the development of innate immune cells. Mice that are homozygous null for Il15ra are viable and fertile. They are lymphopenic as result of decreased proliferation and homing of lymphocytes to peripheral lymph nodes. As a result, marked hypocellularity of lymph nodes is observed. Deficiencies are seen in levels of natural killer cells, natural killer T cells, CD8+ T lymphocytes, TCR delta/gamma intraepithelial lymphocytes and memory phenotype CD8+ T cells.
Loss of IL15RA expression has also been shown to induce a functional oxidative shift in fast muscles, substantially increasing fatigue resistance and exercises capacity. Knockout mice run greater distances and have greater ambulatory activity than control animals. | ||
| 003692 | B6;129X1-Sncatm1Rosl/J | Repository- Live |
| Homozygous null mice are viable, fertile, normal in size and do not display any gross abnormalities. No gene product (mRNA or protein) is detected in brain tissue. A wild-type complement of dopamine neurons, fibers and synaptic terminals is present and the overall brain architecture appears to be intact. They suffer from a reduction in total striatal dopamine and exhibit an attenuated locomotor response when given amphetamine. Normal dopamine release is observed upon stimulation of the nigrostriatal terminal with a single electrical pulse. When multiple stimuli are applied however, null mice exhibit an accelerated recovery of dopamine release. A similar acceleration is seen in wildtype mice in the presence of increased extracellular calcium. The phenotype observed in homozygous Snca-null mice suggests that Snca is an activity-dependent negative regulator of dopamine neurotransmission. | ||
| 008467 | B6;129X1-Wnt7btm2Amc/J | Repository- Live |
| Mice homozygous for the Wnt7bc3 allele are viable and fertile, with loxP sites flanking exon 3 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region deleted in the cre-expressing tissue(s). Unlike other Wnt7b mutant alleles, this Wnt7bc3 conditional allele is not affected by alternative exon 1 splicing. These Wnt7bc3 mice may be useful in generating conditional mutations for studying the role of Wnt7b (and other Wnt family members) in development and canonical Wnt signaling cascades, including lung differentiation and growth. In addition, these mice may also be useful in conjunction with other Wnt7 mutant strains including Wnt7b knockout mice (Stock No. 004693) and Wnt7a mutant mice (Stock No. 004715).
When bred to a strain expressing Cre recom ..... | ||
| 002717 | B6;C-Cntn1m1J/GrsrJ | Repository- Live |
| Mice homozygous for the Cntn1m1J mutation are smaller than their wild-type littermates by 4 to 7 days of age, and appear emaciated by 2 weeks of age. They are ataxic, most die by 18 to 20 days of age, and all die by 30 days of age. Histological assessment found normal neuromuscular junctions, normal Purkinje cell dendritic arborization, and no morphological anomalies in brain. The twitch and titanic force generated by excised extensor digitorum longus muscles was found to be normal when normalized for the muscle weight of these smaller mutants. Necropsies showed pale livers, little food in the stomachs, and gas bubbles in the intestines. | ||
| 012433 | B6;C3-Tg(ACTA1-rtTA,tetO-cre)102Monk/J | Repository- Live |
| These transgenic mice have a tetracycline (doxycycline) inducible Cre-mediated recombination system that is specific for skeletal muscle myocytes. Two transgenic constructs were coinjected to generate this strain. The first transgene contains cre recombinase under the control of the tetO, tetracycline-responsive regulatory element and a second transgenic construct contains the reverse tetracycline-controlled transactivator, rtTA (Tet-On), under the control of the human ACTA1, actin, alpha 1, skeletal muscle promoter. Mice hemizygous for the transgenic inserts are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Cre mRNA expression is detected in mice treated with doxycycline (dox) specifically in limb muscle. In the absence of dox, very weak Cre mRNA expression is detected in skeletal muscle. When crossed with a reporter strain, inducible Cre recombinase activity is restricted to skeletal muscle tissues. Slight Cre ..... For more information please see the full phenotype on the strain data sheet | ||
| 008605 | B6;C3-Tg(CAG-DsRed,-EGFP)5Gae/J | Repository- Live |
| Hemizygous IRG transgenic mice are viable and fertile, with widespread expression of a loxP-flanked optimized red fluorescent protein variant (DsRed-Express) directed to embryonic and adult tissues by the CAG promoter prior to exposure to Cre recombinase. When bred to cre-expressing mice, the resulting offspring have the DsRed-Express cassette deleted in the cre-expressing tissue(s), allowing expression of the enhanced green fluorescent protein (EGFP) cassette located just downstream. These IRG transgenic mice are a double-fluorescent, Cre-reporter strain; with widespread expression of red fluorescence prior to Cre recombinase exposure, and green fluorescence following cre-mediated recombination in a pattern determined by cre expression, and should provide a versatile tool for analyzing complex cellular relationships in a wide variety of tissues. For example, when using IRG transgenic mice along with Nestin-Cre mice (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 010827 | B6;C3-Tg(FOXJ1-EGFP)85Leo/J | Repository- Live |
| These transgenic mice express Green Fluorescent Protein in ciliated cells of tracheal, bronchial, nasal epithelium, oviduct, testis and in ciliated ependymal cells lining brain ventricles. Transgene expression is restricted to ciliated cells as detected by immunohistochemical analysis of formaldehyde-fixed, paraffin-embedded sections of tissue containing ciliated epithelium and confocal microscopy of thick sections of formaldehyde-fixed, agarose embedded tissue. In mature cultures of tracheal epithelial cells, all ciliated cells are GFP fluorescent and all GFP fluorescent cells are ciliated. In vitro, transgene expression coincides with onset of centriole formation. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of development, physiology and pathology of the lung and other tissues with ciliated epithelium. | ||
| 016576 | B6;C3-Tg(PDGFB-LRRK2*R1441C)574Djmo/J | Repository- Live |
| R1441C-LRRK2 transgenic mice have a minimal cytomegalovirus (CMV) enhancer and human platelet derived growth factor, B polypeptide (PDGFB) promoter/enhancer elements driving expression of a mutated full length human leucine-rich repeat kinase 2 (LRRK2*R1441C) cDNA. Hemizygotes are viable, fertile, and normal in size. The LRRK2 cDNA was modified to harbor the LRRK2*R1441C mutation associated with autosomal dominant, late-onset Parkinson's disease originally identified in family D from Western Nebraska. LRRK2 protein, also known as Dardarin, contains multiple functional domains and may play a role in regulating alpha-synuclein-mediated neuropathology through modulating the intracellular trafficking and accumulation of SNCA protein. R1441C-LRRK2 is selectively overexpressed in the cerebral cortex and cerebellum. These mice display reduced levels of cortical catecholamines, a progressive impairment of locomotor activity and the accumulation of autopha ..... For more information please see the full phenotype on the strain data sheet | ||
| 008169 | B6;C3-Tg(Prnp-MAPT*P301S)PS19Vle/J | Repository- Live |
| These transgenic mice express the P301S mutant human microtubule-associated protein tau, MAPT, under the direction of the mouse prion protein, Prnp, promoter. The expression of the mutant human MAPT is five-fold higher than the expression of the endogenous mouse MAPT protein. Hyperphosphorylated, insoluble mutant human MAPT protein in the brain accumulates with age causing decreased microtubule binding. At three months of age, transgenic mice exhibit clasping and limb retraction when lifted by the tail, which progresses to limb weakness. By 10 months of age the mice exhibit a hunched back and paralysis, followed by inability to feed. Transgenic mice have a median lifespan of approximately nine months with approximately 80% dying by 12 months. Histological analysis reveals neuron degeneration in hippocampus and ventricular dilatation (brain atrophy) by eight months of age, although significant neuron degeneration in the hippocampus occurs at approximately nine months of a ..... For more information please see the full phenotype on the strain data sheet | ||
| 004479 | B6;C3-Tg(Prnp-SNCA*A53T)83Vle/J | Repository- Live |
| Mice homozygous for the transgenic insert are viable and normal in size. These transgenic mice express human A53T variant alpha-synuclein (full-length, 140 amino acid isoform) under the direction of the mouse prion protein promoter. At eight months of age, some homozygous mice develop a progressively severe motor phenotype. Presentation of the phenotype may manifest at 14-15 months of age (on average). Lax grooming, weight loss and diminished mobility precede movement impairment, partial limb paralysis, trembling and inability to stand. Immunohistochemistry analysis of mutants between eight to 12 months of age reveals widely distributed alpha-synuclein inclusions, with dense accumulation in the spinal cord, brainstem, cerebellum and thalamus. The appearance of alpha-synuclein aggregate inclusions parallels the onset of the motor impairment phenotype. Axons and myelin sheaths exhibit progressive ultrastructural degeneration. Immunoelectron microscopy and biochemical analysis show the in ..... For more information please see the full phenotype on the strain data sheet | ||
| 009613 | B6;C3-Tg(Scnn1a-cre)3Aibs/J | Repository- Live |
| Hemizygous Scnn1a-Tg3-Cre mice are viable and fertile, with cre expression directed to cortex, thalamus, midbrain, and cerebellum by the Scnn1a promoter/enhancer regions within the BAC transgene. The donating investigators may not have assessed expression in tissues other than brain. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in the offspring. These Scnn1a-Tg3-Cre mice may be useful for generating conditional mutations for studying gain or loss of function and/or fate mapping in subgroups of brain tissues (including cortex, thalamus, midbrain, and cerebellum).
For characterization information, see images at the Allen Institute for Brain Science website (Scnn1a-Tg3-Cre images). | ||
| 009103 | B6;C3-Tg(Wfs1-cre/ERT2)3Aibs/J | Repository- Live |
| Hemizygous Wfs1-Tg3-CreERT2 mice are viable and fertile. As the Cre-ERT2 fusion gene is under control of the Wfs1 promoter/enhancer regions within the BAC transgene, cre activity is directed to cortex, hippocampus, striatum, thalamus and cerebellum only following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OHT or tamoxifen) and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to tamoxifen. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone ma ..... For more information please see the full phenotype on the strain data sheet | ||
| 014650 | B6;C3-Tg(tetO-TARDBP*)4Vle/J | Repository- Live |
| These transgenic mice express the mutant human TARDBP, TAR DNA binding protein, hTDP-43-deltaNLS, with a defective nuclear localization signal, under the direction of the tetO, tetracycline operator promoter. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. It is not known if homozygotes are viable. When mated to a mutant strain expressing tetracycline-controlled transactivator protein (tTA), expression of the hTDP-43-deltaNLS protein may be regulated with tetracycline or its analog doxycycline (DOX) in the double mutant offspring. When mated to Camk2a-tTA mice which express tTA in forebrain neurons (See for example: Stock No. 003010; Stock No. 007004; Stock No. 010712), the resulting bitransgenic mice ex ..... For more information please see the full phenotype on the strain data sheet | ||
| 000231 | B6;C3Fe a/a-Csf1op/J | Repository- Live |
| Mice homozygous for the osteopetrosis spontaneous mutation (Csf1op) are viable and exhibit osteopetrosis. The osteoclasts are the primary cell type affected in homozygous mutant mice. This results in a generalized macrophage deficiency, monocytopenia, and defective bone remodeling. Homozygous mutant mice also have abnormal calcium regulation, impaired dental growth and female mice fail to lactate. Total leukocyte counts are reduced and marrow cells are decreased to one-tenth of normal control mice. Homozygous mutant mice have a deficient microglia and macrophage response, and therefore may be useful tools to study the role of glia in neurological disease if mated to transgenic models of neurodegenerative disease. | ||
| 012705 | B6;CBA-Tg(ATXN3*)84.2Cce/IbezJ | Repository- Live |
| MJD84.2 transgenic mice (also called SCA3-YAC-84Q transgenic mice) are viable and fertile. These mice harbor a YAC transgene that expresses a human ataxin 3 (ATXN3; also called Machado-Joseph disease (MJD), MJD1, or spinocerebellar ataxia 3 (SCA3)) gene modified with an expanded 84 CAG repeat motif that is associated with MJD/SCA3 in humans. Hemizygous mice (MJD84.2) harbor two copies of the transgene at a single genomic integration site, with transgene expression levels and patterns almost identical to endogenous MJD. Transgene expression is widespread (detected in the cerebellum, cerebral cortex, heart, lung, spleen, liver, and skeletal muscle). Stable transmission of the MJD1/CAG84 transgene has been demonstrated for multiple generations with a predicted frequency of about 50%. Hemizygous mice exhibit attenuated weight gain and a progressive neurological phenotype. The neurological phenotype is characterized by prominent gait abnormalities (~ 4 weeks), mild tremor, moderate ..... For more information please see the full phenotype on the strain data sheet | ||
| 014647 | B6;CBA-Tg(Pdx1-cre)6Cvw/J | Repository- Live |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Cre recombinase under the control of the mouse Pdx1 (pancreatic and duodenal homeobox 1) promoter. Mosaic Cre recombinase activity is detected in the pancreatic epithelium, antral stomach and duodenum in neonates and in pancreatic beta islet cells in adults. No Cre recombinase activity is detected ectopically to the Pdx1 expression domain. When crossed with a strain containing loxP site-flanked sequences, Cre-mediated recombination results in deletion of the floxed sequences in the cre-expressing tissues of the offspring. It is not known if homozygotes are viable. | ||
| 004654 | B6;CBA-Tg(Pou5f1-EGFP)2Mnn/J | Repository- Live |
| Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Enhanced Green Fluorescent Protein under the control of the POU domain, class 5, transcription factor 1, promoter and distal enhancer. Primordial germ cell specific markers, alkaline phosphatase II and stage-specific embryonic antigen, are co-expressed in EGFP positive cells. 9.5 and 10.5 dpc (days post-coitum) migratory primordial germ cells from hemizygotes and homozygotes can be sorted and isolated by flow cytometry. This strain represents an effective tool for studying genetic imprinting and early embryonic development. | ||
| 007910 | B6;CBA-Tg(Thy1-Brainbow1.0)LLich/J | Repository- Live |
| These Thy1-Brainbow 1.0 (line L) transgenic mice are viable and fertile. The mice possess multiple fluorescent protein sequences uniquely flanked with pairs of incompatible Lox sites alternated to create mutually exclusive recombination events; allowing stochastic expression of multiple fluorescent proteins from a single transgene. Prior to Cre-mediated recombination, the fluorescent protein immediately adjacent to the promoter, dTomato (RFP), is expressed in peripheral and central neurons. When bred to Cre recombinase expressing mice, the resulting offspring can have one of three expression outcomes for each transgene in each cell of the cre expressing tissue(s): dTomato (RFP) (no recombination), mCerulean (CFP), or mYFP. Integration of tandem transgene copies yields combinatorial fluorescent protein expression in each cell, and thus many possible cell colors, providing a way to distinguish adjacent neurons and visualize other cellular interactions. Of note, the singl ..... For more information please see the full phenotype on the strain data sheet | ||
| 011070 | B6;CBA-Tg(Thy1-EGFP)SJrs/NdivJ | Repository- Live |
| Mice harboring the Thy1-GFP transgene are viable and fertile with enhanced green fluorescent protein (EGFP) expression under the control of a modified Thy1 promoter region (containing the sequences required for neuronal expression but lacking the sequences required for expression in non-neural cells). These thy1-GFP-S mice (derived from founder line S) have EGFP expression in sparse subsets of neurons within specific populations; providing a bright, vital Golgi-like stain. Thy1-GFP-S mice show EGFP labeling in the superficial layers of the neocortex, including most/all interneuron subtypes, with pyramidal/interneuron ratios of approximately 4:1 that match the distribution in the non-labeled population. While this is similar to Thy1-GFPM mice (Stock No. 007788), the labeling distribution for line S is different from line M. In addition, less than 10% of cerebellum mossy fibers show EGFP labeling and no EGFP expressio ..... For more information please see the full phenotype on the strain data sheet | ||
| 015814 | B6;CBA-Tg(Thy1-spH)64Vnmu/FrkJ | Repository- Live |
| These transgenic mice express spH, the pH-sensitive variant of the green fluorescent protein (ecliptic pHluorin) fused to the mouse synaptic vesicle-associated membrane protein 2 (Vamp2), under the control of the mouse thymus cell antigen 1 (Thy1) promoter. In founder line spH64, transgene expression is detected in many regions of the brain. spH expression is detected mainly in GABAergic or inhibitory synaptic terminals of dissociated hippocampal neurons. Synaptic activity, as determined by fluorescence, is detectable starting at approximately 10 days in vitro in cultured hippocampal neurons. | ||
| 005956 | B6;D1Lac-Scd1ab-2J/J | Repository- Live |
| The overall appearance of mice homozygous for either the Scd1ab-J allele or the Scd1ab-2J allele (Stock No. 002304 or 005956) includes slightly hunched posture, dry, scaly skin, thin fur sometimes detectable by 7 days of age, and small eyes with encrusted eyelids stuck shut. They have hypoplasia of the sebaceous glands and other hair follicle abnormalities that result in scarring alopecia. These mice have a paucity of adipose tissue, thin subcutis, and a distinctive odor. Hepatic cholesterol ester and triglyceride synthesis has been shown to be deficient in Scd1ab-J homozygotes and could not be restored through diet. Early studies of skin lipids in the original asebia mutant (Scd1ab) revealed a deficiency in wax esters, wax diesters, and sterols esterified with very long-chain fatty acids along with an in ..... For more information please see the full phenotype on the strain data sheet | ||
| 013137 | B6;D2-Tg(Akr1b7-RFP)9Amc/J | Repository- Live |
| These transgenic mice express Red Fluorescent Protein (TagRFP-T variant) under the direction of the mouse Akr1b7, aldo-keto reductase family 1, member B7, promoter.
Transgene expression is detected at high levels in the adrenal glands and endothelial cells of renal medullary arterioles of transgenic embryos aged E15.5.
Renal vasculature associated expression is observed in Smooth Muscle Actin immunohistochemical positive cells that are closely associated with FLK1 and PECAM positive intrarenal arteries. Other possible sites of expression have not been characterized.
Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make this strain homozygous. This strain was transferred from the collection of the GenitoUrinary Development Molecular Anatomy Project (GUDMAP). | ||
| 015853 | B6;DBA-Tg(Cited1-TagRFP)26Amc/J | Repository- Live |
| These transgenic mice express the Tag-RFPT variant of Red Fluorescent Protein under the direction of the mouse Cited1, Cbp/p300-interacting transactivator with Glu/Asp-rich carboxy-terminal domain 1, promoter. TagRFP is the optimized monomeric derivative of the tetrameric eqFP578 from the sea anemone, Entacmaea quadricolor.
RFP fluorescence is detected in the cap mesenchyme in the kidney and the male reproductive systems of hemizygous embryos, 15.5 embryonic days of age. Immunohistochemical analysis reveals that the TagRFP-T transgene is expressed in the expected Cited1 expression domain. Other possible sites of expression have not been characterized. Mice that are hemizygous for the knock in allele are viable, fertile, normal in size and do not display physical or behavioral abnormalities.
This strain was transferred from the collection of the GenitoUrinary Development Molecular Anatomy Project (GUDMAP). | ||
| 008344 | B6;DBA-Tg(Fos-tTA,Fos-EGFP*)1Mmay Tg(tetO-lacZ,tTA*)1Mmay/J | Repository- Live |
| The TetTag mouse is a bi-transgenic mutant that has tetracycline (or tetracycline analog) inducible expression of beta-galactosidase in activated neurons. Two independently generated transgenic strains were crossed to produce this bi-transgenic TetTag strain. In the first transgenic construct, the tetracycline-controlled transactivator (tTA) protein and a two hour half-life Green Fluorescent Protein (shEGFP) are expressed under the direction of the fos, FBJ osteosarcoma oncogene, minimal promoter. The second transgenic construct expresses a nuclear-localizing beta-galactosidase gene and the doxycycline insensitive tetracycline regulated transactivator (containing point mutation, H100Y), under the control of the tetO, tetracycline-responsive regulatory element. In the absence of tetracycline or a tetracycline analog (such as doxycycline), selective expression of beta-galactosidase is observed in activated neurons. Doxycycline administration prevents expression beta-galactosidase ..... For more information please see the full phenotype on the strain data sheet | ||
| 014160 | B6;DBA-Tg(S100b-EGFP/cre/ERT2)22Amc/J | Repository- Live |
| These transgenic mice express the eGFPCreERT2 (Enhanced Green Fluorescent Protein and cre/ESR1) fusion gene under the direction of the mouse S100b, S100 protein, beta polypeptide, neural, promoter. Transgene expression is detected in chondrocytes in developing bone and in neural cells in the dorsal root ganglia (DRG). GFP fluorescence is not detectable by fluorescent microscope examination of whole embryos, bones or neural tube sagittal slices from embryos aged 15.5dpc. Tamoxifen induced Cre recombinase activity is detected in a subset of the GFP immunoreactive-positive cells in bone and to a lesser extent in the dorsal root ganglia. GFP immunoreactive-positive cells co-localize with S100b immunoreactive-positive cells in bone and DRG. Other possible sites of expression have not been characterized. Mice that are hemizygous for the transgene are viable, fertile, normal in size and do not display physical or behavioral abnormalities. This strain was transfe ..... For more information please see the full phenotype on the strain data sheet | ||
| 014159 | B6;DBA-Tg(Tmem100-EGFP/cre/ERT2)30Amc/J | Repository- Live |
| These transgenic mice express the eGFPCreERT2 (Enhanced Green Fluorescent Protein and cre/ESR1) fusion gene under the direction of the mouse Tmem100, transmembrane protein 100, promoter. Transgene expression is detected in developing nephrons of the kidney, Wolfian and Mullerian ducts and vasculature of the urogenital system of hemizygous 15.5 dpc embryos. GFP fluorescence is detected in embryos 15.5dpc in age in the proximal region of the early renal vesicle, at later stages eGFP is present in the parietal epithelium adjacent to Wilms Tumor (WT1) positive cells demarcating the future podocytes of Bowman's capsule and is limited to the Tmem100 expression domain. Tamoxifen inducible Cre recombinase activity is detected in the developing kidney (nephrogenic zone), vasculature and Wolfian or Mullerian duct of mutant embryos aged 15.5dpc. Possible cre recombinase activity is detected in small renal arteries. Other possible sites of expression have not been char ..... For more information please see the full phenotype on the strain data sheet | ||
| 010803 | B6;FVB-Tg(Adipoq-cre)1Evdr/J | Repository- Live |
| Mice hemizygous for this Adipoq-Cre BAC transgene are viable and fertile, with expression of a Cre recombinase directed to adipose tissue by the promoter/regulatory regions of the mouse adiponectin (Adipoq) locus on the BAC transgene. Transcription/translation from the BAC Adipoq locus is disabled, and Cre recombinase expression levels are similar to that of endogenous Adipoq expression. These mice express Cre recombinase effectively in white adipose tissue (WAT) and brown adipose tissue (BAT), but not in macrophages (including adipose-tissue resident macrophages, alveolar macrophages, or thioglycollate-stimulated peritoneal macrophages). The donating investigator reports highly efficient Cre recombinase activity, with no ectopic expression. The phenotype of homozygous mice was not determined by the donating investigator. These Adipoq-Cre BAC transgenic mice may be useful in generating conditional mutations for studying adipose tissue function and storage, obesity, ..... For more information please see the full phenotype on the strain data sheet | ||
| 009159 | B6;FVB-Tg(Cnp-EGFP/Rpl10a)JD368Htz/J | Repository- Live |
| These BAC TRAP transgenic mice express the EGFP-L10a fusion gene, EGFP/Rpl10a, under the control of the mouse Cnp (2',3'-cyclic nucleotide 3' phosphodiesterase) promoter. The transgene expression pattern corresponds to endogenous Cnp expression. Green fluorescent protein is detected in mature oligodendrocytes. Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. Transgenic male mice are infertile. Attempts at cryopreserving sperm from male transgenic mice have failed. This mutant mouse strain may be useful in affinity purification of polysomal mRNAs (translating ribosome affinity purification or TRAP) from mature oligodendrocytes and tracking mature oligodendrocytes by fluorescence. | ||
| 012944 | B6;SJL-Il6ratm1.1Drew/J | Repository- Live |
| These Il6rafl/fl mutant mice possess loxP sites flanking exons 4-6 of the interleukin 6 receptor alpha chain (Il6ra) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice that express tissue-specific Cre recombinase, resulting offspring lack detectable Il6ra in the cre-expressing tissues. This strain may be useful for studying the role of Il6 in immune response, re-epithelialization, angiogenesis, macrophage infiltration, and wound healing.
For example, when bred to a strain expressing Cre recombinase in the myeloid cell lineage (see Stock No. 004781 for example), this mutant mouse strain may be useful in studies of inflammation and wound healing. When bred to a strain expressing Cre recombinase in liver (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 003800 | B6;SJL-Tg(ACTFLPe)9205Dym/J | Repository- Live |
| This transgenic strain expresses a variant of the Saccharomyces cerevisiae FLP1 recombinase gene under the direction of the human ACTB promoter. The FLPe recombinase variant exhibits enhanced thermostability with recombination activity being four-fold and ten-fold that of wildtype FLP at 37C and 40C, respectively. Mice that are hemizygous for the transgenic allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Recombinase activity is detected in a wide variety of tissues (spinal cord, heart, gonad, adrenal) as early as embryonic day 10.5. This deleter strain is a suitable alternative to, and complement with the Cre-loxP system for in vivo genetic engineering. | ||
| 005249 | B6;SJL-Tg(Krt1-15-cre/PGR)22Cot/J | Repository- Live |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice have a synthetic steroid RU 486 inducible Cre-mediated recombination system driven by the mouse keratin complex 1, acidic, gene 15 promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the human progesterone receptor. The mutant human progesterone receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, RU 486. Restricted to the cytoplasm, the Cre/PGR protein can only gain access to the nuclear compartment after exposure to RU 486. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating RU 486-induced, Cre-mediated targeted deletions. This strain represents an effective tool for generating tissue-specific targeted mutants that would be useful to study epi ..... For more information please see the full phenotype on the strain data sheet | ||
| 010576 | B6;SJL-Tg(MMTV-rtTA)4-1Jek/J | Repository- Live |
| The donating investigator claims homozygous mice are viable and fertile. These MMTV-rtTA mice have expression of the reverse tetracycline-controlled transactivator (rtTA) protein directed primarily to the breast epithelia of the mammary ductal system by the mouse mammary tumor virus (MMTV) promoter. The donating investigator also reports some rtTA expression in salivary glands (particularly in the males) as well as prostate glands. When mated to a mutant strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE, TetRE or tetO), expression of the target gene may be induced with administration of the tetracycline analog doxycycline (dox) in the double mutant offspring. These MMTV-rtTA mice are a Tet-On tool that allows conditional, dox-inducible expression of genes primarily in mammary gland epithelial cells and may be useful in studying the endocrine function of mammary tissues and/or breast cancer (for example). | ||
| 008850 | B6;SJL-Tg(Mt1-LDLR)93-4Reh/AgnJ | Repository- Live |
| Mice hemizygous for this MMT-I-hLDLR transgene (hLDLRTg mice) are viable and fertile, with human low density lipoprotein receptor (hLDLR) expression controlled by the mouse metallothionein 1 gene (Mt1) promoter sequences. The donating investigator reports that homozygous mice are not viable. Expression of hLDLR mRNA is highest in liver, moderate in kidney, small intestine, and heart, and lowest in brain and pancreas. Treatment with cadmium sulfate (CdSO4) stimulates transcription from the metallothionein promoter and results in higher levels of hLDLR expression. This overexpression of functional LDLR in transgenic mice results in greatly increased clearance of LDLR ligands (LDL, apoprotein B-100 and apoprotein E) from plasma when compared to wild-type mice. These hLDLRTg mice may be useful for studying the role of apolipoproteins and their receptors, lipid transport and lipoprotein metabolism in a wide variety of disease (including atherosclerosis, Alzheimer's disease, and hepat ..... For more information please see the full phenotype on the strain data sheet | ||
| 012355 | B6;SJL-Tg(Pvalb-COP4*H134R/EYFP)15Gfng/J | Repository- Live |
| Mice hemizygous for the Prv-mhChR2-YFP BAC transgene are viable and fertile with expression of the mhChR2::YFP fusion protein directed to neuronal populations by the mouse parvalbumin (Pvalb or Prv) promoter/enhancer regions on the BAC transgene. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 that was modified to harbor a gain-of-function H134R substitution (mhChR2; also called hChR2-H134R) fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mhChR2-expressing neurons with blue light (450-490 nm) leads to rapid ..... For more information please see the full phenotype on the strain data sheet | ||
| 013094 | B6;SJL-Tg(Sox10-cre)507Mcln/J | Repository- Live |
| Mice hemizygous for the S4F:cre transgene are viable and fertile, containing the SRY-box containing gene 10 (Sox10) promoter and a c-Fos minimal promoter sequence directing expression of Cre recombinase predominantly to neural crest derived cells. Specifically, Cre recombinase expression is observed in craniofacial skeletal components, sympathetic and parasympathetic neuronal/glial populations as well as epidermal melanocyte precursors. Expression is also evident in non-neural crest derived tissues including oligodendrocytes and the ventral neural tube. When these transgenic mice are bred with mice containing a loxP-flanked sequence, Cre-mediated recombination is expected to result in deletion of the floxed sequences in the Cre recombinase-expressing tissues of the offspring. These mice may be important for lineage tracing, gene function characterization, and genome manipulations. | ||
| 012348 | B6;SJL-Tg(Thy1-COP3/EYFP)8Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-VChR1-YFP transgene are viable and fertile with expression of the VChR1::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The VChR1::YFP fusion protein is composed of a synthetic, mammalian codon-optimized, red-shifted channelrhodopsin-1 derived from Volvox carteri (VChR1) fused in-frame with an enhanced yellow fluorescent protein (EYFP). Compared with ChR2, VChR1 has a markedly (~70 nm) red-shifted action spectrum with a maximum at ~535 nm (green light). The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this VChR1 functions as a green light-driven cation channel that depolarizes the cell and causes action potentials. As such, illumination of VChR1-expressing neurons leads to rapid and reversible photostimulation of action potential firing/neural activity in these cells. The donating investigator spec ..... For more information please see the full phenotype on the strain data sheet | ||
| 012350 | B6;SJL-Tg(Thy1-COP4*H134R/EYFP)20Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-mhChR2-YFP transgene are viable and fertile with expression of the mhChR2::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 (optimized with an N-terminal beta2 nictinic acytlcholine receptor signal peptide and C-terminal ER-export and Golgi-export motifs) that harbors a gain-of-function H134R substitution fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mhChR2-expressing neurons with blue light ..... For more information please see the full phenotype on the strain data sheet | ||
| 012332 | B6;SJL-Tg(Thy1-HOP/EYFP)2Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-eNpHR-YFP transgene are viable and fertile with expression of the eNpHR::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The donating investigator specifically reports that Thy1-eNpHR-YFP mice derived from founder line 2 exhibit high expression of EYFP in layer 5 pyramidal neurons at cortex, dentate gyrus, thalamus, superior colliculus, inferior culliculus, brainstem, amydagala and cerebellum. These Thy1-eNpHR-YFP line 2 transgenic mice may be useful for rapid control of motor behavior by addition or removal of light, for ex vivo and in vivo studies of neural circuitry/connectivity following illumination, or for fluorescent labeling of neural tissues.
The eNpHR::YFP fusion protein, designed with halorhodopsin from the halophilic bacterium Natronomonas pharaonis (NpHR) fused in-frame with an enhanced yellow fluorescent protein (EYFP), was optimized for expression in mammalian systems ..... | ||
| 012334 | B6;SJL-Tg(Thy1-HOP/EYFP)4Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-eNpHR-YFP transgene are viable and fertile with expression of the eNpHR::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The donating investigator specifically reports that Thy1-eNpHR-YFP mice derived from founder line 4 exhibit high EGFP expression in layer 2/3 and layer 5 pyramidal neurons at cortex, dentate gyrus, thalamus, superior colliculus, inferior culliculus, brainstem, amydagala and cerebellum. These Thy1-eNpHR-YFP line 4 transgenic mice may be useful for rapid control of motor behavior by addition or removal of light, for ex vivo and in vivo studies of neural circuitry/connectivity following illumination, or for fluorescent labeling of neural tissues.
The eNpHR::YFP fusion protein, designed with halorhodopsin from the halophilic bacterium Natronomonas pharaonis (NpHR) fused in-frame with an enhanced yellow fluorescent protein (EYFP), was optimized for expression in mammali ..... | ||
| 007610 | B6;SJL-Tg(Thy1-cre/ERT2,-EYFP)VGfng/J | Repository- Live |
| These transgenic mice ("SLICK" for single-neuron labeling with inducible Cre-mediated knock-out) have a tamoxifen inducible Cre-mediated recombination system and Enhanced Yellow Fluorescent Protein driven by 2 bidirectional copies of the mouse thymus cell antigen 1 promoter. Hemizygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make the strain homozygous. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted neuron-specific deletions only in neurons where the Thy1 is active. These cells will be evident by the expression of Yellow Fluorescent Protein. Transgenic mice express YFP constitutively in neurons. The Donating Investigator reports that founder line V mice express the transgene sparsely in neurons of the central nervous system.
This strain is one of ..... | ||
| 014555 | B6;SJL-Tg(Tph2-COP4*H134R/EYFP)5Gfng/J | Repository- Live |
| Mice hemizygous for the TpH2-mhChR2-YFP BAC transgene (or TpH2-ChR2-YFP BAC transgene) are viable and fertile, with expression of the mhChR2::YFP fusion protein directed to serotonergic neuronal populations by the mouse tryptophan hydroxylase 2 (Tph2 or TpH2) promoter/enhancer regions on the BAC transgene. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 that was modified to harbor a gain-of-function H134R substitution (mhChR2; also called hChR2-H134R) fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mhChR2-ex ..... For more information please see the full phenotype on the strain data sheet | ||
| 010577 | B6;SJL-Tg(tetO-Erbb2*)8-4Jek/J | Repository- Live |
| The donating investigator reports that homozygous mice are viable and fertile. These TetRE-ErbB2 (TRE-ErbB2 or TRE-Neu) transgenic mice have expression of an activated form of the rat ErbB2 regulated by the tetracycline operator (tetO; also called tetracycline-responsive element (TRE, TetRE) or tet-operator) and cytomegalovirus minimal promoter. When mated to a mutant strain expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), expression of the constitutively active ErbB2 protein may be regulated with the tetracycline analog doxycycline (dox) in the double mutant offspring.
The amino acid mutation within the transmembrane domain of the ErbB2 receptor protein kinase facilitates its oligomerization and activation independent of a ligand; resulting in hyperplasia in tissues where it is expressed.
These TetRE-ErbB2 mice may be bred to generate bi-transgenic mutant mice with conditional (inducible/r ..... For more information please see the full phenotype on the strain data sheet | ||
| 003627 | B6C3-Tg(HD82Gln)81Dbo/J | Repository- Live |
| Mice expressing this transgene appear normal at birth through 1-2 months. Mice fail to gain weight, develop tremors, hypokinesis and lack coordination. They exhibit an abnormal gait and frequent hind limb clasping. Life expectancy is 5-6 months. Studies using huntingtin antibodies indicated numerous immunoreactive nuclear inclusions in multiple neuron populations. Neuritic damage is evident. | ||
| 000314 | B6CBACa Aw-J/A-EdaTa/J-XO | Repository- Live |
| XO or monsomy X mice lack a second sex chromosome. The condition is inherited as an X-linked dominant trait with male lethality. XO mice exhibit some degree of growth retardation, high frequency hearing loss, reduced thyroid activity, reduced body temperature and some behavioral abnormalities. Unlike Turner Syndrome in humans, XO females are fertile. The two-step mating system for this strain (described under Mating System) incorporates the X-linked coat color marker tabby so that mice can be identified by a combination of coat color and sex. This strain may be useful for studies of Turner Syndrome or X-linked recessive alleles. | ||
| 003544 | B6Ei;AKR-rhg/J | Repository- Live |
| Homozygotes are much smaller than their wildtype littermates at birth and hair development is retarded at 3 weeks of age, but similar to normal by 10 weeks of age. | ||
| 004850 | B6EiC3Sn-Rb(12.Ts171665Dn)2Cje/CjeDnJ | Repository- Live |
| Like B6EiC3Sn a/A - Ts(1716)65Dn (Stock No. 001924), this strain has three copies of most of the genes on mouse Chromosome 16 that are homologues of human Chromosome 21 genes. Transmission of the chromosome 16 segmental trisomy through the female germline is significantly improved over Ts65Dn (43% versus 24%). Dendritic spines on granule cells in the fascia dentata are enlarged in size and decreased in density (Villar AJ, et al. 2005). Unlike Ts65Dn, males are fertile. Mice are 20% smaller in size than controls. This strain serves a model for Down syndrome. | ||
| 005252 | B6EiC3Sn.BLiA-Ts(1716)65Dn/DnJ | Repository- Live |
| Segmentally trisomic Ts(1716)65Dn mice provide a postnatal model for Down syndrome. Ts65Dn mice have three copies of most of the genes on mouse Chromosome 16 that are homologues of human Chromosome 21 genes. These extra genes, along with the centromere and about 5% of proximal Chromosome 17 are contained in a small extra chromosome derived from a reciprocal translocation. The trisomic mice on this genetic background, with the wild-type allele of Pde6b, are similar to the Ts(1716)65Dn trisomic mice (Stock No. 001924) in that they display slightly shorter body length and lower body weight, reduced grip strength, nocturnal hyperactivity, and impaired performance in the Morris water maze. Any differences in the Morris water maze tests for the two genetic backgrounds were found to be very subtle. Distinct from Stock No. 001924, this genetic background is homozygous for the wild-type allele of Pde6b a ..... For more information please see the full phenotype on the strain data sheet | ||
| 001203 | C3FeB6F1/J A/Aw-J | Repository- Live |
| 008393 | C3H;101-Dync1h1Swl/PopJ | Repository- Live |
| Mice heterozygous for the radiation-induced Sprawling mutation of the cytoplasmic dynein heavy chain 1 gene (Dync1h1Swl) are viable and fertile (the donating investigator reports that less than 50% of males breed successfully). Heterozygous mice display an early-onset hereditary proprioceptive sensory neuropathy with muscle spindle deficiency. Mice are distinguishable around one week after birth by the presence of hindlimb flexion during tail suspension, and around three to four weeks of age develop a typical unsteady gait characterized by jerky and wobbly locomotion. At rest, the hindlimbs are splayed and flexed forward and hindpaws are incapable of gripping structures. Defective proprioception is suggested as proprioceptive sensory neurons are severely compromised in the lumbar dorsal root ganglia of newborns and the H reflex is defective despite normal motor nerve function in the hindlimbs. Homozygous mice die in utero before embryonic day (E)8.5, indicating ..... For more information please see the full phenotype on the strain data sheet | ||
| 013728 | C57BL/6-Tg(tetO-NOS2,-lacZ)240iMhus/J | Repository- Live |
| These iNOSβgal transgenic mice express the human nitric oxide synthase 2, inducible (NOS2 or iNOS) gene and a β-galactosidase (lacZ) reporter, both regulated by the bidirectional tetracycline operator, tetO. Homozygous mice are viable, fertile, and normal in size. NOS isoforms reduce molecular oxygen to superoxide, reactive oxygen species, and reactive nitrogen species (all of which can cause cellular toxicity and tissue damage). When mated to a mutant strain expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), LacZ and iNOS expression may be regulated with the tetracycline analog doxycycline (DOX) in the double mutant offspring. When bred to a strain expressing tTA driven by α-myosin heavy chain (α-MHC), cardiomyocyte specific overexpression of lacZ and iNOS result in embryonic lethality, cardiac enlargement, cardiomyopathy, bradyarrhythmia, and sudd ..... For more information please see the full phenotype on the strain data sheet | ||
| 010543 | C;129-Hsf1tm1Ijb/J | Repository- Live |
| Mice that are heterozygous for this targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. A truncated gene product (mRNA) is detected by Northern blot analysis of embryonic cells. No gene product (protein) is detected by Western blot analysis of non-treated and heat shocked cells or brain, testis, heart and liver tissue. The prenatal lethal phenotype of homozygous mice is more severe on the 129 background than on BALB/c, C57BL/6, or ICR backgrounds. Surviving homozygotes have slowed growth with body weights approximately 78% of normal at eight weeks of age. Homozygotes exhibit abnormal chorioallantoic placenta (thinned spongiotrophoblast layer). Homozygous females are infertile due to impaired meiosis and zygotic cell division. Homozygotes are more resistant to experimentally induced skin tumors and exhibit a lower tumor burden than wild-type controls. Cultured MEFs from homozygotes are less sensitive to glucose depriv ..... For more information please see the full phenotype on the strain data sheet | ||
| 010685 | C;129S-Adora2atm1Jfc/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No functional gene product (protein) is detected by receptor autoradiography analysis of the brain. Experimentally induced cerebral infarction volume and resulting neurological function impairment are reduced in homozygotes. Treatment with receptor agonist, CGS 21680, does not elicit decreased locomotor activity in homozygotes, as compared to wildtype. Homozygotes have reduced spontaneous activity and increased resistance to the addictive substances amphetamine and cocaine. This mutant mouse strain may be useful in studies of behavior, ischemic brain injury, stroke, responses to addictive substances and T cell response to inflammation. | ||
| 004081 | C;129S-Vhltm1Jae/J | Repository- Live |
| This strain contains loxP sites flanking the Vhl promoter and exon 1 resulting in a conditional null allele. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Cre-mediated recombination results in the deletion of the promoter and exon 1. Studies in which liver-specific inactivation of the Vhl gene was achieved by breeding this strain with albumin promoter driven-Cre mice (see Stock No. 003574 for example) resulted in hemizygous mice that exhibit cavernous hemangiomas of the liver, a rare component of the human von Hippel-Lindau (VHL) disease. This strain represents an effective tool for generating tissue specific-targeted mutants useful in studies examining VHL and tumor suppression in general.
When bred to a strain expressing Cre recombinase in the myeloid cell lineage (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 004597 | C;129S4-Ptentm1Hwu/J | Repository- Live |
| These mice possess loxP sites flanking exon 5 of the targeted gene. Mice homozygous for the "floxed" allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele.
For example, when crossed to a strain expressing Cre recombinase in astrocytes (see Stock No. 012887), this mutant mouse strain may be useful in studies of neurogenesis. When crossed to a strain expressing Cre recombinase in the central nervous system (see Stock No. 004600), this mutant mouse strain may be useful in studies of glia differentiation and cerebellar development. | ||
| 008234 | CB6-Tg(CAG-EGFP/CETN2)3-4Jgg/J | Repository- Live |
| Transgenic GFP-CETN2 mice are viable and fertile, expressing an enhanced green fluorescent protein-labeled human Centrin-2 (EGFP-CETN2) under the control of the chicken beta-actin promoter (with cytomegalovirus immediate early enhancer). Distinct and uniform GFP fluorescence corresponding to the two centrioles of the centrosome are observed in every tissue examined from embryonic day 14.5 through adult, independent of cell-cycle stage. Overexpression of CETN2 from the transgene is not reported to lead to any aberrant phenotype or alter the average number of centrosomes per cell. As intracellular GFP-aggregates are observed in specific regions exclusively in the adult brain, the donating investigator cautions against the use of this model in studying the centrosome in adult brain. These GFP-CETN2 mice allow fluorescent staining of the centrioles of the centrosome, and may be useful for studying mitosis, microtubule organization, cell-cycle regulation, signal transduction, transcription ..... For more information please see the full phenotype on the strain data sheet | ||
| 007677 | CB6-Tg(Gad1-EGFP)G42Zjh/J | Repository- Live |
| Mice hemizygous for this GAD67-GFP transgene are viable and fertile. GAD67-GFP (line G42) mice selectively express enhanced green fluorescent protein (EGFP) in the calcium-binding protein parvalbumin (Pv)-expressing subclass of basket interneurons (soma, dendrites, and axons) and also in putative presynaptic boutons. Transgene expression (EGFP expression) is published as early as postnatal day 0 (P0) with high expression levels throughout postnatal development. EGFP expression remains restricted to ~50% of Pv-expressing interneurons in adulthood. The donating investigator additionally reports transgene expression as early as embryonic day 14 (E14). EGFP expression is not reported in other interneuron classes positive for somatostatin (SOM), cholecystokinin (CCK), calretinin (CR), and VIP. These GAD67-GFP (line G42) mice may be useful for fluorescent labeling of the Pv-expressing subset of GABAergic neurons, allowing reliable and efficient characterization of perisomatic innervation ..... For more information please see the full phenotype on the strain data sheet | ||
| 002718 | CByJ.Cg-hop/J | Repository- Live |
| Mice homozygous for the hop-sterile spontaneous mutation (hop) are viable, females are fertile but males are sterile. Homozygous mutant mice walk with a characteristic hopping gait using the hindlegs simultaneously. There is preaxial polydactyly of both fore- and hindfeet. Defects in spermatogenesis result in abnormal sperm tail development. Tailed sperm are completely absent from the lumen of the testicular tubules. The second meiotic division is frequently abnormal or incomplete, often leaving four centrioles per cell. These centrioles usually fail to form flagella, and tail development is arrested. | ||
| 013732 | FVB-Tg(NPEPPS)1Skar/J | Repository- Live |
| These mice express a human aminopeptidase puromycin sensitive (hPSA or NPEPPS) gene directed by its endogenous promoter/enhancer regions on a BAC transgene. Mice hemizygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. PSA is a cytosolic aminopeptidase that hydrolyzes N-terminal amino acids. PSA is considered to have neuroprotective qualities due to its ability to degrade certain proteins associated with neurodegenerative diseases (TAU and polyglutamine expansion repeat-containing proteins). hPSA overexpression is seen in the cerebral cortex, spinal cord, cerebellum, hippocampus, and brain stem at a 2-3 fold greater level than endogenous PSA. hPSA activity is also increased in muscle, kidney, and liver. These mice may be useful for studying PSA protection in neurodegenerative disorders. | ||
| 008311 | FVB.129S2(B6)-Hmox1tm1Poss/J | Repository- Live |
| Mice that are homozygous for this targeted mutation are slightly smaller in size than wildtype littermates and exhibit poor grooming and hypoactivity. As early as 20 weeks of age, homozygotes develop anemia with diminished serum iron and increased serum ferritin. Histological analysis reveals iron accumulation in kidney and liver. Elevated oxidized proteins and lipid peroxidation develop in the liver and kidney. Homozygotes develop progressive chronic inflammatory
disease, including enlarged spleen and lymph nodes, inflammatory infiltrates, glomerulonephritis, fibrosis. Homozygous male mice have smaller testis than wildtype controls. Homozygotes occur at a lower than expected frequency, or are not produced, from heterozygous crosses and have decreased postnatal survival. An almost undetectable abnormal gene product (mRNA) is detected by Northern blot analysis of total splenic RNA. This mutant mouse strain may be useful in studies of hemochromatosis, inflammation and iron meta ..... For more information please see the full phenotype on the strain data sheet | ||
| 008820 | FVB.B-WldS/UmonJ | Repository- Live |
| The Wallerian degeneration slow spontaneous mutation, Wlds arose on the C57BL/Ola background. On the congenic FVB/N background, mice that are homozygous for this mutation exhibit delayed Wallerian degeneration compared to wildtype controls. Wallerian degeneration is the process of degeneration, after transection, of axons distal to the sever site of a peripheral nerve, and includes infiltration of macrophages, demyelination and initiation of Schwann cell mitosis. The Wlds mutation is widely expressed and is detected in neural tissue. | ||
| 010920 | FVB;129P2-Gt(ROSA)26Sortm1(birA)Mejr/J | Repository- Live |
| These ROSA26HABirA mice contain an HA (hemagglutinin) tagged bacterial birA, bifunctional protein (biotin ligase), gene inserted into the Gt(ROSA)26Sor locus. When crossed with a strain containing an Avi-tagged sequence of interest, biotinylation of the target protein results. Biotinylation is highly specific, quantative and allows purification of the target protein complexes. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. birA gene product (protein) is detected in all tissues by Western blot analysis. Secretory proteins are not efficiently biotinylated due to the location of the BirA protein in cytoplasm. This mutant mouse strain would be a useful tool for the isolation and purification of proteins and protein complexes from tissues. | ||
| 010710 | FVB;129S6-Sncatm1Nbm Tg(SNCA)1Nbm/J | Repository- Live |
| These PAC-Tg(SNCAWT);Snca-/- mice are viable and fertile, harboring a Snca knockout allele and a transgene encoding the human α-synuclein. As homozygotes, expression of endogenous mouse α-synuclein is abolished and replaced by human α-synuclein from the two total insertions of the PAC-Tg(SNCAWT). While brain RNA expression of SNCAWT is more than 50-fold greater compared to normal endogenous mouse α-synuclein, protein levels are only 1 to 1.5-fold greater. In colon however, both RNA and protein expression of SNCAWT are ~100-fold greater than normal endogenous mouse α-synuclein. PAC-Tg(SNCAWT);Snca-/- mice do not show any enteric nervous system abnormalities or widespread α-synuclein aggregation in brain or colon. No detectable motor behavior impairments, autonomic abnormalities, olfactory dysfunction, dopaminergic deficits, Lewy body inclusions or neurodegeneration are ..... For more information please see the full phenotype on the strain data sheet | ||
| 010788 | FVB;129S6-Sncatm1Nbm Tg(SNCA*A30P)1Nbm Tg(SNCA*A30P)2Nbm/J | Repository- Live |
| These double transgenic homozygous mice (dbl-PAC-Tg(SNCAA30P);Snca-/- mice) are viable and fertile, harboring a Snca knockout allele and two independently inserted transgenes encoding the human A30P-mutant α-synuclein associated with autosomal dominant Parkinson's disease. As homozygotes, expression of endogenous mouse α-synuclein is abolished and replaced by α-synuclein*A30P from the PAC-Tg(SNCAA30P). Because PAC-Tg(SNCAA30P) line 1 inserted on the X chromosome and line 2 inserted on a somatic chromosome, homozygous females have four total insertions and homozygous males have three total insertions. While brain RNA expression of SNCAA30P is more than 10-fold greater compared to normal endogenous mouse α-synuclein, protein levels are only 1 to 1.5-fold greater. In colon however, both RNA and protein expression of SNCAA30P are ~80-fold greater than normal endogenous mouse α-synuclein. ..... For more information please see the full phenotype on the strain data sheet | ||
| 010799 | FVB;129S6-Sncatm1Nbm Tg(SNCA*A53T)1Nbm Tg(SNCA*A53T)2Nbm/J | Repository- Live |
| These double transgenic homozygous mice (dbl-PAC-Tg(SNCAA53T);Snca-/- mice) are viable and fertile, harboring a Snca knockout allele and two independently inserted transgenes encoding the human A53T-mutant α-synuclein associated with autosomal dominant Parkinson's disease. As homozygotes, expression of endogenous mouse α-synuclein is abolished and replaced by α-synuclein*A53T from the four total insertions of the PAC-Tg(SNCAA53T). While brain RNA expression of SNCAA53T is ~10-fold greater compared to normal endogenous mouse α-synuclein, protein levels are only 1 to 1.5-fold greater. In colon however, both RNA and protein expression of SNCAA53T are ~80-fold greater than normal endogenous mouse α-synuclein. By three months of age, dbl-PAC-Tg(SNCAA53T);Snca-/- mice show robust abnormalities in enteric nervous system function (impaired colonic motility [males only] and prolonge ..... For more information please see the full phenotype on the strain data sheet | ||
| 009682 | NMRI-Tbcepmn/J | Repository- Live |
| Mice that are homozygous for this spontaneous mutation are viable but die prematurely. Onset of locomotor impairment with corresponding motor neuron and muscular degeneration occurs at 2 to 3 weeks of age. Atrophy and paralysis starts in the hind limbs and pelvic girdle and is progressive. Homozygotes die by 6 to 7 weeks of age due to respiratory failure. Neurodegeneration starts in the motor endplates, progresses to loss of axons and results in apoptosis of the cell bodies. Electrophysiological deficiencies are detected by 13 days of age, before the neurodegeneration is clinically visible. Electron microscopic analysis of sciatic and phrenic nerves reveals a reduced number of microtubules. TBCE protein is destabilized, producing a reduction in tubulin and microtubules in motor neuron axons. Progressive microtubule loss occurs in axons distal to proximal and corresponds to axon degeneration. The mutation arose in the NMRI/Pan outbred line and has been identified as a Trp524Gly ..... For more information please see the full phenotype on the strain data sheet | ||
| 011066 | NOD.Cg-Prkdcscid Il2rgtm1Wjl Tg(CSF2)2Ygy Tg(IL3)1Ygy Tg(KITLG)3Ygy/YgyJGckRolyJ | Repository- Live |
| These mutant mice carry the Prkdcscid and Il2rgtm1Wjl alleles and the Tg(IL3)1Ygy, Tg(CSF2)2Ygy and Tg(KITLG)3Ygy transgenes. The Tg(CSF2)2Ygy transgene contains the porcine colony stimulating factor 2 (granulocyte-macrophage) sequence (CSF2) under the control of the human cytomegalovirus promoter. The Tg(IL3)1Ygy transgene contains the porcine interleukin 3 sequence under the control of the human cytomegalovirus promoter. The Tg(KITLG)3Ygy transgene contains the porcine kit ligand (KITL) under the control of the human cytomegalovirus promoter. The 3 transgenes were coinjected together in the original transgenic strain used to generate this mutant strain. | ||
| 002043 | STOCK A/A-Dab1scm/J | Repository- Live |
| Mice homozygous for the scrambler spontaneous mutation (Dab1scm) are recognized by an unstable gait and whole-body tremor. The cerebella of 30-day-old scrambler homozygotes are hypoplastic and devoid of folia; however, neither seizures nor abnormal brain wave patterns have been observed. Scrambler is similar to the reeler mutation in phenotype and pathology and, like reeler, probably results from defective neuronal migration. Female homozygotes mate and breed. Homozygous scrambler mutants have an ataxic gait which in the male may be contributory factor in the failure to mate. Normal life span for both sexes. | ||
| 009597 | STOCK Adam17tm1.2Bbl/J | Repository- Live |
| Mice homozygous for this Taceflox allele are viable and fertile, with loxP sites flanking exon 2 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have the floxed sequences deleted in the cre-expressing tissue producing a null allele. As the proinflammatory cytokine TNF-α and other other cell receptors are synthesized as membrane-bound precursors that need to be proteolytically released by functional TNF-α converting enzyme (TACE or Adam17 [a disintegrin and metallopeptidase domain 17]), these Taceflox mutant mice may be useful in generating conditional mutations for studying TNF-sheddase function, TNF-related autoimmune diseases. | ||
| 003810 | STOCK Adrb1tm1Bkk Adrb2tm1Bkk/J | Repository- Live |
| Mice that are homozygous null for the Adrb1 and Adrb2 genes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Stimulation of beta adrenergic receptor function in these mice by agonists or exercise reveals significant impairments in chronotropic range, vascular reactivity and metabolic rate. A severely attenuated chronotropic and hypotensive response is observed after administration of the non-selective beta adrenergic receptor agonist isoproterenol. An abnormal response to epinephrine is also seen, with bradycardia and a monophasic hypertensive blood pressure change being observed rather than the tachycardia and biphasic hypertensive/ hypotensive response seen in wildtype mice. When exercised, heart rates in null mice are lower than that of wild type mice. No difference is noted in the resting heart rate. | ||
| 012458 | STOCK Adrbk1tm1Gwd/J | Repository- Live |
| These GRK2f/f mutant mice possess loxP sites flanking exons 3-6 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre in a ubiquitous manner embryos die at E~13.5. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exons 3-6 deleted in the cre-expressing tissues. This strain may be useful for studying the regulation of beta-adrenergic receptor signaling or other receptors regulated in a GRK2-dependent manner. | ||
| 012899 | STOCK Agrptm1(cre)Lowl/J | Repository- Live |
| Mice homozygous for the Agrp-Ires-cre allele are viable and fertile, with IRES-Cre inserted in exon 3 of the agouti related protein, Agrp. As such, cre expression is directed by the endogenous promoter/enhancer regions. Specifically, Cre recombinase expression is observed in agouti-related protein (AgRP) secreting neurons. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in the offspring. These mice may be useful for studying the physiological functions of GABA neurotransmission in ArGP neurons in the hypothalamus. | ||
| 012882 | STOCK Ascl1tm1.1(Cre/ERT2)Jejo/J | Repository- Live |
| In Ascl1-CreERT2 mice, the entire coding region of the endogenous mouse achaete-scute complex homolog 1 (Ascl1 or Mash1) gene is replaced by a CreERT2 fusion protein. Cre activity is induced following tamoxifen administration. As such, when Ascl1-CreERT2 mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Ascl1-expressing cells of the offspring. The creERT2 fusion protein is expressed in all Ascl1 expressing neural progenitor cells in the embryo and the adult brain, including subsets of neurons throughout central nervous system (CNS) and peripheral nervous system (PNS), and in neuroendocrine cells in lung and kidney. Homozygotes die within hours of birth due to CNS and PNS disruptions in neural development. Mice heterozygous for this allele are viable, fertile, and normal in size. These mice may be useful for studying the lineage of distin ..... For more information please see the full phenotype on the strain data sheet | ||
| 012881 | STOCK Ascl1tm1Reed/J | Repository- Live |
| In this strain the entire coding region of the endogenous mouse achaete-scute complex homolog 1 (Ascl1 or Mash1) gene is replaced with a nuclear localized green fluorescent protein (GFP) gene, abolishing gene function. GFP, driven by the Ascl1 promoter sequence, is expressed in all Ascl1-expressing neural progenitor cells in the embryo and the adult brain, including subsets of neurons throughout the central nervous system (CNS) and the peripheral nervous system (PNS), and in neuroendocrine cells in lung and kidney. Homozygotes die within hours of birth due to CNS and PNS disruptions in neural development. Mice heterozygous for the targeted mutation are viable, fertile, and normal in size. These mice may be useful for studying the lineage of distinct cell populations, neuronal turnover, and neuronal replacement upon traumatic injury. | ||
| 013072 | STOCK Atf4tm1Tow/J | Repository- Live |
| In this strain, a neomycin phosphotransferase resistance (neo) cassette replaces the entire coding region of the endogenous mouse activating transcription factor 4 (Atf4) gene, abolishing gene function. Mice homozygous for the Atf4 allele exhibit low viability, with delayed bone formation during embryonic development and low bone mass throughout postnatal life. They exhibit a reduction in oxidative stress-induced gene expression, resistance to oxidative death, and decreased consumption of the antioxidant glutathione. They also have decreased insulin sensitivity, smaller fat pads, and delayed hair growth as compared with control mice. Adults are severely microphthalmic, with no recognizable lens, anterior chamber, iris, or vitreous body. These mice may be useful for studying cell proliferation defects associated with blindness, osteoporosis, and stress responses. | ||
| 011121 | STOCK Axltm1Grl/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When combined with the mutations Tyro3tm1Grl (Stock No. 007937) and Mertktm1Grl (Stock No. 011122), mice exhibit a lymphoproliferative disorder, autoimmunity, increased apoptosis in multiple tissues, blindness, abnormal spermatogenesis and reduced (in females) fertility or infertility (in males). This mutant mouse strain may be useful in studies of autoimmunity, germ cell development and apoptosis. | ||
| 008882 | STOCK Bcl2tm1Irt/J | Repository- Live |
| Mice homozygous for this Bcl2flox conditional allele are viable and fertile, with a loxP-flanked neo cassette upstream of exon 2, as well as a loxP site downstream of exon 2 of the Bcl2 (B-cell leukemia/lymphoma 2) gene. When bred to mice that express Cre recombinase, the resulting offspring can have one of three resulting genotypes in the cre-expressing tissue(s); only the neo selection cassette deleted, only exon 2 deleted, or both the neo selection cassette and exon 2 deleted. The two latter genotypes result in loss of Bcl2 protein expression and are reported to confer the null phenotype. These Bcl2flox mutant mice may be useful in generating conditional mutations for studying apoptosis, mitochondrial permeability, cell survival signaling, cancer, neurological disorders, and immunity.
For example, when crossed to a strain expressing Cre recombinase in myeloid cell lineages (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 004339 | STOCK Bdnftm3Jae/J | Repository- Live |
| These mice possess loxP sites on either side of exon 5 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
When bred to a strain expressing Cre recombinase under the control of a tetracycline-responsive promoter element (see Stock No. 006224, 006234, 006244) and a strain expressing a tetracycline-controlled activator protein in brain tissues (see Stock No. 003763), this mutant mouse strain may be useful in studies of hippocampal-dependent learning and long-term potentiation. When bred to a strain expressing Cre recombinase in neuronal cells (see Stock No. 003966 for example), this ..... | ||
| 004585 | STOCK Cav1tm1Mls/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical abnormalities. Mutant mice exhibit exercise intolerance when challenged and are slightly hyperphagic. No gene product (protein) is detected by Western blot analysis in adipose, lung and heart tissues or in cultured mouse embryonic fibroblasts (MEFs). A decrease in the level of co-expressed caveolin-2 protein is immunodetected. At age 4-5 months, mutant mice are often smaller than their wildtype littermates. By one year of age, mutant mice weigh 5 to 7 grams less than wildtype, and are resistant to diet-induced obesity. Progressive adipose pathology results in reduced white adipose tissue with abnormally small adipocytes and enlarged, hyperplastic brown adipose tissue. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Isolated aortic tissue segments have a diminished vasoconstriction ..... For more information please see the full phenotype on the strain data sheet | ||
| 012706 | STOCK Ccktm1.1(cre)Zjh/J | Repository- Live |
| The Cck-IRES-Cre allele harbors an internal ribosome entry site and Cre recombinase in the 3' UTR of the cholecystokinin locus (Cck). As such, cre expression is directed by the endogenous Cck promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When Cck-IRES-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Cck-expressing cells in the offspring.
The donating investigator reports Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Cck expression pattern with highly efficient recombination). They report Cre recombinase activity is observed in cholecystokinin positive neurons (interneurons) of the cortex. Characterization of cre expression in tissues other than brain is not ..... | ||
| 006873 | STOCK Cebpbtm1Vpo/J | Repository- Live |
| Significant numbers of mice homozygous for this C/EBP-beta mutationon this mixed genetic background die perinatally due to hypoglycemia and a failure to mobilize glycogen. Homozygous males that survive to adulthood are fertile, but females are sterile, and display altered mammary duct formation. Macrophages isolated from homozygous mutant mice have impaired bactericidal activity. Surviving homozygotes exhibit fasting hypoglycemia, with reduced plasma insulin, plasma lipids, and free fatty acids (FFAs), and impaired hepatic glucose production. Further, they have a blunted response to glucagon and adrenaline primarily due to altered levels of hepatic cAMP production and reduced protein kinase A activity. Homozygous mice are resistant to obesity and have increased carbon dioxide production from increased metabolism in the brown adipose tissue and muscle. On a high-fat diet, homozygotes are protected from obesity and fatty liver due to reduced hepatic expression of lipogenic genes. Homozyg ..... For more information please see the full phenotype on the strain data sheet | ||
| 013701 | STOCK Cep290tm1Jgg/J | Repository- Live |
| These mice possess loxP sites on either side of exon 36 and 37 of the Cep290 (centrosomal protein 290) gene. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the gene. This strain may be useful in studies of retinal degeneration, cilia/flagella development, and fertility. | ||
| 002364 | STOCK Cftrtm1Unc Tg(FABPCFTR)1Jaw/J | Repository- Live |
| These FABP-hCFTR-CFTR bitransgenic mice harbor the FABP-hCFTR transgene (human fatty acid binding protein 1 liver (FABP1) promoter directing expression of a human cystic fibrosis transmembrane conductance regulator (ATP-binding cassette sub-family C, member 7) (CFTR) gene) and a targeted mutation of the cystic fibrosis transmembrane conductance regulator homolog gene (Cftrtm1Unc). Mice homozygous for both the Cftr targeted mutation and the FABP-hCFTR transgene have normal longevity up to nine months (longest time examined). There is correction of ileal goblet cell and crypt cell hyperplasia and cAMP-stimulated chloride secretion. There is little or no expression of the transgene in the lung. This more robust model may be used to assess the effects of the null mutation on the nose and lungs, and may be useful as a mouse model of Cystic Fibrosis.
Of note, colonies maintained at The Jackson Laboratory report poor breeding performance when using ..... | ||
| 010910 | STOCK Corttm1(cre)Zjh/J | Repository- Live |
| The Cst-T2A-Cre (Cort-T2A-Cre) allele harbors a a T2A oligopeptide that mediates ribosomal skipping (foot-and-mouth disease virus 2A from the insect Thosea asigna virus) and Cre recombinase in the 3' UTR of the cortistatin locus (Cort). As such, cre expression is directed by the endogenous Cort promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When Cst-T2A-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Cort-expressing cells (CST positive neurons) of the offspring.
The donating investigator reports Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Cort expression pattern with highly efficient recombination). They report Cre recombinase activity is observed in so ..... | ||
| 003392 | STOCK Crb1rd8/J | Repository- Live |
| 013170 | STOCK Dclk1tm1.2Jgg/J | Repository- Live |
| These mice possess loxP sites on either side of exon 3 of the Dclk1 (doublecortin-like kinase 1) gene. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing mouse, this strain is useful in eliminating tissue-specific expression of DCX-domain containing isoforms of this gene. This strain may be useful in studies of neuronal migration. | ||
| 013173 | STOCK Dclk2tm1.2Jgg/J | Repository- Live |
| Homozyous Dclk2 (doublecortin-like kinase 2) targeted mutation mice lack expression of the gene and show no significant phenotype in brain structure. This strain may be useful in studies of epilepsy.
When combined with a Dcx (doublecortin) knockout allele, compound mutant mice exhibit spontaneous seizures and morphological defects of hippocampal CA pyramidal cells. Most double mutants reportedly die at a young age (approximately 3 weeks). | ||
| 013172 | STOCK Dclk2tm1Jgg/J | Repository- Live |
| These mice possess loxP sites on either side of exon 2 of the Dclk2 (doublecortin-like kinase 2) gene. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the gene. This strain may be useful in studies of neurodevelopment and epilepsy. | ||
| 005992 | STOCK Efna2tm1Jgf Efna5tm1Ddmo/J | Repository- Live |
| Mice homozygous for both targeted mutations are viable, fertile, and normal in size. While the donating investigator reports that 10-20% of females homozygous at both loci neglect their litters, no such neglect is reported in the colonies at The Jackson Laboratory (Aug 2009). Double homozygous mice have no endogenous protein expression in inferior colliculus (IC) or superior colliculus (SC), and thus lack the concentration gradient created by the endogenous proteins across the midbrain in wildtype mice. Temporal and nasal retinal axon termination is severely altered: multiple ectopic aborizations in the SC indicate abnormalities in both anteroposterior and dorsoventral topography. Following surgical ablation of portions of the midbrain (including IC and SC), cross-modal innervation by retinal neurons is greater in double homozygous mutants compared to wildtype. Mice heterozygous at both loci are reported to have greater reproductive performance compared to double homozygous mice. Furth ..... For more information please see the full phenotype on the strain data sheet | ||
| 009340 | STOCK Eif2ak3tm1Dron/HotaJ | Repository- Live |
| These mice harbor a targeted mutation of the Eif2ak3 (eukaryotic translation initiation factor 2 alpha kinase 3 [also called Perk]) locus that abolishes endogenous gene expression. To date (Feb 2010), the donating investigator has not been able to generate homozygous mice on a C57BL/6J congenic background. The following phenotype describes mice on a mixed albino Swiss Webster;129/SvEv genetic background. Heterozygous mice are viable and fertile. Homozygous (Perk-/-) mice appear runty within a few days of birth and develop a rapid and progressive decline in endocrine and exocrine pancreatic function. This results in a complex pleiotropic phenotype including hyperglycemia, exocrine pancreatic insufficiency, diabetes, growth retardation, inability to breed, and early mortality. The phenotype of the Perk-/- mice is very similar to that observed in humans with Wolcott-Rallison syndrome; the consistent feature of which is severe diabetes mellitus developing in infancy. Heterozygous mi ..... For more information please see the full phenotype on the strain data sheet | ||
| 014151 | STOCK Eif2c2tm3.1Ghan/J | Repository- Live |
| A point mutation in the Eif2c2 (eukaryotic translation initiation factor 2C, 2; also called Ago2) gene inactivates catalytic activity in this strain but does not disrupt gene expression. Homozygous neonates are anemic and die shortly after birth. Mice show a loss of miR-451, a small RNA important for erythropoiesis. Heterozygous targeted mutant mice are viable and fertile. There are no known phenotypic differences between the mouse carrying the floxed neo cassette (see Stock No. 14150) and this strain from which the cassette has been deleted. This strain may be useful in studies of microRNA biogenesis and erythropoiesis. | ||
| 008407 | STOCK Epas1tm1Mcs/J | Repository- Live |
| The Hif-2α 2-loxP allele, also called Hif-2&alphafl or Epas12lox, contains loxP sites flanking exon 2 of the endothelial PAS domain protein 1 locus (Epas1 or Hif-2α). Homozygous mice are are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon deleted in the cre-expressing tissue(s).
For example, when bred to a strain with inducible Cre recombinase expression in cardiac cells (see Stock No. 005657 for example), this mutant mouse strain may be useful in studies of erythropoiesis. When bred to a strain with tamoxifen inducible widespread Cre recombinase expression(see Stock No. 008085 for example), this mutant mouse strain may be useful in studie ..... | ||
| 012916 | STOCK Epha4tm1.1Bzh/J | Repository- Live |
| These Epha4flox mutant mice possess loxP sites flanking exon 3 of the Eph receptor, A4 (Epha4) targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 3 deleted in the process-rich layers of the hippocampus. This strain may be useful for studying axon guidance, spine morphogenesis, synaptic plasticity, neuronal circuitry (including that of the central pattern generator), neural injury and repair, vascular formation, and various cell-cell communications in and outside the nervous system. | ||
| 014108 | STOCK Epn3tm1.1Pdc/J | Repository- Live |
| These Epn3-/- mice lack the entire coding region of the Epsin 3 (Epn3) gene. Homozygous mice are viable, fertile, and normal in size. Epn3 is expressed specifically in in the parietal cells of the stomach as well as in keratinocytes migrating across collagen in cutaneous wounds. | ||
| 015830 | STOCK Erc1tm2.1Sud/J | Repository- Live |
| A 5'UTR exon and the first coding exon of the Erc1 (ELKS/RAB6-interacting/CAST family member 1; ELKS1, CAST2) gene are flanked by loxP sites in these floxed mutant mice. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Normal expression of the targeted gene is demonstrated by the floxed allele. | ||
| 015831 | STOCK Erc2tm1.2Sud/J | Repository- Live |
| A 5'UTR exon and the first coding exon of the Erc2 (ELKS/RAB6-interacting/CAST family member 2; ELKS2, CAST1) gene are flanked by loxP sites in these targeted mutant mice. An in-frame tetracysteine tag is located in exon 1. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Normal expression of the targeted gene is demonstrated by the floxed allele.
Widespread cre excision of the floxed exons blocks expression (see Stock No. 008391). | ||
| 010698 | STOCK Fgf2tm2Doe/J | Repository- Live |
| Mice homozygous for the Fgf2lmw-ko (Fgf2lmw or FGF2 LMWKO) allele are viable and fertile with no reported abnormalities in endothelial cell migration and proliferation. As the targeted allele disrupts expression of the fibroblast growth factor 2 low molecular weight (Fgf2 lmw) isoform, the 18 kDa isoform is not expressed (as demonstrated in brain, aorta, lung, and endothelial cells from homozygous mice). The Fgf2 high molecular weight (hmw) isoforms (20.5 and 21 kDa) are still expressed in the nucleus from the targeted allele. Homozygous mice have significantly reduced bone mineral density and fewer mineralized nodules, coincident with increased expression of the Wnt antagonist secreted frizzled receptor 1 (sFRP-1) in bone tissue. Homozygous deficiency of the Fgf2 lmw isoform is associated with significantly impaired recovery in postischemic cardiac/contractile function after ischemia-reperfusion (I-R) injury. | ||
| 010720 | STOCK Fgf2tm3Doe/J | Repository- Live |
| Mice homozygous for the Fgf2hmw-ko (Fgf2hmw or FGF2 HMWKO) allele are viable and fertile with no histological, immunohistochemical, or morphometric abnormalities in myocardial architecture or blood vessel and cardiac capillary density. As the targeted allele disrupts expression of the two Fgf2 high molecular weight (Fgf2 hmw) isoforms, the 20.5 and 21 kDa isoforms are not expressed (as demonstrated in heart, liver, and brain tissues from homozygous mice). The Fgf2 low molecular weight (lmw) isoform (18 kDa) is still expressed in the cytoplasm and nucleus from the targeted allele. Homozygous deficiency of the Fgf2 hmw isoforms is associated with significant improvement in postischemic cardiac/contractile function after ischemia-reperfusion (I-R) injury. | ||
| 007569 | STOCK Fgfr2tm1Dor/J | Repository- Live |
| Mice homozygous for this Fgfr2flox allele possess loxP sites flanking exons 8-10 of the targeted gene and are viable and fertile. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have sequences encoding the alternatively spliced Ig domain IIIb, as well as the IIIc and TM domains, deleted in the cre-expressing tissue(s). These Fgfr2-flox mutant mice may be useful in generating conditional mutations to study the role of fibroblast growth factor receptors in vertebrate development; including early embryogenesis, regional specification of the brain, limb morphogenesis, and normal bone, craniofacial, and lens development.
For example, when crossed to a strain expressing Cre recombinase in the central nervous system, especially astrocytes (see Stock No. 004600), this mutant mouse strain may be useful in studies of astroglial migration. When crossed to ..... | ||
| 008464 | STOCK Foxa2tm2.1(cre/Esr1*)Moon/J | Repository- Live |
| This strain expresses the tamoxifen-inducible cre/Esr1 from the targeted locus. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions specifically in the developing endoderm, notochord, and floorplate. Heterozygotes and homozygotes are normal in size, viability and fertility. | ||
| 010963 | STOCK Fxntm1Mkn Tg(FXN)YG22Pook/J | Repository- Live |
| The YG22 transgenic founder line carries a single copy of the human FXN gene with one GAA trinucleotide repeat sequence of 190 repeats. High levels of human FXN gene product (mRNA or protein) are detected by RT-PCR and Western blot analysis. 40-50% of the endogenous mouse Fxn gene product (protein) is detected by Western blot analysis in mice heterozygous for the targeted mutation alone. Mice that are homozygous for the targeted allele and hemizygous for the transgene exhibit an age dependent, tissue specific expansion of the GAA repeat, with expansion accumulation in the CNS (particularly cerebellum), similar to the human pathology. The GAA triplet repeat exhibits intergenerational instability. Mice that are homozygous for the targeted allele and hemizygous for the transgene exhibit progressive retinal degeneration, impaired and decreased locomotor activity and coordination, and an increase in body weight. At 9 months of age, muscle strength is decreased. Alt ..... For more information please see the full phenotype on the strain data sheet | ||
| 010702 | STOCK Gad2tm1(cre/ERT2)Zjh/J | Repository- Live |
| The Gad2-CreERT2 knock-in allele both abolishes Gad2 gene function and expresses a CreERT2 fusion protein (creERT2 fusion protein) from the Gad2 promoter/enhancer elements. Heterozygous mice are viable and fertile with no reported abnormalities. Homozygous mice are expected to have a knockout phenotype similar to other null mutations of this gene and may exhibit increased seizure activity (although no early death is reported). Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Gad2-CreERT2 mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Gad2-expressing cells of the offspring. The donating investigator reports tamoxifen-inducible Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Gad2 expression pattern with highly efficient inducibility). ..... | ||
| 010802 | STOCK Gad2tm2(cre)Zjh/J | Repository- Live |
| The Gad2-IRES-Cre allele harbors an internal ribosome entry site and Cre recombinase in the 3' UTR of the Gad2 (glutamic acid decarboxylase 2) locus. As such, cre expression is directed by the endogenous Gad2 promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When Gad2-IRES-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Gad2-expressing cells (GAD2 positive neurons) of the offspring.
The donating investigator reports Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Gad2 expression pattern with highly efficient recombination). The donating investigator did not examine cre expression in tissues other than brain. For characterization information, see image ..... | ||
| 008194 | STOCK Gata4tm1.1Sad/J | Repository- Live |
| Mice homozygous for this Gata4loxP conditional allele are viable and fertile, with loxP sites flanking exons 3-5 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (coding for both zinc finger DNA-binding domains and the nuclear localization signal essential for GATA4 function) deleted in the cre-expressing tissue(s). These GATA binding protein 4 conditional mice may be useful in generating conditional mutations for studying GATA4 function during organogenesis (such as cardiogenesis) or in adult mice.
For example, when crossed to a strain expressing Cre recombinase in cardiac myocytes (see Stock No. 009074), this mutant mouse strain may be useful in studies of cardiac hypertrophy, stress-compensation and myocyte viability. When bred to a strain expressing Cre recombinase in heart muscle (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 008211 | STOCK Gli1tm2Alj/J | Repository- Live |
| Mice homozygous for the Gli1lz (or Gli1lacZ) allele are viable and semi-fertile, with a "knock-in" of β-galactosidase (lacZ) inserted into the first coding exon (exon 2) and replacing the genomic fragment encoding the entire N-terminal and zinc-finger domains of the targeted locus (exons 2-7); abolishing endogenous gene function even if alternative splicing occurs. Under control of the upstream promoter/enhancer elements, lacZ expression is observed in a pattern indistinguishable from wildtype gene mRNA expression. As Gli1 transcription is a readout of high level Hedgehog signaling, these Gli1lz (or Gli1lacZ) mice may be useful for studying Hedgehog/Sonic Hedgehog signaling in axis patterning, proliferation, and cell fate specification of Hedgehog responding cells at different stages of embryogenesis. | ||
| 007913 | STOCK Gli1tm3(cre/ERT2)Alj/J | Repository- Live |
| Mice homozygous for this Gli1-CreERT2 targeted allele are viable and fertile (although homozygous males are reported to have breeding problems). Under control of the endogenous upstream promoter/enhancer elements, tamoxifen-inducible cre activity is observed in cells that have received positive Hedgehog/Sonic Hedgehog signaling. The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to tamoxifen. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone may be coadministered. When these Gli1-CreERT2 mice are ..... For more information please see the full phenotype on the strain data sheet | ||
| 007922 | STOCK Gli2tm2.1Alj/J | Repository- Live |
| Mice homozygous for this Gli2lzki allele harbor a β-galactosidase "knock-in" (lzki) allele that also abolishes endogenous gene function. As such, homozygous mice die at birth with many defects including absence of Sonic Hedgehog-expressing floor plate cells, reduction of Nkx2.2-expressing V3 interneurons in the spinal cord, and defects in midbrain, cerebellum and lung development. Under control of the upstream promoter/enhancer elements, lacZ expression is observed in a pattern identical to the wild-type gene. Heterozygotes are viable and fertile. These Gli2lzki mice may be useful for studying Hedgehog/Sonic Hedgehog signaling in the development of many organs (such as central nervous system and axis patterning), as well as the role of Gli2 in adult organs. | ||
| 007926 | STOCK Gli2tm6Alj/J | Repository- Live |
| Mice homozygous for this Gli2flox conditional allele are viable and fertile, with loxP sites flanking exons 7 and 8 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have these exons deleted in the cre-expressing tissue(s). This results in a frameshift mutation following splicing of mRNA from exon 6 to 9 and is reported to confer the null phenotype. These Gli2flox mutant mice may be useful in generating conditional mutations for studying Hedgehog/Sonic Hedgehog signaling in the development of many organs (such as central nervous system and axis patterning), as well as the role of Gli2 in adult organs. | ||
| 008873 | STOCK Gli3tm1Alj/J | Repository- Live |
| Mice homozygous for this Gli3flox conditional allele are viable and fertile, with loxP sites flanking exon 8 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have exon 8 deleted in the cre-expressing tissue(s). This results in a frameshift mutation upstream of the DNA-binding domain following splicing of mRNA from exon 7 to 9 and is reported to confer the null phenotype. These Gli3flox mutant mice may be useful in generating conditional mutations for studying Hedgehog/Sonic Hedgehog signaling in the development of many organs (such as central nervous system and limb patterning), as well as the role of Gli3 in adult organs.
When bred to a strain expressing Cre recombinase in the nervous system (see Stock No. 003771 for example), this mutant mouse strain may be useful in studies of mid/hind brain development. When bred to a str ..... | ||
| 013731 | STOCK Gt(ROSA)26Sortm1(CAG-Brainbow2.1)Cle/J | Repository- Live |
| Mice homozygous for the R26R-Confetti conditional allele are viable and fertile, with a CAG promoter, loxP site, and STOP cassette preventing transcription of the downstream Brainbow 2.1 sequences. The Brainbow 2.1 region contains two loxP-flanked dimers, each uniquely positioned in head-to-tail tandem. One dimer has nuclear-localized green fluorescent protein (hrGFPII) and a reverse-oriented cytoplasmic yellow fluorescent protein (mYFP). The other dimer has cytoplasmic red fluorescent protein (tdimer2(12)) and a reverse-oriented membrane-tethered cyan fluorescent protein (mCerulean). The Brainbow2.1 region may be written as loxP-STOP-loxP-GFP-PFY-Pxol-loxP-RFP-PFC-Pxol to show the transcriptional direction of each part. When bred to mice that express Cre recombinase, the resulting offspring may have a recombination event that stochastically places one of the four fluorescent proteins into position directly downstream of the CAG promote ..... For more information please see the full phenotype on the strain data sheet | ||
| 006331 | STOCK Gt(ROSA)26Sortm1(DTA)Jpmb/J | Repository- Live |
| Homozygous "ROSA26-eGFP-DTA" mice are viable, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator reports that some homozygous males are subfertile. Mutant mice display widespread expression of EGFP, but DTA transcription is prevented by a strong transcriptional stop sequence. When bred to mice that express Cre recombinase under the control of a promoter of interest, the loxP-flanked EGFP and stop sequence are removed, and DTA expression is activated, resulting in the specific ablation of cre-expressing cells. This strain may be useful on its own as a fluorescent reporter or in combination with cre-expressing mice to produce conditional deletions of specific groups of cells. Transgenic mice also may have applications in toxicology and protein synthesis research.
For example, when crossed to a strain expressing Cre recombinase in the midbrain and dorsal spinal cord (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 008159 | STOCK Gt(ROSA)26Sortm1(Notch1)Dam/J | Repository- Live |
| These mice contain a sequence encoding an intracellular portion of the mouse Notch1 gene (amino acids 1749-2293), but lacking the c-terminal PEST domain, and Green Fluorescent Protein, GFP, inserted into the GT(ROSA)26Sor locus. Expression of the Notch1 fragment and GFP is blocked by a loxP-flanked STOP fragment placed between the coding sequence and the GT(ROSA)26Sor promoter. The GFP expression is localized to the nucleus by an IRES sequence. The truncated cytoplasmic fragment encoded by the Notch1 sequence causes constitutive signaling activity. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants for studying the effects of Notch pathway activation. Homozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
For example, when crossed to a strain expressing a tamoxifen inducible Cre recombinase in all c ..... | ||
| 005130 | STOCK Gt(ROSA)26Sortm1(Smo/EYFP)Amc/J | Repository- Live |
| These mice contain an Enhanced Yellow Fluorescent Protein/Smoothened homolog (Drosophila) fusion gene inserted into the Gt(ROSA)26Sor locus. The mutant allele consists of a fusion product involving Enhanced Yellow Fluorescent Protein (EYFP) and the constitutively active W539L point mutation of the mouse smoothened homolog (Drosophila) gene (SmoM2). Expression of the Smo/EYFP fusion gene is blocked by a loxP-flanked STOP fragment placed between the Gt(ROSA)26Sor promoter and the Smo/EYFP sequence. When used in conjunction with a Cre recombinase-expressing strain, successful Cre-mediated excision results in the constitutive expression of mouse smoothened homolog (Drosophila) and unrestrained Hedgehog signaling in Cre-expressing tissues. Expression of the SmoM2 fusion protein can be monitored using EYFP-specific fluorescence protocols. Mice that are homozygous for the mutant allele are viable, fertile, normal in size and do not display any gross physical ..... For more information please see the full phenotype on the strain data sheet | ||
| 011004 | STOCK Gt(ROSA)26Sortm1(rtTA*M2)Jae Col1a1tm3(tetO-Pou5f1,-Sox2,-Klf4,-Myc)Jae/J | Repository- Live |
| Mice homozygous for both targeted mutations (R26-rtTA and Col1a1::tetO-4F2A) are viable and fertile. These double mutant R26rtTA;Col1a14F2A mice have widespread expression of the optimized form of reverse tetracycline-controlled transactivator (rtTA-M2) protein directed to multiple tissues by the Gt(ROSA)26Sor promoter. In the absence of the tetracycline analog doxycycline (dox), expression of the dox-inducible 4F2A cassette from the Col1a1 locus is not detected. Following dox administration, this single-gene transgenic mouse strain expresses the polycistronic 4F2A cassette (four mouse reprogramming genes Oct4 [Pou5f1], Sox2, Klf4, and c-Myc [Myc]). Somatic expression of these reprogramming factors allows multiple somatic cell types to be directly reprogrammed to generate induced pluripotent stem cells (iPSCs) by culture in dox (see details below). Because the reprogramming factors are carried on a single polycistronic con ..... For more information please see the full phenotype on the strain data sheet | ||
| 011011 | STOCK Gt(ROSA)26Sortm1(rtTA*M2)Jae Col1a1tm4(tetO-Pou5f1,-Sox2,-Klf4,-Myc)Jae/J | Repository- Live |
| Mice homozygous for both targeted mutations (R26-rtTA and Col1a1::2lox-tetO-4F2A) are viable and fertile. These double mutant R26rtTA;Col1a12lox-4F2A mice have widespread expression of the optimized form of reverse tetracycline-controlled transactivator (rtTA-M2) protein directed to multiple tissues by the Gt(ROSA)26Sor promoter. In the absence of the tetracycline analog doxycycline (dox), expression of the loxP-flanked, dox-inducible 4F2A cassette from the Col1a1 locus is not detected. Following dox administration, this single-gene transgenic mouse strain expresses the polycistronic 4F2A cassette (four mouse reprogramming genes Oct4 [Pou5f1], Sox2, Klf4, and c-Myc [Myc]). Somatic expression of these reprogramming factors allows multiple somatic cell types to be directly reprogrammed to generate induced pluripotent stem cells (iPSCs) by culture in dox (see details below). Because the 4F2A reprogramming factors are f ..... For more information please see the full phenotype on the strain data sheet | ||
| 005572 | STOCK Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/J | Repository- Live |
| Homozygous mutant mice are viable, fertile, normal in size and do not display any behavioral abnormalities. When these gene targeted mice are bred to transgenic strains expressing Cre recombinase, functional rtTA and EGFP activity is observed in the double mutant offspring in the tissues that express cre. These double mutant mice may be bred to transgenic strains carrying genes of interest under the regulation of tetracycline responsive elements (TRE; tetO) to generate triple mutant mice in which the tissue specificity of the Cre-transgenic line and the doxycycline inducibility of the rtTA/TRE-controlled transgenes can be combined to regulate expression of the target gene. Of note, mutant mice are also available on a C57BL/6J genetic background (see Stock No. 005670). | ||
| 008600 | STOCK Gt(ROSA)26Sortm1(tTA)Roos/J | Repository- Live |
| Mice heterozygous for the ROSA:LNL:tTA conditional mutation of the Gt(ROSA)26Sor locus are viable and fertile, with a loxP-flanked STOP cassette preventing transcription of a downstream optimized/modified tetracycline-controlled transactivator protein ("mtTA"). Applying both Cre-lox and Tet-Off technologies, these ROSA:LNL:tTA mutant mice may be useful to generate compound mutant mice in which expression of a tetracycline-responsive promoter element (TRE; also called tet-operator or tetO)-driven gene of interest can be both directed to the cell types defined by the chosen Cre recombinase expression, as well as turned off by the addition of tetracycline (or its analog doxycycline (dox)). | ||
| 013124 | STOCK Gt(ROSA)26Sortm3(Gli3)Amc/J | Repository- Live |
| These RosaGli3TFlag c/c mice contain a floxed-neomycin resistance (neo) cassette and polyadenylation signal, cDNA encoding a FLAG-tagged GLI-Kruppel family member (Gli3) repressor gene, an internal ribosome entry site (IRES), and a Venus yellow fluorescent protein (YFP) under control of the ubiquitous Gt(ROSA)26Sor locus. Breeding these mutant mice to mice that express Cre-recombinase will also result in Floxed-neo-stop excision. When these mice are crossed to mice containing Cre-recombinase under direction of a paired related homeobox 1 (Prrx1) promoter (see Stock No. 005584), active in early limb mesenchyme, the mice produce Gli3TFlag at levels that are comparable with the endogenous protein. Mice exhibited a variety of limb defects including a variable preaxial forelimb polydactyly, limb truncation, and reduced mineralization. These mice may be useful for understanding Sonic hedgehog signaling and iden ..... For more information please see the full phenotype on the strain data sheet | ||
| 007576 | STOCK Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo/J | Repository- Live |
| Mice homozygous for this mT/mG mutation are viable and fertile. These mice possess loxP sites on either side of a membrane-targeted tdTomato (mT) cassette and express strong red fluorescence in all tissues and cell types examined. Tail or whole body epifluorescence is sufficient to identify mT/mG homozygotes. When bred to Cre recombinase expressing mice, the resulting offspring have the mT cassette deleted in the cre expressing tissue(s), allowing expression of the membrane-targeted EGFP (mG) cassette located just downstream. The donating investigator reports that the ACTB promoter allows stronger and persistent expression of the fluorescent proteins (especially in adult cells) compared to the endogenous Gt(ROSA) locus alone. This double-fluorescent system allows direct live visualization of both recombined and non-recombined cells at single cell resolution, offering an internal control for phenotypic analysis of Cre-induced mosaic mutants and providing a second marker fo ..... For more information please see the full phenotype on the strain data sheet | ||
| 009674 | STOCK Gt(ROSA)26Sortm4(HIF2A*)Kael/J | Repository- Live |
| These LSL-HIF2dPA mice conditionally express a form of hemagglutinin (HA)-tagged human HIF2a (HIF2&alpha, HIF2dPA) cDNA that escapes recognition by the von Hippel-Lindau tumor suppressor protein by virtue of proline to alanine substitutions. When crossed with a tissue-specific cre strain, excision of a floxed stop cassette enables expression of the cDNA driven by the endogenous mouse Gt(ROSA)26Sor promoter. There is no expression until the mice are exposed to Cre recombinase. This strain may be useful in studies of von Hippel-Lindau disease mechanisms.
For example, when crossed to a strain expressing Cre recombinase in liver (see Stock No. 003574), this mutant mouse strain may be useful in studies of VHL disease. | ||
| 012266 | STOCK Gt(ROSA)26Sortm5(ACTB-tTA)Luo/J | Repository- Live |
| Mice homozygous for this ROSA26-ZtTA (or ZtTA) conditional allele are viable and fertile, although the donating investigator reports that heterozygous mice are more healthy and fertile than homozygous mice. This ROSA26-ZtTA (or ZtTA) conditional allele is designed with a loxP-flanked β-geo transcriptional STOP cassette preventing transcription of the downstream tetracycline-controlled transactivator protein (tTA). When bred to mice that express Cre recombinase, offspring will have the STOP cassette deleted and subsequent expression of the tTA in the cre-expressing cells. The donating investigator reports that the CMV enhancer/chicken beta-actin core promoter (pCA) allows stronger and persistent expression of the downstream tTA (especially in adult cells) compared to the endogenous Gt(ROSA)26Sor locus alone. Applying both Cre-lox and Tet-Off technologies, these ZtTA mutant mice may be useful to generate compound mutant mice in which expression of a tetracyclin ..... For more information please see the full phenotype on the strain data sheet | ||
| 013123 | STOCK Gt(ROSA)26Sortm6(Gli1)Amc/J | Repository- Live |
| These RosaGli1Flag c/c mice contain a floxed-neomycin resistance (neo) cassette and polyadenylation signal, cDNA encoding a FLAG-tagged GLI-Kruppel family member (Gli1) gene, an internal ribosome entry site (IRES), and a Venus yellow fluorescent protein (YFP) under control of the ubiquitous Gt(ROSA)26Sor locus. Breeding these mutant mice to mice that express Cre-recombinase will also result in Floxed-neo-stop excision. When these mice are crossed to mice containing Cre-recombinase under direction of an atonal homolog 1 (Math1) promoter, active in dividing granule neuron precursor cells and medulloblastoma tumors, the mice produce Gli1Flag at levels higher than the endogenous protein in the cerebellum. These mice may be useful for understanding Sonic hedgehog signaling and identifying targets of Gli1 action in developing ventral neural tube. | ||
| 003342 | STOCK Hbatm1Paz Hbbtm1Tow Tg(HBA-HBBs)41Paz/J | Repository- Live |
| This strain was engineered so that it no longer expresses mouse Hba and Hbb, but does express human HBA and HBB. It mimics the genetic, hematologic and histopathologic features that are found in humans afflicted with sickle cell anemia, including irreversibly sickled red blood cells, anemia and multiorgan pathology. A significant percentage of sickle cell mice do not survive to adulthood. | ||
| 012640 | STOCK Hdac2tm1.2Rdp/J | Repository- Live |
| These HDAC2KO mutant mice lack exons 5-6 of the mouse histone deacetylase 2 (Hdac2) gene. Mice that are homozygous for this allele are viable, fertile, although the donating investigator reports that homozygous mice are born at a twofold lower frequency than expected from a normal Mendelian ratio. These mice have an increased synapse number and enhanced memory formation. This strain may be useful for studying the functional and structural synaptic changes and neuronal adaptive responses implicated in memory formation and storage. | ||
| 014178 | STOCK Hey2tm1Eno/J | Repository- Live |
| These mice possess loxP sites on either side of exons 2 and 3 of the targeted gene, which encode amino acids 29-82. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 2 and 3 deleted in the cre-expressing tissue(s).
When bred to a strain with Cre recombinase expression in vascular smooth muscle (see Stock No. 004746 for example), this mutant mouse strain may be useful in studies of ventricular septal defect cardiac development. When bred to a strain with Cre recombinase expression in developing heart, pharynx, this mutant mouse strain may be useful in studies of cardiac development. | ||
| 014543 | STOCK Hgftm1.1(HGF)Aveo Prkdcscid/J | Repository- Live |
| Mice homozygous for both the hHGFki and Prkdcscid alleles, also called immunocompromised hHGFki mice, are viable and fertile.
The hHGFki allele is a "humanized" knock-in mutation that replaces the mouse hepatocyte growth factor (HGF) coding region downstream of the signal sequence with the human HGF cDNA sequence. As a result, the endogenous mouse promoter drives expression of human HGF. While the human HGF activates both the human and murine form of its tyrosine kinase receptor (met proto-oncogene (MET; c-Met)), the murine HGF is unable to activate human MET. Mice homozygous for hHGFki express only the human form of HGF. In homozygous hHGFki mice, HGF expression from the knock-in allele is observed in developing embryo, as well as adult liver, kidney and lung. hHGFki homozygous mice exhibit an increase in serum HGF after clotting. Mice homozygous for the Prkdcscid mutation exhibit T- and B-cell deficiency. | ||
| 005051 | STOCK KitW-sh/HNihrJaeBsmJ | Repository- Live |
| Kit mutations affect melanogenesis, hematopoiesis and gametogenesis. The sash mutation affects melanoblast survival. Melanoblast density is severely reduced in homozygotes by E12 (Cable et al., 1995). Homozygote are white with black eyes and some pigment around the ears. Heterozygotes are black with a white sash at the midline. The KitW-sh mutation affects Kit expression in a tissue specific manner. Kit expression is abolished in mast cells and mutant mice have a mast cell deficit (Tono et al., 1992, Berrozpe et al., 1999). However, young animals (<4 weeks) have been reported to have mast cells in skin (Yamakazi et al., 1994). KitW-sh mRNA is expressed normally in the cerebellum and is weakly expressed in testis and spleen (Tono et al., 1992). In contrast to the KitW and KitW-v mutations, KitW-sh germ cells and erythrocytes are not affected. Homozygtes have some ..... For more information please see the full phenotype on the strain data sheet | ||
| 012874 | STOCK Map3k11m1J/GrsrJ | Repository- Live |
| Mice homozygous for the Map3k11m1J mutation can be identified easily as early as 3 to 4 days of age by the dorsal lines of dark red skin that run from head to tail along the spine and from left to right across the crown of the head, base of the neck in front of the shoulders, and between the base of the ribs and the pelvis. These lines fade away and by 3 weeks of age are no longer evident even when the homozygote is shaved to expose the skin. Homozygotes have necrotic dental pulp, which also improves with age. | ||
| 004779 | STOCK Mapttm1(EGFP)Klt/J | Repository- Live |
| Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. A knock-in of the EGFP coding sequence into the first exon disrupts expression of the Mapt gene and produces a cytoplasmic EGFP fused to the first 31 amino acids. No gene product (isoform proteins) is detected in whole brain lysates by Western blot analysis. EGFP signal is detected beginning at 9.0 days post coitum in the trigeminal ganglion and by 10.75 days post coitum fluorescent signal is detected throughout the developing central nervous system. EGFP expression persists to adult and closely patterns the expression of neuron specific beta-tubulin III, as detected by the TuJ1 antibody. The expression of cytoplasmic EGFP in the central nervous system of this mutant allows for non-invasive visualization of elongating nerve axons. | ||
| 014610 | STOCK Mecp2tm3.1Bird/J | Repository- Live |
| A targeted mutation was designed to insert an enhanced green fluorescent protein sequence (EGFP) sequence in the 3' UTR of the methyl CpG binding protein 2 (Mecp2) gene. Homozygous females and male carriers are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Mecp2 is located on the X-chromosome, and exhibits increased expression in the central nervous system during neuronal maturation. Mutations in the Mecp2 gene can cause Rett Syndrome, an autism-spectrum neurodevelopmental disorder. Under control of the endogenous Mecp2 promoter, these mice express EGFP in neurons throughout the brain at levels consistent with endogenous MECP2 expression in wildtype mice from the colony. These mice may be useful for visualizing MECP2 expressing neuronal cells. | ||
| 008458 | STOCK Mirc1tm1.1Tyj/J | Repository- Live |
| The miR-17~92 (Mir17, Mir18, Mir19a, Mir20a, Mir19b-1, Mir92-1) cluster, overexpressed in human cancers, is flanked by loxP sites in this targeted mutation strain. Mice homozygous for the floxed miR17~92 allele (miR17~92fl/fl) are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. | ||
| 008460 | STOCK Mirc3tm1.1Tyj/J | Repository- Live |
| The miR-106b~25 (Mir106b, Mir93, Mir25) cluster, located in intron 13 of the Mcm7 (minichromosome maintenance deficient 7 (S. cerevisiae)) gene, is deleted in this targeted mutant strain. Mice homozygous for this null allele (miR-106b~25delta) are viable and fertile and do not display any gross physical or behavioral abnormalities. This strain may be useful in characterizing this genetic region, a paralog of the miR-17~92 region. Expression of Mcm7 is unaffected. | ||
| 014120 | STOCK Mkxtm1.2Jian/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross behavioral abnormalities. By 2 weeks of age, homozygotes have wavy tails that are obvious when the mice are running. In the tails of homozygotes, tendon morphology is abnormal (crimp patterning), smaller in size than wildtype controls and tendon insertions on vertebrae are not easily seen. Limb tendons are also smaller with abnormal morphology. Tendon fibrils from mutants exhibit smaller diameter when compared to wildtype controls as early as postnatal day 5. Tendon sheaths from homozygotes are thicker and have more cell layers than wildtype controls. | ||
| 009079 | STOCK Mll1tm2(MLLT3)Thr/KsyJ | Repository- Live |
| The Mll-AF9 knock-in allele encodes a MLL-AF9 fusion protein that mimics the t(9;11)(p22;q23) translocation identified in acute myeloid leukemia (AML) patients. While homozygous mice are not viable, heterozygotes are viable and fertile but females are poor mothers and may not survive pregnancy. Expression of the MLL-AF9 fusion protein results in development of leukemia beginning around six months of age; almost all of which are AMLs. Detectable proliferation of myeloid cells is observed in bone marrow by as little as six days after birth, and this early accumulation of myeloid precursors likely confers a greater chance of acquiring secondary mutations that cooperate in the appearance of overt cancer. These Mll-AF9 knock-in mice may be useful for studying hematopoietic development, cancer, and AML. | ||
| 007022 | STOCK Mnx1tm4(cre)Tmj Smn1tm1Msd Tg(SMN2*delta7)4299Ahmb Tg(SMN2)89Ahmb/J | Repository- Live |
| Mice homozygous for the Tg(SMN2*delta7)4299Ahmb and Tg(SMN2)89Ahmb transgenes and the Smntm1Msd targeted mutation allele exhibit symptoms and neuropathology similar to patients afflicted with severe proximal spinal muscular atrophy (SMA), and a similar phenotype observed in Stock no. 005025. At birth, triple mutants are noticeably smaller than normal littermates. By day 5, signs of muscle weakness are apparent and become progressively more pronounced over the following week as the mice display an abnormal gait, shakiness in the hind limbs and a tendency to fall over. In addition, this strain carries the Mnx1 For more information please see the full phenotype on the strain data sheet | ||
| 014179 | STOCK Mov10l1tm1.1Eno/J | Repository- Live |
| These mice possess loxP sites on either side of exon 20, which encodes a helicase domain. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 20 deleted in the cre-expressing tissue(s).
When bred to a strain with widespread expression of Cre recombinase, this mutant mouse strain may be useful in studies of retrotransposon activiation in male germ cells. Global homozygous deletion results in male infertility due to apoptosis of pachytene spermatocytes. | ||
| 013169 | STOCK Nphp1tm1Jgg/J | Repository- Live |
| Homozygous Nphp1 (nephronophthisis 1 (juvenile) homolog (human)) targeted mutation mice lack protein expression (examined in testes) and gradually develop a mild retinal degeneration that is slightly evident at 2 months of age. | ||
| 005692 | STOCK Nphs1tm1Rkl/J | Repository- Live |
| Mice that are heterozygous for the Nephrin KO/GFP knock-in mutation are viable and fertile. Homozygous mice die within a few days after birth with massive glomerular vascular leak and an absence of glomerular epithelial slit diaphragms. No gene product is detected by Western blot of kidney tissue of homozygotes. Green fluorescent protein (GFP) is detected in glomeruli of homozygotes and heterozygotes. Newborn homozygotes show extensive proteinuria, while heterozygotes show none. These Nephrin KO/GFP knock-in mice may be useful in studying nephrotic syndrome or any of the diseases where plasma ultrafiltration is affected. | ||
| 007658 | STOCK Npr2tm1Gar/J | Repository- Live |
| Homozygous females are not fertile due to the failure of their reproductive tract development. Homozygous males are also infertile; although spermatogenesis and accessory structures appear unaffected, abnormalities in the neuronal control of penile erection have been found. Null mice are notably smaller than their wildtype and heterozygous littermates several days after birth. Heterozygous mice show a slight reduction in naso-anal length. A dramatic impairment of endochondral ossification and an attenuation of longitudinal vertebra or limb-bone growth are also seen in null animals. They show self-clasping and priapism, suggesting neuronal disorders, but no histological abnormalities are seen in the brain or spinal cord. Survival is reduced. Lethal tonic-clonic seizure attacks have been observed. mRNA is not detected in the brain, growth-plate cartilage, or primary cultures of dermal fibroblasts as determined by Northern blot analysis. This strain may be useful in studies of bo ..... For more information please see the full phenotype on the strain data sheet | ||
| 001618 | STOCK Oca2p Prop1df/J | Repository- Live |
| Mice homozygous for the Ames dwarf spontaneous mutation (Prop1df) resemble mice homozygous for the Snell's dwarf mutation (Pit1dw). Homozygous Ames dwarf mutant mice show growth retardation after the first postnatal week, and weight at 2 months is only about one-half normal. Females and most males are sterile. There is no detectable growth hormone or prolactin. Ames dwarf mice have a secondary immune deficiency presumably resulting from the lack of growth hormone. | ||
| 012871 | STOCK Pik3r1tm1Lca/J | Repository- Live |
| Mice homozygous for this p85αloxP allele are viable and fertile, with loxP sites flanking exon 7 of the targeted gene. The Pik3r1 locus encodes three proteins (p85α, p55α, and p50α) that arise from alternative transcription initiation sites; and exon 7 is the first common exon for all three isoforms. When bred to mice that express Cre recombinase, the resulting offspring will have exon 7 deleted in the cre-expressing tissue(s); splicing of upstream exons (exon 6, 1b, or 1c) directly into the downstream exon 8 results in a frameshift mutation that introduces an immediate stop codon. Such a deletion should prevent the translation of the SH2 and p110-binding domains, eliminating the ability to form a functional protein from any of the three transcription initiation sites. These mutant mice may be useful in generating conditional mutations for studying class IA phosphoinositide 3-kinases (PI3Ks) in cell growth, cell proliferation cell ..... For more information please see the full phenotype on the strain data sheet | ||
| 014141 | STOCK Prkaa1tm1.1Sjm/J | Repository- Live |
| These Prkaa1 mutant mice possess loxP sites flanking exon 3 of the protein kinase, AMP-activated, alpha 1 catalytic subunit (Prkaa1) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Prkaa1 belongs to the serine/threonine protein kinase family and is a catalytic subunit of the 5'-prime-AMP-activated protein kinase (AMPK). AMPK is a sensor of the energy status of cells and promotes survival during stress. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exon 3 deleted in the cre-expressing tissues. When bred to transgenic mice expressing Cre recombinase driven by myxovirus (influenza virus) resistance 1 (Mx1) promoter/enhanced elements, PRKAA1 expression is abolished in hematopoietic cells. This strain may be useful for studying cell growth and energy expenditure. | ||
| 003081 | STOCK Ptch1tm1Mps/J | Repository- Live |
| Mice homozygous for the targeted mutation die during embryogenesis and are found to have open and overgrown neural tubes. Heterozygous patched mice are larger than wild-type littermates and have a low incidence of hindlimb defects. Some heterozygotes develop brain tumors beginning around 5 weeks of age. Heterozygotes express lacZ in a pattern mimicking endogenous gene expression pattern. Homozygous embryos display derepressed lacZ expression starting at embryonic day 8.0. | ||
| 006770 | STOCK Rag1tm1Mom Tg(TIE2GFP)287Sato/J | Repository- Live |
| To generate this double mutant strain, B6.Cg-Tg(TIE2GFP)287Sato/1J (Stock No. 004659) was crossed to C.129S7(B6)-Rag1tm1Mom/J (Stock No. 003145). This mutant mouse strain may be useful in studies examining angiogenesis in transplanted tissues. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described for each single mutant. We will modify the strain description if necessary as published results become available. | ||
| 015832 | STOCK Rims1tm3Sud/J | Repository- Live |
| 015833 | STOCK Rims2tm1.1Sud/J | Repository- Live |
| These mice possess loxP sites on either side of exon 26 in the Rims2 (regulating synaptic membrane exocytosis 2) gene. An in-frame ECFP-tetracysteine tag is fused to the floxed exon, enabling immunofluorescent detection. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the α, β, and γ isoforms of the gene. | ||
| 013197 | STOCK Sagtm1Jnc/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mutant mice are photosensitive and if not maintained under low light conditions will develop progressive retinal degeneration. No gene product (protein) is detected by Northern blot analysis of retinas from homozygous mice maintained in cyclic (12 hour light: 12 hour dark) conditions. Photoreceptor loss in homozygotes maintained in cyclic light conditions begins at approximately 100 days of age, progressing to loss of more than half of the photoreceptors by 1 year of age. After 1 week of constant light exposure, homozygotes lose 30% of photoreceptors; after 3 weeks of constant light exposure, more than 60% of photoreceptors are lost. Homozygotes maintained under cyclic light conditions exhibit disorganized and 25% shorter retinal rod outer segment layer, as well as reduced levels of retinal rhodopsin. Recovery phase respon ..... For more information please see the full phenotype on the strain data sheet | ||
| 014645 | STOCK Sec24bY613X/J | Repository- Live |
| Mice heterozygous for this ENU-induced mutation (Sec24bY613X), are viable and fertile, although the donating investigator reports that 33% of homozygous mice are dead or dying by E18.5. Sec24b is a cargo-sorting member of the core complex of the COPII endoplasmic reticulum (ER)-Golgi transport vesicle, and is critical for neural tube closure. These mice contain a premature stop codon in exon 9 of the Sec24 related gene family, member B (Sec24b) gene. Sec24bY613X homozygotes develop craniorachischisis, a fully open neural tube from the midbrain-hindbrain boundary to the most caudal end of the neural tube. These mice exhibit deficits in convergent extension and other planar cell polarity phenotypes. At E18.5, 45% of embryos exhibit omphalocele and 99% exhibit eyelid fusion failure. Also, outer and inner cochlear hair cells periodically fall out of phase and are abnormally aligned. These mutant mice may be useful in studying planar cel ..... For more information please see the full phenotype on the strain data sheet | ||
| 012898 | STOCK Slc17a6tm1Lowl/J | Repository- Live |
| These Vglut2flox mutant mice possess loxP sites flanking exon 2 of the solute carrier family 17 (sodium-dependant inorganic phosphate cotransporter), member 6 (Slc17a6 or Vglut2) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 deleted in the cre-expressing tissue. These mice may be useful for studying the effect of transport, packaging, and release of glutamate from ventromedial hypothalamic (VMH) neurons on hypoglycemia. | ||
| 012897 | STOCK Slc32a1tm1Lowl/J | Repository- Live |
| These Vgatflox/flox mutant mice possess loxP sites flanking exon 2 of the solute carrier family 32 (sodium-dependant inorganic phosphate cotransporter), member 1 (Slc32a1 or Vgat) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 deleted in the cre-expressing tissue. These mice may be useful for studying the physiological effect of GABAergic neurotransmission on the regulation of energy balance.
For example, when crossed to a strain expressing Cre recombinase in agouti-related protein (AgRP) secreting neurons (see Stock No. 012899), this mutant mouse strain may be useful in studies of energy balance. | ||
| 008212 | STOCK Smn1tm1Msd Tg(Prnp-SMN)92Ahmb Tg(SMN2)89Ahmb/J | Repository- Live |
| As described for SMA mice (see Stock No. 005024), mice homozygous for Smn1tm1Msd targeted mutation (Smn null allele) and human SMN2 transgene (SMN2 low copy line 89) exhibit symptoms, neuropathology, and early lethality similar to human type I proximal spinal muscular atrophy (SMA) patients. As an addition to that SMA model, this strain also carries the PrP-SMN transgene; with the mouse prion protein (PrP or Prnp) promoter directing full-length human SMN expression at high levels in neurons (with low expression in skeletal muscle and liver). When the PrP-SMN transgene is derived from PrP92-SMN founder mice, high SMN expression in spinal cord and brain is observed. Homozygous SMN2; Smn; Prp92-SMN mice are rescued from the severe SMA phenotype, have significantly increased lifespan (average of 210 days) and have normal lumbar motor neuron root counts. Homozygous SMN2; Smn; PrP92-SMN mal ..... For more information please see the full phenotype on the strain data sheet | ||
| 007951 | STOCK Smn1tm3(SMN2/Smn1)Mrph Tg(SMN2*delta7)4299Ahmb Tg(SMN2)89Ahmb/J | Repository- Live |
| This triple mutant mouse harbors two transgenic alleles and a single targeted mutation. The Tg(SMN2*delta7)4299Ahmb allele consists of a human SMN2 (survival of motor neuron 2, centromeric) cDNA lacking exon 7 whereas the Tg(SMN2)89Ahmb allele consists of the entire human SMN2 gene. Mice that are homozygous for the targeted mutant Smn1tm3(SMN2/Smn1/SMN2)Mrph allele and homozygous for the two transgenic alleles should function similarly to SMA mutant strain FVB.Cg-Tg(SMN2*delta7)4299Ahmb Tg(SMN2)89Ahmb Smn1tm1Msd/J (Stock No. 005025). The targeted mutant Smn1tm3(SMN2/Smn1/SMN2)Mrph allele is engineered to revert to a fully functional Smn1 allele upon Cre-mediated recombination. This mutant mouse strain may be useful in studies of Spinal Muscular Atrophy.
Importation of this model was supported by the Spinal Muscular Atrophy Foundation. | ||
| 004526 | STOCK Smotm2Amc/J | Repository- Live |
| These mice possess loxP sites on either side of exon 1 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to a strain with the targeted null allele (Stock No. 004288) and a strain expressing Cre recombinase in the skin (Stock No. 004782), this mutant mouse strain may be useful in studies of hedgehog signalling and cell proliferation in the dental epithelium. When bred to a strain with the targeted null allele (Stock No. 004288) and a strain expressing Cre recombinase in the nervous system (Stock No. 003771), this mutant mouse strain may be useful in studies of hedgehog signalling and cerebellar foliation. When bred to ..... | ||
| 013093 | STOCK Sox2tm1.1Lan/J | Repository- Live |
| These Sox2flox mutant mice possess loxP sites flanking the coding exon of SRY-box containing gene 2 (Sox2). Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice that express tissue-specific Cre recombinase, the resulting offspring will have no Sox2 expression in cre-expressing tissues. This strain may be useful for studying eye and lens development. | ||
| 013044 | STOCK Ssttm2.1(cre)Zjh/J | Repository- Live |
| The Sst-IRES-Cre (or SOM-IRES-Cre) allele harbors an internal ribosome entry site and Cre recombinase in the 3' UTR of the somatostatin locus (Sst). As such, cre expression is directed by the endogenous Sst promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When Sst-IRES-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Sst-expressing cells in the offspring.
The donating investigator reports Cre recombinase activity is specific and efficient; largely recapitulating the endogenous somatostatin expression pattern with efficient recombination. They report Cre recombinase activity is observed in somatostatin positive neurons (including dendritic inhibitory interneurons such as Martinotti cells and Oriens-Lacunosum-Molecular ..... | ||
| 014143 | STOCK Stk11tm1.1Sjm/J | Repository- Live |
| These Stk11 mutant mice possess loxP sites flanking exons 3-6 of the serine/threonine kinase 11 (Stk11) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Stk11 is a member of the serine/threonine kinase family and regulates cell polarity and cell division, and controls cell energy expenditure. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exons 3-6 deleted in the cre-expressing tissues. When bred to transgenic mice expressing Cre recombinase driven by myxovirus (influenza virus) resistance 1 (Mx1) promoter/enhanced elements, STK11 expression is abolished in hematopoietic cells. This strain may be useful for studying cell growth and tumor suppression.
For example, when crossed to a strain expressing tamoxifen-inducible Cre recombinase (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 015836 | STOCK Syt12tm1.1Sud/J | Repository- Live |
| Exon 4 of this Syt12 (synaptotagmin XII) targeted mutation strain is flanked by loxP sites and carries a serine to alanine mutation at residue 97 (S97A). Serine 97 is a protein kinase A (PKA) phosphorylation site and the point mutation abolishes the increase of spontaneous neurotransmitter release by Syt12 overexpression in primary cortical culture. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the gene. Floxed mice express the targeted gene at levels comparable to wild type, as demonstrated by Western blot of whole brain. | ||
| 012719 | STOCK Tgfb3tm1(cre)Vk/J | Repository- Live |
| Mice heterozygous for the Tgfb3-cre allele are viable, fertile, and normal in size. Homozygotes die at birth due to cleft palate. Expression of Cre recombinase is driven by the transforming growth factor β 3 (Tgfb3) locus. Specifically, Cre recombinase expression is observed in the heart, pharyngeal arches, otic vesicle, mid brain, limb buds, midline palatal epithelium, and whisker follicles during embryo and fetus development. When these transgenic mice are bred with mice containing a loxP-flanked sequence, Cre-mediated recombination results in deletion of the floxed sequences in the Cre-expressing tissues of the offspring. This strain may be useful for studying the palatal epithelium during facial development and the vasculature of the central nervous system. | ||
| 012620 | STOCK Trp53tm1Brd Brca1tm1Aash Tg(LGB-cre)74Acl/J | Repository- Live |
| BLG-Cre; Brca1F22-24/F22-24; p53+/- mice carry the beta-lactoglobulin (BLG)-Cre transgene, are homozygous for floxed exons 22-24 of the breast cancer 1 (Brca1) allele, and are heterozygous for p53 tumor-suppressor gene (p53) deficiency. Mice of this genotype are viable, fertile, normal in size and do not display any behavioral abnormalities. BLG-Cre; Brca1F22-24/F22-24; p53+/- females have expression of the BLG-Cre transgene during lactation; which leads to loss of Brca1 function in the mammary gland. This results in formation of mammary tumors exhibiting high grade central necrosis and metaplastic elements in the form of spindle cell and squamous cell differentiation; as seen in human basal-like breast cancers and BRCA1 mutation carriers. Heterozygosity for the mutant p53 allele accelerates the formation of mammary tumors. This strain may be useful for studying human basal-like cancer and breast ..... For more information please see the full phenotype on the strain data sheet | ||
| 008813 | STOCK Trpa1tm2Kykw Tg(CAG-cre/Esr1*)5Amc/J | Repository- Live |
| These compound mutant mice carry a floxed allele of the Trpa1 (transient receptor potential cation channel, subfamily A, member 1) gene in addition to a tamoxifen inducible cre transgene driven by the chicken beta actin promoter/enhancer coupled with the cytomegalovirus (CMV) immediate-early enhancer (see Stock No. 004682). Restricted to the cytoplasm, the cre/Esr1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. Tamoxifen administration induces cre recombination within the Trpa1 allele, excising the S5/S6 transmembrane domains. Animals not treated with tamoxifen display no observable phenotype. | ||
| 014581 | STOCK Trpm8tm1Apat/J | Repository- Live |
| These mutant mice express farnesylated enhanced GFP gene (EGFPf) from the endogenous Trpm8 locus. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No wildtype gene product (mRNA) is detected although low levels of a truncated mRNA splice variant is sometimes detected by RT-PCR analysis of total RNA derived from dorsal root ganglia (DRG) isolated from homozygotes. No Trpm8 locus mRNA is detected by in situ hybridization of DRG isolated from homozygotes. In thermotaxis assays performed in a cage equipped with surface temperature gradients, homozygous mice spend less time in the warmer area compared to wildtype controls. Homozygotes display diminished responses to application of acetone and injection of icilin. Noxious cold sensation of colder temperatures (sub zero) is normal. Mutant mice do not display cold-induced analgesia in response to pain. EGFPf-positive n ..... For more information please see the full phenotype on the strain data sheet | ||
| 005680 | STOCK Tsc1tm1Djk/J | Repository- Live |
| Homozygous mice are viable, fertile, normal in size, have normal expression of hamartin (the targeted gene's protein product), have no growth or behavioral defects, and are devoid of tumors through age 18 months. This mutant carries a "floxed" allele of the endogenous gene. When combined with a mutant carrying a Cre recombinase gene under the control of a promoter of interest, exons 17 and 18 of Tsc1 are deleted in the tissue of interest. This mutant may be useful in many tissue-specific studies including tuberous sclerosis or other hamartoma syndromes, regulation of the actin cytoskeleton and motility, cellular and organismal glucose homeostasis, cell growth responses, apoptosis regulation, and regulation of cell size.
When bred to a strain expressing Cre recombinase in neuronal cells (see Stock No. 003966 for example), this mutant mouse strain may be useful in studies of tuberous sclerosis.
When ..... | ||
| 006104 | STOCK Ush1cdfcr-3J/J | Repository- Live |
| Mice homozygous for the deaf circler 3 Jackson mutation display head bobbing and rapid circling and are deaf. This strain is maintained segregating for coat color alleles resulting in agouti and albino mice. | ||
| 014563 | STOCK Utrntm1Ked Dmdmdx/J | Repository- Live |
| Female mice that are homozygous for the Utrntm1Ked allele and the Dmdmdx allele, and male mice that are homozygous for the Utrntm1Ked allele and hemizygous for the Dmdmdx allele, exhibit a more severe phenotype than single Dmdmdx mutants: earlier onset of muscle dystrophy (degeneration, macrophage infiltration and necrosis), weight loss after weaning, joint contractures, kyphosis, dystrophy of extraocular muscles, abnormal electrocardiograms, infertility and premature death. Growth retardation onset is at weaning. By 4 of 6 weeks of age, the double mutants exhibit reduced body weight, reduced mobility, abnormal breathing pattern and slack posture. Muscle weakness and kyphosis (curvature of the spine) is progressive and the double mutant mice develop a waddling gait. Necrosis of the diaphragm muscle is observed in 6 day old double mutant mice. Muscle fibers with centralized nuclei are seen in ..... For more information please see the full phenotype on the strain data sheet | ||
| 013158 | STOCK Utrntm1Ked/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of kidney, lung and brain tissues. Levels of transcript are significantly reduced, as detected by RNase protection assay. Neuromuscular junctions from homozygotes lack extrasynaptic nerve sprouts, exhibit reduced postsynaptic membrane folding and fewer (approximately 40% reduction) acetylcholine receptors. The amplitude of miniature endplate currents (in extensor digitorum longus muscle) is reduced by 20%. Homozygotes exhibit abnormal Schwann cell compartments and reduced internodal length.
When bred with mice carrying the Dmdmdx allele (see Stock No. 001801) the resulting double mutant mice exhibit a more severe phenotype than single Dmdmdx mutants: earlier onset ..... | ||
| 010908 | STOCK Viptm1(cre)Zjh/J | Repository- Live |
| The Vip-IRES-Cre allele harbors an internal ribosome entry site and Cre recombinase in the 3' UTR of the vasoactive intestinal polypeptide locus (Vip). As such, cre expression is directed by the endogenous Vip promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When Vip-IRES-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Vip-expressing cells in the offspring.
The donating investigator reports Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Vip expression pattern with highly efficient recombination). They report Cre recombinase activity in some GABAergic interneurons, and did not examine cre expression in the intestine or tissues other than brain. | ||
| 016116 | STOCK Waptm2(rtTA)Kuw/J | Repository- Live |
| These mice contain a reverse tetracycline-controlled transactivator (rtTA) protein in the 5' untranslated region of the whey acidic protein (Wap) gene. Homozygous mice are viable, fertile, and normal in size. WAP, expressed late during pregnancy and during lactation in the mammary gland, is the principal whey protein found in rodent milk. When mated to a mutant strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TetO), the Wap-rtTA allele mediates expression of TetO-responder genes in the developing mammary gland upon administration of doxycycline (dox). Since expression of the endogenous WAP locus is elevated during pregnancy and lactation, the expression of TetO responder genes is particularly high during these stages of mammary gland development. The Wap-rtTA mice are useful to express exogenous proteins including teto-regulated oncogenes in the mammary epithelium. | ||
| 010911 | STOCK Wt1tm1(EGFP/cre)Wtp/J | Repository- Live |
| Homozygous mice die between embryonic day (E)13.5 and birth with defects of heart, kidney, gonads, and multiple other organs. Heterozygous (Wt1GFPCre/+) mice are viable and fertile. The Wt1GFPCre "knock-in" allele both abolishes Wt1 gene function and expresses an enhanced green fluorescent protein-Cre recombinase fusion protein (EGFPCre) from the Wt1 promoter/enhancer elements. In heart from heterozygous mice, EGFPCre expression is directed to proepicardium and epicardium from E9.5 to E15.5, and is not found in the myocardium. When bred to mice containing loxP-flanked sequences, the resulting offspring will have Cre-mediated deletion of the floxed sequences in the Wt1-expressing cells (and their descendants). As Wt1 is expressed in the developing genitourinary system and in the mesothelia overlying most visceral organs, these mutant mice may be useful as fluorescent/Cre-lox tools for lineage-tracing/marking Wt1-expressin ..... For more information please see the full phenotype on the strain data sheet | ||
| 010912 | STOCK Wt1tm2(cre/ERT2)Wtp/J | Repository- Live |
| Homozygous mice die between embryonic day (E)13.5 and birth with defects of heart, kidney, gonads, and multiple other organs. Heterozygous (Wt1CreERT2/+) mice are viable and fertile. The Wt1CreERT2 "knock-in" allele both abolishes Wt1 gene function and has expression of the CreERT2 fusion protein (CreERT2) under control of the Wt1 promoter/enhancer elements. In heart from heterozygous mice, CreERT2 expression is directed to proepicardium and epicardium from E9.5 to E15.5, and is not found in the myocardium. CreERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Wt1CreERT2 mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Wt1-expressing cells of the offspring. The donating investigator reports that Cre activity may be observed prior to tamoxifen exposure only in ..... For more information please see the full phenotype on the strain data sheet | ||
| 017007 | STOCK fsq/GrsrJ | Repository- Live |
| At approximately two months of age, flying squirrel homozygotes stiffen throughout their trunk and limbs, particularly on the ventral side of the body, and when picked up take on a rigid spread out posture. As a result they walk with a slight stagger. Homozygotes are not fertile but do live to adulthood. | ||
| 006857 | STOCK ne/J | Repository- Live |
| Mice homozygous for the no eyelid mutation have a range of phenoytpes with varying penetrance including missing eyelid, closed eyelids, microphthalmia, ocular deformities, malformed digits, malformed ear pinnae, renal agenesis, and slight discoloration of the fur on the head. | ||
| 012691 | STOCK Et(icre/ERT2)14374Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap lentiviral transgene are viable and fertile, with expression of an iCreERT2 fusion gene (an optimized variant of Cre recombinase [iCre; improved with mammalian codon usage, removed putative cryptic splice sites, altered stop codon, and reduced CpG content to limit the chances of epigenetic silencing in mammals] fused to Cre-ERT2 [a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain]) under control of the promoter/enhancer regions surrounding the site where the enhancer trap lentiviral transgene randomly inserted. While Cre-ERT2 fusion gene activity is designed to be inducible (observed following tamoxifen administration), some minor Cre recombinase activity is observed without tamoxifen in these mice.
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as:
many cells in hippocampus (including dentate gyrus projections), with very sparse coverage in all oth ..... For more information please see the full phenotype on the strain data sheet | ||
| 012692 | STOCK Et(icre/ERT2)14602Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap lentiviral transgene are viable and fertile, with expression of an iCreERT2 fusion gene (an optimized variant of Cre recombinase [iCre; improved with mammalian codon usage, removed putative cryptic splice sites, altered stop codon, and reduced CpG content to limit the chances of epigenetic silencing in mammals] fused to Cre-ERT2 [a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain]) under control of the promoter/enhancer regions surrounding the site where the enhancer trap lentiviral transgene randomly inserted. Cre-ERT2 fusion gene activity is designed to be inducible (observed following tamoxifen administration).
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as:
scattered cells in most areas of the brain, with more cells in hippocampus (perhaps more staining in CA2 & CA3 regions; dentate gyrus projections are stained more than cell bodies). No Cre ..... For more information please see the full phenotype on the strain data sheet | ||
| 012693 | STOCK Et(icre/ERT2)14624Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap lentiviral transgene are viable and fertile, with expression of an iCreERT2 fusion gene (an optimized variant of Cre recombinase [iCre; improved with mammalian codon usage, removed putative cryptic splice sites, altered stop codon, and reduced CpG content to limit the chances of epigenetic silencing in mammals] fused to Cre-ERT2 [a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain]) under control of the promoter/enhancer regions surrounding the site where the enhancer trap lentiviral transgene randomly inserted. While Cre-ERT2 fusion gene activity is designed to be inducible (observed following tamoxifen administration), some minor Cre recombinase activity is observed without tamoxifen in these mice.
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as:
scattered cells in cortex, hippocampus, with more cells in the CA3 region, midbrain, and granule cell l ..... For more information please see the full phenotype on the strain data sheet | ||
| 001379 | STOCK In(4)56Rk Rd4/J | Repository- Live |
| 000729 | STOCK Rb(11.13)4Bnr/J | Repository- Live |
| 013749 | STOCK Tg(ACTB-EGFP,-tdTomato)11Luo/J | Repository- Live |
| Homozygous MADM-11GT mice are viable and fertile with no gross behavioral or observable abnormalities. The MADM-11GT allele has the CMV enhancer/chicken beta-actin core promoter, the N-terminal portion of a mutant enhanced green fluorescent protein (mut4-EGFP), a beta-globin intronic sequence containing an frt site and a loxP-flanked neomycin resistance gene, and the MYC-tagged C-terminal portion of a red fluorescent protein (tdTomato) all inserted into the Hipp11 locus on chromosome 11 (cytoband A1 at ~3cM between the Eif4enif1 and Drg1 loci). These MADM-11GT mutants are designed for MADM (mosaic analysis with double markers), and must be crossed to MADM-11TG mice harboring a reciprocal mutation at the same locus (see Stock No. 013751). The resulting GT/TG offspring have one copy of each reciprocal mutation on homologous chromosomes ("trans-heterozygou ..... For more information please see the full phenotype on the strain data sheet | ||
| 014092 | STOCK Tg(ACTB-tTA2,-MAPT/lacZ)1Luo/J | Repository- Live |
| Homozygous CAG-stop-tTA2 transgenic mice are viable and fertile. CAG-stop-tTA2 transgenic mice harbor the ii-CAG-stop-tTA2-IRES-tau-lacZ-ii transgene; designed with a loxP-flanked transcriptional STOP cassette preventing transcription of the downstream modified tetracycline-regulated transactivator (tTA2). The ii-CAG-stop-tTA2-IRES-tau-lacZ-ii transgene is flanked by two copies of the chicken β-globin HS4 insulator on each side to preserve expression fidelity (see additional information below). When bred to mice that express a tamoxifen-inducible Cre recombinase (CreERT2), administration of tamoxifen to the double mutant offspring allows the CreERT2 fusion protein to enter the nucleus of the cre-expressing cells; this deletes the STOP cassette and results in expression of tTA2. The donating investigator reports that tau-lacZ fusion protein expression in the tamoxifen-treated double mutant offspring is faint. Of note, the donating investigator h ..... For more information please see the full phenotype on the strain data sheet | ||
| 013751 | STOCK Tg(ACTB-tdTomato,-EGFP)11Luo/J | Repository- Live |
| Homozygous MADM-11TG mice are viable and fertile with no gross behavioral or observable abnormalities. The MADM-11TG allele has the CMV enhancer/chicken beta-actin core promoter, the N-terminal portion of a red fluorescent protein (tdTomato), a beta-globin intronic sequence containing an frt site and a loxP-flanked neomycin resistance gene, and the C-terminal portion of a mutant enhanced green fluorescent protein (mut4-EGFP) all inserted into the Hipp11 locus on chromosome 11 (cytoband A1 at ~3cM between the Eif4enif1 and Drg1 loci). These MADM-11TG mutants are designed for MADM (mosaic analysis with double markers), and must be crossed to MADM-11GT mice harboring a reciprocal mutation at the same locus (see Stock No. 013749). The resulting TG/GT offspring have one copy of each reciprocal mutation on homologous chromosomes ("trans-heterozygous"), and mu ..... For more information please see the full phenotype on the strain data sheet | ||
| 014177 | STOCK Tg(Afp-mCherry)1Hadj/J | Repository- Live |
| Afp::mCherry transgenic mice have the alpha fetoprotein (Afp) promoter/enhancer sequences driving expression of a monomeric red fluorescent protein, mCherry. Hemizygotes are viable, fertile, and normal in size. Under control of Afp, mCherry labels the visceral endoderm and its derivatives, including the visceral yolk sac and gut endoderm. Expression is also seen in fetal liver and pancreas, and in liver, pancreas, digestive tract and brain of postnatal mice. These mice may be useful as a bright and photostable means for visualizing morphogenesis and tissue rearrangements in the developing embryo. | ||
| 007684 | STOCK Tg(Atoh1-cre/Esr1*)14Fsh/J | Repository- Live |
| Mice hemizygous for this Math1-CreERT2 transgene are viable and fertile. Under control of the Math1 (Atoh1) enhancer, tamoxifen-inducible cre activity is observed in neural progenitors of the cerebellar rhombic lip, dorsal hindbrain and spinal cord, as well as in inner-ear primordia (with a limited amount of ectopic expression in the primordium of the hippocampus but not the cortex). The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to tamoxifen. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone ma ..... For more information please see the full phenotype on the strain data sheet | ||
| 003920 | STOCK Tg(CAG-Bgeo/GFP)21Lbe/J | Repository- Live |
| These Z/EG transgenic mice constitutively express lacZ under the control of the CMV enhancer/chicken actin promoter. Expression is widespread with notable exceptions being liver and lung tissue. Expression is observed throughout all embryonic and adult stages. When crossed with a Cre recombinase-expressing strain, lacZ expression is replaced with enhanced GFP expression in tissues expressing cre. This double reporter system makes it possible to distinguish a lack of reporter expression from a lack of Cre recombinase expression while providing a means to assess cre excision activity in live animals and cells. Although homozygotes are viable, attempts to breed homozygous mice proved unsuccessful. | ||
| 005441 | STOCK Tg(CAG-DsRed*MST)1Nagy/J | Repository- Live |
| Mice homozygous for this Actb-DsRed.T3 transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the red fluorescent protein variant DsRed.MST under the control of the chicken beta actin promoter coupled with the cytomegalovirus (CMV) immediate early enhancer. All tissues of homozygotes fluoresce red. Mice hemizygous for the transgene express red fluorescent protein less intensely than homozygotes. Expression is observed throughout all embryonic and adult stages and very high expression is found in pancreas, skeletal muscle, heart and seminal vesicle. | ||
| 003116 | STOCK Tg(CAG-EGFP)D4Nagy/J | Repository- Live |
| This transgenic strain carries the Enhanced Green Fluorescent Protein (Clontech) driven by chicken beta-actin promoter and CMV intermediate early enhancer. The transgene was found to have integrated on the X chromosome. Mice of this strain, and cells derived from them, can be distinguished from wildtype on the basis of fluorescence. Transgene expression is seen as early as ~embryonic day 2.75, as morula stage embryos begin to compact. Expression of EGFP is spatiotemporally widespread, though levels differ between different lineages (e.g., expression is slightly higher in the heart). As the transgene is located on the X chromosome, transgenic males will exclusively transmit the EGFP transgene to their female offspring, providing the basis for a non-invasive sexing assay based on green fluorescence. These mice may be useful for sex discrimination prior to overt sexual dimorphism (embryonic day 12.5), monitoring X-inactivation, and may be a source of fluorescently marked cells/tiss ..... For more information please see the full phenotype on the strain data sheet | ||
| 011106 | STOCK Tg(CAG-GFP*)1Hadj/J | Repository- Live |
| Mice harboring the lipid modified CAG-GFP* transgene are viable and fertile, normal in size and do not display any gross physical or behavioral abnormalities. The CAG promoter directs widespread expression of a glycosylphosphatidylinositol-tagged (GPI) green fluorescent protein (GFP) fusion throughout embryonic development and adulthood. Expression is targeted to the plasma membrane, Golgi membranes and some secretory vesicles. Expression is enriched in the apical regions of the plasma membrane. Hemizygotes and homozygotes exhibit identical distribution patterns, however, homozygotes exhibit increased fluorescence. This mutant mouse strain may be useful for in vivo imaging of cell morphology, plasma membrane dynamics and lipid localization. | ||
| 013753 | STOCK Tg(CAG-KikGR)33Hadj/J | Repository- Live |
| CAG::KikGR33 transgenic mice express a Kikume Green-Red (KikGR) photoconvertible fluorescent protein under the control of a CMV enhancer/chicken beta-actin promoter (CAGGS) promoter. Mice homozygous for the transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. KikGR, engineered from Favia favus coral, changes color from green to red upon activation in embryos, adult mice, and embryonic stem (ES) cells. At basal state, green fluorescence is seen in all cells. A single cell or group of cells at basal state, exposed to 405 nm wavelength light, undergo photo conversion and fluoresce red. Since KikGR is developmentally neutral and non-toxic, the movement of these fluorescent cells, and their progeny, can be imaged during embryonic development. Mice from founder line 33 exhibits widespread expression of KikGR, while mice from founder line 75 (Stock No. ..... For more information please see the full phenotype on the strain data sheet | ||
| 009678 | STOCK Tg(CAG-RAB9A)500Repa/J | Repository- Live |
| These transgenic mice express HA-tagged human RAB9A, member RAS oncogene family, gene (RAB9A) under the control of the CAG promoter (CAGGS, chicken beta actin promoter/enhancer coupled with the cytomegalovirus immediate-early enhancer). Transgene expression is detected in liver, brain, kidney, and skin, and is highest in brain and liver. Expression is approximately 30-fold higher than endogenous RAB9 protein in the liver. Mice that are hemizygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make the strain homozygous. This mutant mouse strain may be useful in studies of Niemann-Pick, type C (NP-C) disease.
Double mutant mice that carry this transgene and are homozygous for the Npc1m1N allele (see Stock No. 003092) exhibit a less severe phenotype than mice homozygous for t ..... | ||
| 003273 | STOCK Tg(CMV-rtTA)4Bjd/J | Repository- Live |
| Homozygous transgenic mice are viable, fertile, and display no overt phenotype. These mice carry the gene encoding the reverse tetracyline-controlled transactivator protein (rtTA) under the control of a human cytomegalovirus early promoter (PhCMV). When these mice are mated to a strain carrying a luciferase reporter gene coupled to a tetracycline-responsive promoter element (TRE; tetO), luciferase expression in the bitransgenic offspring is induced up to 105-fold by treatment with doxycycline (dox) in organs and tissues where PhCMVis known to be active, (i.e. muscle, kidney, thymus and pancreas). Little to no luciferase expression is induced in tissues where PhCMV is not active (i.e. lung, brain, liver and lymphocytes). These mice may be mated to strains containing a gene of interest coupled to a TRE to study the target gene expression effects under tissue-specific, dox-inducible regulation. Dox may be administered in the animals? water suppl ..... For more information please see the full phenotype on the strain data sheet | ||
| 009615 | STOCK Tg(Cartpt-cre)1Aibs/J | Repository- Live |
| Hemizygous Cart-Tg1-Cre mice are viable and fertile, with cre expression directed to cortex, hippocampus, and cerebellum by the Cartpt promoter/enhancer regions within the BAC transgene. The donating investigators may not have assessed expression in tissues other than brain. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in the offspring. These Cart-Tg1-Cre mice may be useful for generating conditional mutations for studying gain or loss of function and/or fate mapping in subgroups of brain tissues (including cortex, hippocampus, and cerebellum).
For characterization information, see images at the Allen Institute for Brain Science website (Cart-Tg1-Cre images). | ||
| 008241 | STOCK Tg(Cspg4-DsRed.T1)1Akik/J | Repository- Live |
| Mice hemizygous for the NG2DsRedBAC transgene are viable and fertile, expressing an optimized red fluorescent protein variant (DsRed.T1) under the control of the mouse NG2 (Cspg4) promoter/enhancer. DsRed.T1 fluorescence is detected in NG2 cells (oligodendrocyte progenitor cells) throughout the postnatal central nervous system, including the gray and white matter of the brain, cerebellum and spinal cord, and vascular mural cells; but not in mature oligodendrocytes, astrocytes, resting microglia, or neurons. DsRed.T1 fluorescence intensity is highest in cell bodies and can also be detected in distal processes, suggesting that tetrameric DsRed.T1 remains soluble and is not toxic to cells. In addition, DsRed.T1 fluorescence may be readily detected without using anti-DsRed antibodies and is suitable for identifying NG2 cells in live slices or for purifying NG2 cells via FACS. These NG2DsRedBAC transgenic mice may be useful for fluorescent labeling of NG2 cells (oligodendrocyte p ..... For more information please see the full phenotype on the strain data sheet | ||
| 003208 | STOCK Tg(DR4)1Jae/J | Repository- Live |
| MEFs prepared from the DR-4 mouse strain displayed resistance to concentrations of the drugs G418, 6-thioguanine, puromycin and hygromycin well above those used normally for the selection of drug-resistant ES cells. This mouse strain represents an economical donor for the production of multiple-drug resistant mouse embryonic fibroblasts (MEFs). | ||
| 008861 | STOCK Tg(Ela1-Cre/ERT2)1Stof/J | Repository- Live |
| These transgenic mice have a tamoxifen-inducible, Cre-mediated recombination system driven by the rat elastase 1, pancreatic (Ela1) promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the human estrogen receptor ligand binding domain (CreERT2). The mutant human estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the Cre/ESR1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. No cre activity is detectable without tamoxifen treatment. When these transgenic mice are bred with mice containing a loxP flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the flanked sequences in Ela1
expressing cells; making them useful in fate mapping of pancreatic acinar cells.
Hemizygous mutant mice are viable, fertile, normal in ..... For more information please see the full phenotype on the strain data sheet | ||
| 005938 | STOCK Tg(Eno2-cre)39Jme/J | Repository- Live |
| Mice hemizygous for this NSE39-Cre transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These NSE39-Cre mice harbor a transgenic insert consisting of the cre recombinase gene under the control of the promoter region of the rat neuron specific enolase (NSE or Eno2) gene. As such, Cre recombinase activity is directed to neurons with expression in many tissue types. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the flanked genome.
Specifically, these NSE39-Cre transgenic mice may also be useful in studies of spinal muscular atrophy (SMA) along with mice harboring a conditional (floxed) Smn1 gene (see Stock No. 006138 or Stock No. 006146).
Additional SMA strains expressing cre in striated muscle are av ..... For more information please see the full phenotype on the strain data sheet | ||
| 004623 | STOCK Tg(Fos-lacZ)34Efu/J | Repository- Live |
| These TOPGAL transgenic mice are a reporter strain that express Beta-galactosidase in the presence of the lymphoid enhancer binding factor 1/transcription factor 3 (LEF/TCF) mediated signaling pathway and activated Beta-catenin. The transgene contains the lacZ gene under the control of a regulatory sequence consisting of three consensus LEF/TCF-binding motifs upstream of a minimal c-fos promoter. Transgenic mice display TOPGAL activity (Beta-galactosidase activity) during early embryonic development in a subset of pluripotent embryonic basal cells of the epithelium and dermis of developing hair follicles, but not during the next stage of hair follicle development; formation of hair germs. TOPGAL transgene activity reappears in hair follicles at E16.5 and TOPGAL expression is strongly upregulated in the postnatal hair shaft precursor cells in both whisker and body hair anagen follicles (active periods of hair growth). TOPGAL expression ceases during catagen (regression and ..... For more information please see the full phenotype on the strain data sheet | ||
| 011062 | STOCK Tg(Gdf9-cre)5092Coo/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice express Cre recombinase under the control of the mouse growth differentiation factor 9 (Gdf9) promoter. Cre recombinase expression is detected in oocytes of the primordial follicles by postnatal day 3 and in oocytes, but not somatic cells, of all follicles at the primary, secondary and later stages by 24 days. When crossed with a strain containing loxP site flanked sequence, Cre-mediated recombination results in deletion of the flanked sequence in the offspring. This mutant mouse strain may be useful in studies of studies of folliculogenesis and oocyte development. | ||
| 012841 | STOCK Tg(Ggt1-cre)M3Egn/J | Repository- Live |
| These transgenic mice express Cre recombinase under the control of the rat Ggt1, gamma-glutamyltransferase 1, promoter. Cre recombinase expression is detected by Northern blot in the kidney beginning at age 7 days. No transcript was detected in brain, liver, spleen, muscle, lung or adrenal gland. Cre recombinase protein is detected immunohistochemically in cortical proximal tubules. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in deletion of the targeted gene in the cortical tubular epithelium. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator reports that homozygotes are viable and fertile. | ||
| 005418 | STOCK Tg(HIST1H2BB/EGFP)1Pa/J | Repository- Live |
| Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express an "H2B-EGFP" fusion protein (coding sequence for the human HIST1H2BB gene [histone 1 H2bb] followed C-terminally by Enhanced Green Fluorescent Protein gene [EGFP, BD Biosciences]) under the control of the chicken beta actin promoter/enhancer coupled with the cytomegalovirus (CMV) immediate-early enhancer. Nucleosomes and chromatin in all cells fluoresce. Fluorescence is detectable during all phases of mitosis. The donating investigator reports occasional silencing of the transgene when transmitted through the female germ line. This mutant mouse strain may be useful for in vivo subcellular high-resolution and 3-dimensional studies of dividing cells. | ||
| 016252 | STOCK Tg(Hoxb7-Venus*)17Cos/J | Repository- Live |
| Hoxb7-myr-Venus transgenic mice have the homeobox B7 promoter/enhancer sequences driving expression of a myristoylated yellow fluorescent protein, myr-Venus. Hemizygotes are viable, fertile, and normal in size. Under control of Hoxb7, myr-Venus labels the membranes of individual cells in the Wolffian duct and branching ureteric bud (UB) of the kidney during all stages of urogenital development. This strain allows for the visualization of the shapes and arrangements of individual cells. In contrast, mice containing the Tg(Hoxb7-EGFP)33Cos allele (Stock No. 016251) are useful for viewing tissues specific to the UB lineage. | ||
| 014600 | STOCK Tg(I12b-cre/ERT2,-ALPP)37Fsh/J | Repository- Live |
| These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the mouse Dlx1/2, distal-less homeobox 1, distal-less homeobox 2, forebrain enhancer/ promoter (I12b). The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain, and the human placental alkaline phosphatase (ALPP or PLAP). The mutant mouse estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the Cre/ESR1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing loxP site flanked sequences, the flanked sequences will be deleted in the cre-expressing tissues in the offspring upon administration of tamoxifen. Tamoxifen administration induces Cre recombination in the ventral telencephalon and diencephalon as early as em ..... For more information please see the full phenotype on the strain data sheet | ||
| 008755 | STOCK Tg(Ins2-rtTA)2Efr Tg(teto-DTA)1Gfi/J | Repository- Live |
| This strain was generated by breeding Stock No. 008168 and Stock No. 008250 together at The Jackson Laboratory. The resulting double transgenic colony was established as Stock No. 008755. The Ins2-rtTA (or RIP7-rtTA) transgene expresses the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the rat insulin 2 (Ins2) promoter. The tet-DTA (or tetO-DTA) (transgene expresses diphtheria toxin A (DTA) under the control of a tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator) and a cytomegalovirus minimal promoter. Mice harboring both of these transgenes has doxycycline-inducible expression of DTA in pancreatic beta cells; i.e. addition of the tetracycline analogue doxycycline (dox) results in ablation of pancreatic beta cells. | ||
| 004782 | STOCK Tg(KRT14-cre)1Amc/J | Repository- Live |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the Cre recombinase under the control of the human keratin 14 promoter. Cre transcript is detected in the skin. When crossed to a reporter line containing Gt(ROSA)26Sortm1Sor, Beta-galactosidase activity is detected in the oral ectoderm at 11.75 dpc, and at 14.5 dpc activity is detected in the skin and throughout the dental epithelium. This strain represents an effective tool for generating tissue-specific targeted mutants that would be useful to study developmentally critical gene function in the ectoderm and its derivatives.
View cre expression characterization. | ||
| 005107 | STOCK Tg(KRT14-cre/ERT)20Efu/J | Repository- Live |
| These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the human keratin 14 (KRT14) promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain. The mutant mouse estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen (tamoxifen). Restricted to the cytoplasm, the cre/Esr1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted keratinocyte-specific deletions. Oral tamoxifen administration induces Cre recombination in toe, back skin and tongue. Topically administered tamoxifen induces Cre-mediated recombination in a specific localized area of the skin, occuring in 50 to 60% of the ..... For more information please see the full phenotype on the strain data sheet | ||
| 003553 | STOCK Tg(MMTV-cre)4Mam/J | Repository- Live |
| This transgenic strain expresses P1 Cre recombinase under the control of the MMTV LTR promoter. The MMTV LTR promoter directs a widespread pattern of expression. High levels of recombination have been detected in the virgin and lactating mammary gland, salivary gland, seminal vesicle, skin, erythrocytes, B and T cells. Little background recombination was observed in the lung, kidney, liver and brain tissues (less than 10%). The donating investigator indicates that this strain may be suitable for use in applications where it is desirable to delete genes in the virgin and lactating mammary gland, skin, erythroid cells, and other secretory tissues and skin. | ||
| 009075 | STOCK Tg(Myh6-Ppp3ca)37Eno/J | Repository- Live |
| Calcineurin A (Ppp3ca) expression is driven by the cardiomyocyte-specific alpha myosin heavy chain (alpha MHC) promoter in this transgenic strain. Mice develop cardiac hypertrophy that progresses to dilated cardiomyopathy with interstitial fibrosis, congestive heart failure and sudden death between 6 and 12 months of age. This strain may be useful as a model of human heart disease. | ||
| 009074 | STOCK Tg(Myh6-cre)1Jmk/J | Repository- Live |
| These transgenic mice express nuclear-localizing Cre recombinase under the control of the mouse Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha; alpha-MHC) promoter. Cre recombinase expression is detected in a majority of cardiac myocytes. Approximately 70% efficiency has been demonstrated when crossed with one floxed allele strain. Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Evidence suggests that this transgene is X-linked. | ||
| 005650 | STOCK Tg(Myh6-cre/Esr1*)1Jmk/J | Repository- Live |
| The alpha-MHC-MerCreMer transgene has the mouse Myh6 promoter (myosin, heavy polypeptide 6, cardiac muscle, alpha; alpha-MHC) directing expression of a tamoxifen-inducible Cre recombinase (MerCreMer) to juvenile and adult cardiac myocytes. Mice homozygous for the alpha-MHC-MerCreMer transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre recombinase expression in heart tissue is confirmed by western blot. Southern blot confirmed heart cell specificity compared to brain, kidney, lung, liver, and skeletal muscle. Insertion of this transgene and its protein show no changes in echocardiography, heart mass or pathology, or hypertrophy marker genes compared to nontransgenic littermates. Of note, the MerCreMer double fusion protein has substantially greater Cre recombinase activity with less promiscuity compared with the CreMer single fusion protein. When alpha-MHC-MerCreMer transgenic mice are bred with mice containing For more information please see the full phenotype on the strain data sheet | ||
| 014158 | STOCK Tg(Pax4-cre)1Dam/J | Repository- Live |
| Pax4-cre transgenic mice have the mouse paired box gene 4 (Pax4) promoter directing expression of an enhanced green fluorescent protein fused to a Tet-off cassette (EGFP/tTA). The transgene also contains a tetracycline-responsive element with a CMV minimal promoter (tetO-CMVmin) driving expression of a Cre-recombinase gene. In the absence of tetracycline/doxycycline, Cre recombinase expression is observed in Pax4-expressing cells (pancreatic progenitor cells). While designed to concomitantly allow tetracycline/doxycycline-dependant inhibition of Cre recombinase expression, the donating investigator confirms no such inhibition is observed. Also, no GFP expression is observed with or without tetracycline/doxycycline administration. Therefore, Pax4-cre transgenic mice function only for Cre recombinase expression in Pax4-expressing cells. When bred with mice containing a loxP-flanked sequence, Cre-mediated recombination will result in deletion of ..... For more information please see the full phenotype on the strain data sheet | ||
| 014099 | STOCK Tg(Pmch-cre)1Lowl/J | Repository- Live |
| Mch-cre transgenic mice have the murine pro-melanin-concentrating hormone (Mch) promoter/enhancer regions within the BAC transgene directing expression of Cre-recombinase. Hemizygous Mch-cre mice are viable, fertile, and normal in size, with cre expression directed specifically to MCH-neurons of the hypothalamus and zona incerta. When these transgenic mice are bred with mice containing a loxP-flanked sequence, Cre-mediated recombination is expected to result in deletion of the floxed sequences in the Cre recombinase-expressing neurons of the offspring. MCH neurons regulate many physiological functions by projecting through the brain. These mice may be useful for studying MCH-neuronal activities in controlling energy balance, glucose homeostasis, sleep, locomotion, and reward-related behaviors. | ||
| 005965 | STOCK Tg(Pomc1-cre)16Lowl/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre activity is demonstrable in brain area neurons involved in the control of food intake (arcuate nucleus (hypothalamus) and solitary tract nucleus (hindbrain)). When bred with a mouse containing a loxP site-flanked sequence of interest, Cre-mediated recombination results in deletion of the flanked genome in tissues that normally express Pomc1. The mice may be useful in studies of obesity, food intake, hunger, endocrine and exocrine function, and for tissue specific gene targeting. | ||
| 008477 | STOCK Tg(RARE-Hspa1b/lacZ)12Jrt/J | Repository- Live |
| These transgenic mice express beta-galactosidase (lacZ) gene under the control of the retinoic acid responsive element (RARE). Sporadic beta-galactosidase activity is detected in less than half of embryonic day 3.5 blastocysts. Beta-galactosidase activity in embryos 11.5 embryonic days in age and older mimics the expression pattern of retinoic acid receptor, beta (Rarb). Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When maintained as homozygotes, this strain can lose beta-galactosidase staining capacity. The donating investigator reports that lacZ staining is lost when their mice are bred onto the C57BL/6 genetic background. This strain serves as a reporter strain, with retinoic acid signaling being indicated by beta-galactosidase activity. This mutant mouse strain may be useful in tracking retinoic acid signaling pattern. | ||
| 009606 | STOCK Tg(Six2-EGFP/cre)1Amc/J | Repository- Live |
| Hemizygous Six2-TGCtg mice are viable and fertile, harboring a BAC transgene with a Tet-off-eGFPCre under control of the Six2 promoter/enhancer regions within the BAC transgene. The Tet-off-eGFPCre contains both the tetracycline-controlled transactivator protein (tTA) as well as the tetracycline operator (tetO; also called tetracycline-responsive element [TRE] or tet-operator) upstream of an EGFPCre fusion protein. Sequence updates published after this transgene was created revealed an upstream Six2 ATG start site that is in-frame with the tTA; thus an apparent and unintended fusion was created with the tTA (80 amino acids potentially added) that renders transgene expression unaffected by tetracycline/doxycycline administration. It is not known whether the "mutant" tTA is resistant to tetracycline/doxycycline inactivation and still binds to TRE to activate EGFPCre expression or if the TRE acts as a minimal promoter adjacent to the Six2 promoter in the pr ..... For more information please see the full phenotype on the strain data sheet | ||
| 012586 | STOCK Tg(Slc1a3-cre/ERT)1Nat/J | Repository- Live |
| This BAC transgenic line expresses CreERT under the control of the Slc1a3 (solute carrier family 1 (glial high affinity glutamate transporter); GLAST) promoter. When crossed with a strain containing a loxP site flanked sequence, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted glia and neural progenitor cell-specific deletions. Injection of 4-hydroxytamoxifen leads to recombination specifically in Muller glia in the retina, in astrocytes of the brain, and in neural progenitors, including those that give rise to hippocampal neurons and olfactory neurons in the rostral migratory stream. This strain is a useful tool in studies of neurodevelopment. | ||
| 004783 | STOCK Tg(Sox2-cre)1Amc/J | Repository- Live |
| Mice hemizygous for the Sox2Cre transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Cre recombinase under the control of the mouse SRY-box containing gene 2 promoter. When these transgenic mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in Sox2-expressing tissues in the offspring. Specifically, Cre recombinase activity is detected in the epiblast cells at embryonic day 6.5, with little or no activity in other cells at gastrulation. Some activity is also detected in extra embryonic derivatives of the epiblast, the yolk sac mesoderm and amnion. No Cre recombinase activity is detected in primitive endoderm derived tissues, visceral endoderm. The phenotype of homozygous mice has not been characterized to date (April 2011). These Sox2Cre transgenic may be useful for generating epiblast-derived specific ..... For more information please see the full phenotype on the strain data sheet | ||
| 008208 | STOCK Tg(Stra8-cre)1Reb/J | Repository- Live |
| Homozygous Stra8-cre transgenic mice are viable and fertile, with expression of an optimized variant of Cre recombinase (iCre) directed by the 1.4 kb mouse Stra8 (stimulated by retinoic acid gene 8) genomic promoter fragment. Postnatal Cre-recombinase expression is first observed in testes at postnatal day (P)3 (early-stage spermatogonia), increases out to P7 (pre-leptotene-stage spermatocytes), and is not detected in other tissues examined (including ovaries). In addition, no cre expression is reported in male or female embryos. When Stra8-cre transgenic males are bred with female mice containing a loxP-flanked sequence, Cre-mediated recombination will result in deletion of the floxed sequence, specifically during these stages of spermatogenesis. These Stra8-cre transgenic mice may be useful in generating conditional knockouts in postnatal, premeiotic, male germ cells for studying spermatogenesis. | ||
| 013752 | STOCK Tg(TCF/Lef1-HIST1H2BB/EGFP)61Hadj/J | Repository- Live |
| TCF/Lef:H2B-GFP transgenic mice express an H2B-EGFP fusion protein (coding sequence for the human HIST1H2BB gene [histone 1 H2bb] followed C-terminally by Enhanced Green Fluorescent Protein gene) under the control of six copies of a T cell specific transcription factor/lymphoid enhancer-binding factor 1 (TCF/Lef1) response element and a heat shock protein 1B (Hspa1b) minimal promoter. Mice homozygous for the transgene are viable, fertile, and normal in size. Wnt (wingless-related MMTV) family members are required for triggering embryonic axis formation and for proper development. Wnt signaling results in phosphorylation and nuclear localization of β-catenin, a transcriptional co-activator protein, which, together with the TCF/Lef family of transcription factors, induces the transcription of downstream genes. TCF/Lef:H2B-GFP transgenic mice contain 6 copies of nuclear localized TCF/Lef1 DNA binding sites, which provides increased sensitivity to Wnt/&be ..... For more information please see the full phenotype on the strain data sheet | ||
| 003658 | STOCK Tg(TIE2GFP)287Sato/J | Repository- Live |
| This strain expresses Green Fluorescent Protein (GFP) under the direction of the endothelial-specific receptor tyrosine kinase (Tek, formerly, Tie2) promoter. Endothelial cells expressing GFP can be visualized via fluorescent microscopy or purified by FACS. | ||
| 004746 | STOCK Tg(Tagln-cre)1Her/J | Repository- Live |
| Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Cre recombinase under the control of the mouse transgelin (smooth muscle protein 22-alpha) promoter. Cre recombinase expression (mRNA) closely patterns endogenous transgelin expression, with the highest levels detected in the aorta, intestine and uterus. Low levels of transcript are detected in all other organs tested, likely reflecting the vascular smooth muscle compartments in the these tissues. Cre recombinase activity is observed in vascular smooth muscle cells of hepatic and pulmonary arteries, with no activity detected outside the vascular walls. When crossed with a strain containing a loxP site-flanked sequence of interest, Cre-mediated recombination results in deletion of the flanked sequence in vascular smooth muscle cells. This strain represents an effective tool for generating tissue specific-ta ..... For more information please see the full phenotype on the strain data sheet | ||
| 005493 | STOCK Tg(Tek-rtTA,TRE-lacZ)1425Tpr/J | Repository- Live |
| Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice harbor co-injected transgenic constructs. The reverse tetracycline-controlled transactivator (rtTA) protein is expressed under the direction of the endothelial-specific receptor tyrosine kinase enhancer/promoter (Tek). The second transgenic construct expresses a nuclear-localizing beta-galactosidase gene (lacZ) under the control of a tetracycline-responsive element (TRE). In the presence of tetracycline or a tetracycline analog (such as doxycycline), selective expression of lacZ is observed in the nuclei of vascular endothelium in a wide variety of tissues (aorta, heart, brain, lung, kidney, liver, spleen, uterus, prostate, stomach, skeletal muscle, large and small intestine). Expression is observed as early as embryonic day 9.5. In the absence of tetracycline, some lacZ expression occurs in the smaller branches of ..... For more information please see the full phenotype on the strain data sheet | ||
| 013162 | STOCK Tg(Thy1-Clomeleon)12Gjau/J | Repository- Live |
| These transgenic mice express Clomeleon, a fluorescent fusion protein containing CFP and topaz YFP that acts as a ratiometric indicator for chloride ions, under the control of the mouse Thy1, thymus cell antigen 1, theta, promoter (Thy1.2). Transgene expression in founder line CLM12 is detected at high levels in the thalamus, cerebellar nuclei. No expression is detected in layers 1 and 2 of the neocortex, hippocampal regions CA2 and CA3, cerebellar purkinje cells, or retinal ganglion cells. In the presence of low chloride ion concentrations, YFP fluoresces as a FRET (Fluorescence Resonance Energy Transfer) acceptor for CFP. As the chloride ion concentration increases, YFP fluorescence decreases and CFP fluorescence increases. Using an appropriate calibration curve, the ratio of YFP and CFP fluorescence peaks indicate [Cl-]. Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The ..... For more information please see the full phenotype on the strain data sheet | ||
| 013163 | STOCK Tg(Thy1-Clomeleon)13Gjau/J | Repository- Live |
| These transgenic mice express Clomeleon, a fluorescent fusion protein containing CFP and topaz YFP that acts as a ratiometric indicator for chloride ions, under the control of the mouse Thy1, thymus cell antigen 1, theta, promoter (Thy1.2). Transgene expression in founder line CLM13 is detected at high levels in the hippocampal dentate gyrus and CA1 region, amygdala, and nuclei and mossy fibers of the cerebellum. No expression is detected in the external plexiform layer, mitral cells or internal plexiform layer of the olfactory bulb, layer 1 of the neocortex, cerebellar granule or purkinje cells, or retinal biopolar and amacrine cells. In the presence of low chloride ion concentrations, YFP fluoresces as a FRET (Fluorescence Resonance Energy Transfer ) acceptor for CFP. As the chloride ion concentration increases, YFP fluorescence decreases and CFP fluorescence increases. Using an appropriate calibration curve, the ratio of YFP and CFP fluorescence peaks indicate [Cl-]. Mi ..... For more information please see the full phenotype on the strain data sheet | ||
| 007788 | STOCK Tg(Thy1-EGFP)MJrs/J | Repository- Live |
| Mice harboring the Thy1-GFP transgene are viable and fertile with enhanced green fluorescent protein (EGFP) expression under the control of a modified Thy1 promoter region (containing the sequences required for neuronal expression but lacking the sequences required for expression in non-neural cells). Homozygous or hemizygous Thy1-GFPM mice (derived from founder line M) express EGFP in sparse subsets of neurons within specific populations; providing a bright, vital Golgi-like stain. Less than 10% of all motor axons, retinal ganglion cells, lumbar dorsal root ganglion, and cortex express EGFP. These Thy1-GFPM transgenic mice may be useful in neurobiological studies for fluorescent labeling of neural tissues, especially for mossy fibers in the cerebellum and intense, yet sparse, labeling of a variety of neuronal subsets.
This strain is one of many from the donating investigator with specific/differential fluorescent protein expression in neural tissues (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 012708 | STOCK Tg(Thy1-cre/ERT2,-EYFP)HGfng/PyngJ | Repository- Live |
| The "single-neuron labeling inducible Cre-mediated knockout" (SLICK) transgene is designed with two separate copies of the modified mouse Thy1 promoter region (each containing the sequences required for neuronal expression but lacking the sequences required for expression in non-neural cells) driving expression of a CreERT2 fusion protein and an enhanced yellow fluorescent protein (EYFP). Mice harboring the SLICK transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. mRNA coexpression of both CreERT2 and YFP is highly correlated. YFP expression is directed primarily to projection neurons with variations in the extent and brightness of labeling observed in different founder lines (see below). CreERT2 fusion gene activity is inducible; observed at high levels following tamoxifen administration (see below). When SLICK transgenic mice are bred with mice containing loxP-flanked seque ..... For more information please see the full phenotype on the strain data sheet | ||
| 016584 | STOCK Tg(Tph2-icre/ERT2)6Gloss/J | Repository- Live |
| These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the mouse Tph2, tryptophan hydroxylase 2, promoter. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted deletions. Tamoxifen administration induces Cre recombination in Tph2-expressing neurons in the raphe nucleus. Homozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
This Cre-ERT2 fusion protein consists of iCre recombinase (Codon-improved Cre recombinase) fused to a triple mutant form of the human estrogen receptor which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OHT or tamoxifen) and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can onl ..... | ||
| 011108 | STOCK Tg(Ttr-RFP)1Hadj/J | Repository- Live |
| Mice hemizygous for the Ttr-RFP transgene are viable and fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous mice exhibit reduced viability on this background. Expression of the transgene is directed to the visceral endoderm of early postimplantation embryo (E5.5), yolk sac endoderm, and other endoderm-derived organs including intestine, liver, pancreas, and stomach. In addition, expression is detected in the optic vesicle and regional areas of the brain. This mutant mouse strain may be useful for in vivo imaging, fate mapping and genetic modification of cells of the visceral endoderm. | ||
| 003829 | STOCK Tg(Wnt1-cre)11Rth Tg(Wnt1-GAL4)11Rth/J | Repository- Live |
| When homozygous for both co-injected transgenes, Wnt-1/GAL4/cre-11 transgenic mice are viable, fertile, normal in size and do not display any gross physical abnormalities. Both Cre recombinase and the GAL4 transcriptional activator are expressed under the direction of wingless-related MMTV integration site 1 (Wnt1) promoter/regulatory sequences. Cre recombinase activity is detected in the Wnt1 pattern of expression: in the midbrain by 8.5 dpc and, after neural tube closure, in the dorsal and ventral midlines of the midbrain and caudal diencephalon, midbrain-hindbrain junction and dorsal spinal cord. When Wnt-1/GAL4/cre-11 transgenic mice are bred to mice containing loxP site-flanked sequences, cre-mediated recombination results in deletion of the floxed sequences in the midbrain and developing neural tube of the resulting offspring. | ||
| 008199 | STOCK Tg(dlx6a-cre)1Mekk/J | Repository- Live |
| Homozygous Dlx5/6-Cre transgenic mice are viable and fertile. Expression of Cre recombinase (Cre) is directed to differentiating and migrating forebrain GABAergic neurons during embryonic development by the I56i and I56ii enhancers from the zebrafish dlx5a/dlx6a intergenic region (with the 5' promoter region of zebrafish dlx6a in place to increase the activity of the intergenic enhancers rather than direct tissue-specific expression). When Dlx5/6-Cre transgenic mice are bred with mice containing a loxP-flanked sequence, Cre-mediated recombination will result in deletion of the floxed sequence in the offspring in the offspring. These Dlx5/6-Cre transgenic mice may be useful in generating specific deletions of floxed alleles in GABAergic forebrain neurons. | ||
| 005104 | STOCK Tg(tetO-HIST1H2BJ/GFP)47Efu/J | Repository- Live |
| These transgenic mice express the human histone 1, H2bj, protein (HIST1H2BJ) and Green Fluorescent Protein (GFP) fusion protein, HIST1H2BJ/GFP, under the control of a tetracycline-responsive promoter element (TRE; tetO). Transgenic expression occurs in widespread fashion. When hemizygotes are bred with another transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) to create bitransgenic animals, tissue-specific HIST1H2BJ/GFP transgene expression can be regulated with the tetracycline analog, doxycycline. Pulse-chase administration of doxycycline results in retention of signal in rarely dividing, or infrequently cycling, label-retaining cells (LRCs). Potential constitutive transgene expression should be examined in tissues of interest. | ||
| 012345 | STOCK Tg(tetO-tdTomato,-Syp/EGFP*)1.1Luo/J | Repository- Live |
| Hemizygous TRE-Bi-SG-T line 1.1 transgenic mice are viable and fertile, with no reported phenotypic abnormalities. The TRE-Bi-SG-T transgene has Myc-tagged tdTomato and full-length mouse synaptophysin/mut4EGFP fusion protein (Syp-GFP) expression under the control of the bi-directional tet-responsive promoter (tetO or TRE). When bred with another mouse expressing tetracycline-controlled transactivator protein (tTA) or reverse tetracycline-controlled transactivator protein (rtTA), tdTomato and Syp-GFP fusion protein expression can be regulated with the tetracycline analog doxycycline (dox) in the resulting double mutant offspring. In tTA(-dox) or rtTA(+dox)-expressing cells, tdTomato expression is directed to the entire cell, while GFP expression is directed to the synapse/synaptic vesicle. The donating investigator reports that direct GFP fluorescence and direct tdTomato fluorescence may be visualized in these mice when tTA is present/dox is absent. In addition, the three Myc epi ..... For more information please see the full phenotype on the strain data sheet | ||
| 100401 | WCB6F1/J-KitlSl/KitlSl-d | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Many steel alleles cause severe anemia resulting in death in utero of homozygous mutant mice. However, mice homozygous for some steel mutations and compound heterozygotes for two steel alleles (e.g., KitlSl/KitlSl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtuall ..... For more information please see the full phenotype on the strain data sheet | ||
| 005454 | B6;129S7-Ey3/Boc | Research Strain |
| Mice heterozygous for the eyeless 3 mutation were initially identified as having lens-cornea synechia and eyelessness. Heterozygotes have occasional anophthalmia wherein one or both eyes may be missing or rudimentary. When eyes are present they display a white corneal opacity with a dark spot in the center. Homozygotes are not produced and are believed to die prenatally. | ||
| 002529 | B6;129S7-Vldlrtm1Her/J | Research Strain |
| Mice homozygous for the Vldlrtm1Her targeted mutation are viable and fertile. They are smaller and leaner than normal wildtype siblings. The high level of expression in muscle and adipose tissue suggests a role in VLDL triacylglycerol delivery. Plasma levels of cholesterol, triacylglycerol, and lipoproteins were normal when mice were fed normal, high-carbohydrate or high fat diets. However, homozygous mice do show a modest decrease in body weight, body mass index, and adipose tissue mass as determined by the weights of epididymal fat pads. Many homozygous pups in the colony at the Jackson Lab have patchy fur (hair loss) at weaning but look normal at about 6 weeks of age. In a segregation analysis crossing homozygous females with normal "C57BL6/2J" mice, offspring that were homozygous for this Vldlrtm1Her mutation are associated with subretinal neovascularization and were found to have a neovascularization process similar to a type seen in patients wi ..... For more information please see the full phenotype on the strain data sheet | ||
| 017540 | B6;CAST-GarsNmf249/JRwb | Research Strain |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for GarsNmf249 entry. Mutant mice are smaller than their littermates and develop an unsteady gait about 3 weeks of age (average 3.5weeks of age +/-0.5, n=22). The mice fail to thrive and die between 4-8 weeks of age. Males and females are affected and do not live long enough to mate normally. Although the NMF249 mutation arose in an ENU mutagenized family, it is most likely a spontaneous mutation. The parents showed no overt phenotype and produced only 1 affected mouse in a total of 24 progeny. However, when this animal was mated to a wild-type male (using ovarian transplants), half the offspring was affected, suggesting that a spontaneous dominant mutation may have occurred. Ratios from subsequent matings are consistent with a fully penetrant dominant mutation. In vitro fertilization was attempted using s ..... | ||
| 016848 | STOCK ey4/BOC | Research Strain |
| Mice homozygous for the eyeless 4 mutation display anophthalmia and lens-cornea synechia. | ||
| 006365 | 129-Cckartm1Kpn Cckbrtm1Kpn/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for both of the targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The donating investigator reports that the double mutants have a combined phenotype.
No CCKBR receptor function was detected in competition binding assay of brain (cerebral plasma) membranes. When compared to wildtype, gastric pH in homozygotes is higher, pH 5.2, after overnight fast. Histological analysis reveals diminished parietal cell, enterochromaffin-like cell and antral comatostatin-producing D cell densities. An increase in the number of gastrin-producing G cells is observed. There is an increased number of H+, K+ -ATPase immunoreactive negative cells and abnormal distribution of parietal cells in oxyntic glands. Circulating gastrin levels are 10-fold higher in homozygotes. No CCKAR receptor function was detected in competition binding assay of pancreatic membranes. Homozygotes do not exhibit decreased ..... For more information please see the full phenotype on the strain data sheet | ||
| 006367 | 129-Cckartm1Kpn/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No receptor function was detected in competition binding assay of pancreatic membranes. Mice homozygous for the targeted mutation do not exhibit decreased food intake due to peritoneal injection of cholecystokinin. Baseline food and water intake and body weight is normal in mutant mice. These mutant mice have larger gallbladder volumes and are more likely to develop spontaneous gallstones than wildtype controls. Gastric function is impaired due to diminished intestinal lipid feedback response. Small-intestine transit time is increased in mutant mice. When fed a lithogenic diet, mutant mice have an increase in biliary cholesterol secretion rates, when compared to the wildtype. Although the total number of olfactory-gonadotropin-releasing hormone-1 neuroendocrine (GnRH-1)neurons is the same in embryonic day 14.5 aged mutant and wildtype ..... For more information please see the full phenotype on the strain data sheet | ||
| 006835 | 129-Dag1tm2Kcam/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express cre recombinase, resulting offspring can have exon 2 of the targeted gene deleted in the cre-expressing tissue(s). As the targeted gene has three loxP sites, other genotypes may also result. These mutant mice may be useful in studying muscle disease and regeneration. When bred to a strain expressing Cre recombinase under the control of the human glial fibrillary acidic protein promoter (GFAP) (see Stock No. 004600 for example), this mutant mouse strain may be useful in studies of brain abnormalities observed in congenital muscular dystrophies. When bred to a strain expressing Cre recombinase in the nervous system (see Stock No. 003771 for exampl ..... | ||
| 006053 | 129-Gt(ROSA)26Sortm1(CAG-EGFP)Luo/J | Cryopreserved - Ready for recovery |
| MADM-GG mice are viable with no gross behavioral or observable abnormalities. Regardless of Cre-recombination, these mice express EGFP as their N- and C-terminal coding sequences are interrupted by the beta-actin intron in-frame. High EGFP expression in every cell can be visualized in vivo and in fixed samples. These mutant mice are a control EGFP-expressing strain for use with MADM (mosaic analysis with double markers) mice (see Stock No. 006041 [MADM-GR (EGFP/Dsred2)] and Stock No. 006067 [MADM-RG (Dsred2/EGFP)]). Using the MADM system, a researcher can generate genetic mosaics in which an individual organism contains somatic cells of different genotypes. This allows the researcher to ascertain lineal relationships and pleiotropic gene function in multicellular organisms. These mice may also be useful in studies of cell differentiation and mitosis.
Mice harbor ..... | ||
| 006067 | 129-Gt(ROSA)26Sortm2(CAG-Dsred2/EGFP)Luo/J | Cryopreserved - Ready for recovery |
| MADM-RG mice are viable with no gross behavioral or observable abnormalities. Homozygous females produce less pups to weaning age compared to heterozygotes. These mutants are designed for MADM (mosaic analysis with double markers), and must be crossed to mice harboring a reciprocal mutation at the same locus (see Stock No. 006041 or Stock No. 006075, MADM-GR (EGFP/Dsred2)). The resulting offspring have one copy of each reciprocal mutation on homologous chromosomes ("trans-heterozygous") and must next be bred to a Cre-expressing strain for fluorescent protein expression. Prior to Cre-recombination, double mutant mice do not have colored cells: the chimeric genes do not produce functional proteins because their coding sequences are interrupted by the beta-actin intron in different reading frames. After DNA replication (G2 phase) in double mutant mice, Cre-recombinase introducti ..... For more information please see the full phenotype on the strain data sheet | ||
| 006041 | 129-Gt(ROSA)26Sortm3(CAG-EGFP/Dsred2)Luo/J | Cryopreserved - Ready for recovery |
| MADM-GR mice are viable with no gross behavioral or observable abnormalities. Homozygous mice have low fertility, while heterozygous mice have no reported fertility defects. These mutants are designed for MADM (mosaic analysis with double markers), and must be crossed to mice harboring a reciprocal mutation at the same locus (see Stock No. 006067 or Stock No. 006080, MADM-RG (Dsred2/EGFP)). The resulting offspring have one copy of each reciprocal mutation on homologous chromosomes ("trans-heterozygous") and must next be bred to a Cre-expressing strain for fluorescent protein expression. Prior to Cre-recombination, double mutant mice do not have colored cells: the chimeric genes do not produce functional proteins because their coding sequences are interrupted by the beta-actin intron in different reading frames. After DNA replication (G2 phase) in double mutant mice, Cre-recom ..... For more information please see the full phenotype on the strain data sheet | ||
| 006831 | 129-Sgcbtm1Kcam/J | Cryopreserved - Ready for recovery |
| Homozyous mice are viable and fertile. They develop severe muscular dystrophy and cardiomyopathy with focal areas of necrosis. Severe dystrophic changes including necrosis, dystrophic calcification, fatty infiltration, central nucleation, fibrosis, atrophy and hypertrophy are detected in diaphragm and calf/thigh muscle. Some of these changes occur in 4-week-old animals and accumulate with age. At 20 weeks of age, several regions of focal myocardial necrosis have been observed; small areas of necrotic myocardiocytes may be observed as early as 9 weeks of age. At 30 weeks of age, large areas of fibrosis are detected. Sarcoglycan-sarcospan and dystroglycan complexes are disrupted in skeletal, cardiac, and smooth muscle membranes. Loss of the sarcoglycan-sarcospan complex in vascular smooth muscle results in vascular irregularities in heart, diaphragm, and kidneys. Vascular constrictions in skeletal muscle, cardiac muscle and kidneys is observed. Epsilon-sarcoglycan (SGCE) is also reduced ..... For more information please see the full phenotype on the strain data sheet | ||
| 005213 | 129-Slc10a2tm1Pda/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Male pups tend to be smaller in size than female pups prior to weaning. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of the distal small intestine. Ileal brush border membrane vesicles isolated from homozygotes do not exhibit sodium ion dependent taurocholate uptake, indicating a loss of sodium bile acid cotransporter activity. Total plasma cholesterol levels are slightly higher than normal. Total bile acid pool size is reduced approximately 80% in homozygous mutants, although intestinal lipid absorption is reduced by only about 10%. Bile acid functional turnover rate (daily fecal bile acid excretion/pool size) is elevated 150 fold in male mutants and 75 fold in female mutants. Fecal bile acid excretion is increased 24 fold in male mutants and 11 fold in female mutants. Bile acid composition is ab ..... For more information please see the full phenotype on the strain data sheet | ||
| 006239 | 129-Wnt11tm1Amc/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for this targeted mutation are viable and fertile with normal kidney size and histology. Homozygotes exhibit some embryonic lethality and will die by 2 days post partem. While the cause of death is unclear, these neonates have kidney hypoplasia and reduction of glomeruli. RT-PCR analysis of kidney RNA shows the expected truncated transcript. Homozygotes exhibit ureteric branching morphogenesis defects between embryonic day 11.5-12.5 (T-stage) associated with a reduction in mesenchymal Gdnf expression. These Wnt11 mutant mice may be useful in studies of kidney development, including ureteric bud branching morphogenesis, and Wnt superfamily embryogenesis. | ||
| 009443 | 129;B6-Hint1tm1Ibw/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of MEFs, cerebrum, cerebellum, colon, kidney, thymus, thyroid, stomach,
liver, pancreas, adrenal gland, testis, ovary, heart, lung, spleen, muscle, and skin tissues. No gene product (mRNA) is detected by RT-PCR of MEFs. Homozygotes have smaller thymuses. Homozygotes MEFs exhibit more rapid growth after 8 serial passages, and undergo spontaneous immortalization, as they can be cultured for more than 50 serial passages without morphological changes. Both early and late passage homozygotes MEFs are more resistant to ionizing radiation than wildtype controls. Irradiated MEFs have impaired DNA repair and exhibit chromosome aberrations, and genomic instability. Homozygotes are more sensitive to chemical carcinogens NMBA and DMBA and develop more tumors that are larger and ..... For more information please see the full phenotype on the strain data sheet | ||
| 008243 | 129;B6-Tff3tm1Dkpy/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this intestinal trefoil factor (ITF or Tff3) mutant allele are viable and fertile with no RNA or protein expression of the targeted gene in the gastrointestinal tract. Homozygous mice exhibit impaired physiological migration of intestinal epithelium to the mucosal surface, have impaired mucosal healing and increased susceptibility to dextran sulfate sodium (DSS)- induced colitis, and are more susceptible to chemotherapy and radiation-induced mucositis. These intestinal trefoil factor (ITF or Tff3) mutant mice may be useful in studying gastrointestinal tract injury (including inflammatory bowel diseases), maintenance of the mucosal barrier, migration and turnover of the intestinal epithelium, and therapies for colon cancer. | ||
| 005989 | 129;FVB-Tg(PTH-cre)4167Slib/J | Cryopreserved - Ready for recovery |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre activity is observed only in parathyroid tissue; no activity is seen in thyroid, muscle, lymph node, trachea, thymus, salivary tissues, lung, heart, liver, brain, stomach, spleen, kidney, large intestine, small intestine, and pancreas. When bred with any mouse containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in parathyroid-specific deletion of the flanked genome. These transgenic mice may be useful in generating mouse models of parathyroid-specific deletion of genes of interest, such as multiple endocrine neoplasia type 1, extracellular calcium-sensing receptor, and vitamin D receptor. | ||
| 006820 | 129S-Catsper3tm1Clph/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and do not display any gross physical or behavioral abnormalities. Male homozygotes are infertile due to a defect in sperm motility. Their sperm fails to develop the hyperactive motility pattern required for fertilization. No morphological differences between wildtype and mutant spermatozoa have been observed. No protein product from the targeted gene is detected in testis tissue. Female homozygotes reproduce normally. This strain may be useful in studies of male infertility. | ||
| 006821 | 129S-Catsper4tm1Clph/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and do not display any gross physical or behavioral abnormalities. Male homozygotes are infertile due to a defect in sperm motility. Their sperm fails to develop the hyperactive motility pattern required for fertilization. No morphological differences between wildtype and mutant spermatozoa have been observed. No protein product from the targeted gene is detected in testis tissue. Female homozygotes reproduce normally. This strain may be useful in studies of male infertility. | ||
| 007965 | 129S-Dvl1tm1Awb/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of MEF (mouse embryonic fibroblasts) derived from homozygotes. Homozygotes exhibit diminished social interaction behavior, do not barber or trim whiskers of cagemates, show subordinance in social dominance tests, do not sleep huddled together and do not build nests. Although mutants have an attenuated prepulse inhibition of acoustic and tactile startle (sensorimotor gating of the startle reflex), they do not exhibit any deficits in locomotor or cognitive function. This mutant mouse strain may be useful in studies of social behavior, sensorimotor gating, and possibly psychiatric disorders. | ||
| 008001 | 129S-Dvl2tm1Awb/J | Cryopreserved - Ready for recovery |
| Half of homozygotes exhibit a perinatal lethal phenotype. Surviving homozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Some newborn homozygotes fail to survive and exhibit breathing difficulties, cyanosis and reduced mobility. No gene product (protein) is detected by Western blot analysis of brain lystates. Some nonviable homozygotes display cardiac abnormalities. Most homozygotes (90%) have mild abnormalities of the ribs and vertebrae. 2 to 3% of the homozygous embryos display thoracic spina bifida and exencephaly. This mutant mouse strain may be useful in studies of bone and cardiac development, neural tube closure and spina bifida. | ||
| 008864 | 129S-Ece1tm1Reh/J | Cryopreserved - Ready for recovery |
| Homozygous endothelin converting enzyme 1 targeted mutant mice die before embryonic day 13.5 (E13.5) on a 129 genetic background. Pre-morbid homozygous embryos exhibit peripheral vascular dilation and pericardial effusion, consistent with cardiac failure. There is marked congestion and dilation of the atria and peripheral vessles, as well as generalized edema. The embryos also exhibit severe craniofacial defects. Western blot and enzyme immunoassay confirm that expression of the gene is eliminated in homozygous embryos. These mice closely resemble human DiGeorge syndrome patients who suffer multiple craniofacial and cardiovascular defects. | ||
| 008865 | 129S-Ednratm1Ywa/J | Cryopreserved - Ready for recovery |
| Homozygous endothelin receptor type A targeted mutant embryos are born with numerous defects in craniofacial structures. The mandible appears to have undergone a homeotic transformation into a maxilla. Other maxillary structures are duplicated in the lower jaw, including the palatine, jugal and pterygoid bones. The malleus and incus of the middle ear are dysmorphic and Meckel's cartilage is absent. The hyoid bone of the throat is moved rostrally and fused with the pterygoid bones, resulting in collapse of the trachea and subsequent asphyxia. Defects also exist in the heart, including double outlet right ventricle, transposition of the great arteries, interruption of the aorta and persistent truncus arteriosus. While all mutant mice have cardiac defects, the specific type of defect differs between embryos. Expression of the targeted gene (total embryo RNA) is still observed in homozygous mutant embryos, though there is a shift in size, suggestive of a partial mRNA. Ligand binding ass ..... For more information please see the full phenotype on the strain data sheet | ||
| 007664 | 129S-Efnb1tm1Sor/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites flanking exons 2 through 5 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 2 through 5 deleted in the cre-expressing tissue(s). These Efnb1 conditional mutant mice may be useful in studying cellular signaling in embryonic development and adult mice; specifically receptor tyrosine kinases. For example, when crossed to a strain expressing Cre recombinase in epiblast-derived tissues (see Stock No. 003755), this mutant mouse strain may be useful in embryogenesis research. For example, when bred to a strain expressing Cre recombinase in midbrain/dorsal spinal cord (see Stock No. 007807 or For more information please see the full phenotype on the strain data sheet | ||
| 008866 | 129S-Hcrttm1Ywa/J | Cryopreserved - Ready for recovery |
| Mice lacking orexin/hypocretin gene expression exhibit phenotypes remarkably similar to humans with narcolepsy. These are characterized by behavioral arrests that are similar to cataplexy (occasional direct transitions to REM sleep from wakefulness), and highly fragmented sleep-wake cycles, all of which are important elements of narcolepsy. Homozygotes are viable and fertile. | ||
| 007205 | 129S-Myo1eGt(ROSA)74Sor/J | Cryopreserved - Ready for recovery |
| Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mice are anemic (low hemoglobin concentration, red blood cell count, hematocrit). These mice also exhibit polychromasia (abnormally high number of immature blood cells). Homozygotes occur at lower than Mendelian ratio (15%). Although homozygotes are fertile, pregnancy is occasionally lethal for homozygous females. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Myo1e-mutant mice may be useful in studying vascular development, hematopoiesis and cellular signaling during development and in adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 008002 | 129S-Pafah1b1tm2Awb/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites flanking exons 3 through 6 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Histological analysis of brains from homozygotes reveals slightly wider CA1 and CA3 regions and a split in CA2 region in the hippocampus. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 3 through 6 deleted in the cre-expressing tissue(s). | ||
| 007846 | 129S-Pdgfrbtm1Sor/J | Cryopreserved - Ready for recovery |
| One third of homozygous embryos, aged E16 to E18.5, exhibit purpura and edema with some embryos in this group dying at this stage. Homozygous embryos delivered by Caesarean section at E18.5 die within minutes. Homozygotes exhibit anemia, elevated numbers of nucleated erythrocytes, polychromasia, irregularly shaped mature erythrocytes (anisocytosis), and hemorrhaging. Glomerular capillary tufts are absent and the capsule space is filled with blood cells. No gene product (protein) is detected by Western blot analysis of total protein. A truncated transcript presumed to be due to exon skipping is detected by Northern blot analysis. This mutant mouse strain may be useful in studies of hematopoiesis, kidney development and and cellular signaling during development. | ||
| 008079 | 129S-Ppargtm2Yba/J | Cryopreserved - Ready for recovery |
| These mice express tTA (tetracycline regulated transactivator) and a tetO-driven Flag-tagged Pparg from the endogenous Pparg locus. A fusion transcript (including the 5' portion of Pparg, IRES and tTA (AF1-IRES-tTA)), a Flag-Pparg transcript and a wildtype transcript are detected by Northem blot analysis of white adipose tissue from heterozygotes. The fusion transcript of AF1-IRES-tTA is also detected in brown adipose tissue. Expression of tTA is detected in adipose tissue by Western blot analysis. No Flag-PPARG1 protein was detected in adipose tissue. Weak expression of tTA and the Flag-Pparg transcript is observed in placenta and liver. Endogenous PPARG2 protein is reduced in adipose tissues of heterozygotes. Heterozygotes exhibit "buffalo humps" (swollen interscapular fat pads swollen by hypertrophy and unilocular lipid deposition in mutant brown adipocytes), absence of subcutaneous adipocytes, reduced gonadal white adipose tissue, irregularly residual a ..... For more information please see the full phenotype on the strain data sheet | ||
| 007209 | 129S-Schip1Gt(ROSA)77Sor/J | Cryopreserved - Ready for recovery |
| Homozygotes occur at lower than Mendelian ratio (19%), and 20% die by age 1 week. Heterozygotes viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit abnormalities in neural crest-derived and thoracic skeleton development, and palate bone fusion. These Schip1-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 007199 | 129S-Sgpl1Gt(ROSA)78Sor/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this mutant allele have reduced size and weight gains after birth and do not survive past 8 weeks of age. Homozygotes occur at a lower than Mendelian ratio (19%) from heterozygote X heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Beta-galactosidase staining pattern mimics the endogenous gene expression pattern in adult intestinal epithelial cells. Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mutant mice are anemic (low hemoglobin concentration, reduced red blood cell count, low hematocrit). Mutants exhibit polychromasia (abnormally high number of immature blood cells), kidney defects (blood urea nitrogen level abnormally high, kidney size smaller than wildtype, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells) and abnormalities in palate bone fusion. Homozygotes are infertile. Heterozygote ..... For more information please see the full phenotype on the strain data sheet | ||
| 005066 | 129S-Slc27a2tm1Kds/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by PCR or Western blot analysis. Very long-chain acyl-CoA synthetase (VLCS) enzyme activity is reduced 4-fold in liver and 9-fold in kidney. Liver microsomes and peroxisomes fractions exhibit only a residual (30% of wildtype) VLCS activity level. The very long chain fatty acid (VLCFA) beta-oxidation rate in isolated fibroblasts is reduced by approximately 40% of wildtype activity level. This mutant mouse strain may be useful in studies of X-linked adrenoleukodystrophy and/or fatty acid metabolism. | ||
| 000385 | 129S;AKR-bs/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the spontaneous blind sterile mutation (bs) are characterized by bilateral nuclear cataracts, smaller than normal eyes, and glossy coats. Female mutant mice are fertile but males are sterile. Cataracts are visible in 16 day embryos and continue to adulthood. Adult male mice copulate normally but have smaller than normal testes. Defects in spermatogenesis lead to a reduced number of sperm and those that are formed completely lack acrosomes. | ||
| 003123 | 129S;ICR-Vhltm1Bjg/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Vhltm1Bjg targeted mutation are embryonic lethals. Homozygous mutant embryos show delays in early embryonic development. Development continues to 9.5 days after which mutant embryos undergo necrosis and resorption. On a gross morphological level two structures, the branchial arches and limb buds appear to be more significantly affected. | ||
| 009092 | A.129P-Skitm1Cco/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation die before or shortly after birth due to developmental defects. Homozygotes on the A/J background exhibit exencephaly (severe neural tube closure defects), with a higher embryonic lethality than homozygotes on the C56BL/6 or 129 backgrounds. None exhibit facial clefting. The Donating Investigator reports that homozygotes display flattened or shorter snouts, iris malformation and polydactyly. The penetrance of the phenotype is highly background dependent. Heterozygotes are viable and fertile with timely cranial neural tube closure, and a low incidence of facial clefting. The Donating Investigator reports some heterozygotes on the A/J background exhibit lateral facial clefting. This mutant strain may be useful in studies of facial cleft formation, 1p36 deletion syndrome, oncogene function, apoptosis, and neural tube and skeletal muscle defects. | ||
| 000497 | B6 x (B6xAKR-Frem1heb)F1/J | Cryopreserved - Ready for recovery |
| 000822 | B6 x 129S1/SvEi Oca2+ Tyr+-Vsx2or-J/J | Cryopreserved - Ready for recovery |
| 003483 | B6 x B10.D1-H2q/SgJ-Nox3het-2J/J | Cryopreserved - Ready for recovery |
| 003561 | B6 x B10.PL-H2u/(73NS)Sn-Hxl/J | Cryopreserved - Ready for recovery |
| Hxl is a dominant mutation with 100% penetrance. Heterozygotes and homozygotes have polydactyly. | ||
| 000502 | B6 x B6CBCa Aw-J/A-Myo5aflr Gnb5flr/J | Cryopreserved - Ready for recovery |
| 004591 | B6 x B6Ei.Cg-TWis/EiJ | Cryopreserved - Ready for recovery |
| 000507 | B6 x B6EiC3 a/A-Otcspf/J | Cryopreserved - Ready for recovery |
| 004835 | B6 x B6JCu.Cg-wl/J | Cryopreserved - Ready for recovery |
| Homozygous wabbler-lethal mice are first recognizable at 12 days of age and usually die at about 4 weeks. They have an abnormal wobbly gait and a pronounced tremor when walking. | ||
| 000953 | B6 x BALB/cBy-T4J/J | Cryopreserved - Ready for recovery |
| 002239 | B6 x BALB/cJ-Gdf5bp-3J/J | Cryopreserved - Ready for recovery |
| 002995 | B6 x C.B10-H2b/LiMcdJ-Fbn2fp-2J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the recessive fused phalanges 2 Jackson mutation (Fbn2fp-2J) have syndactyly of the second, third, and/or the fourth digits of the hindlimbs with <20% showing involvement of all three digits. This syndactyly likely results from defective mesenchyme differentiation rather than failed interdigital apoptosis (Arteaga-Solis et al., 2001). This mutant has a less severe phenotype than other Fbn2 mutants do, and shows no involvement of the digits of the forelimbs. Whether this is due to the allele or the genetic background has not been determined. (Chaudhry et al., 2001.) | ||
| 002424 | B6 x C3H/HeJ-Hps6ru-6J/J | Cryopreserved - Ready for recovery |
| 002048 | B6 x C57BLKS-Dock7m Leprdb Myo15sh2-J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the shaker 2 Jackson spontaneous mutation (Myo15sh2-J) are viable and fertile, showing only a slight reduction in both compared to wild-type mice. The shaker 2 Jackson remutation is not visibly different from the original shaker 2 (Myo15sh2, Stock No. 000109). Homozygous mutant mice of both alleles display a phenotype very similar to the behavior and pathology to shaker-1 (Myo7ash1) with the exception that the abnormalities are observed a little earlier in shaker 2 mice. This strain is also carrying the misty (Dock7m) and diabetes (Leprdb) spontaneous mutations. | ||
| 002543 | B6 x IDH2/EiJ | Cryopreserved - Ready for recovery |
| 003602 | B6 x STOCK Cln6nclf-Edardl-3J/J | Cryopreserved - Ready for recovery |
| 000938 | B6 x STOCK Epha4rb/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the rb allele of Epha4 can be visibly identified by 2.5 - 3 weeks of age by a constant hopping gait of the hind limbs; the forelimbs may show a hopping gait or move normally. When picked up by the tail homozygotes clasp their hindlimbs and show reduced ability to hold on to an edge; forelimbs show normal strength. | ||
| 000061 | B6 x STOCK Nox3het/J | Cryopreserved - Ready for recovery |
| Head tilt (Nox3het) is an autosomal recessive mutation that can cause abnormal circling behavior and hyperactivity in affected mice. Homozygotes also exhibit a subtle head tilt. Together, the abnormal behavioral phenotype is consistent with that of a vestibular disorder. Evoked auditory brainstem response profiles are normal indicating that the mutants are not deaf. Nox3het/Nox3het mutants are unable to sense orientation under water and therefore, cannot swim properly. If held by the tail, Nox3het/Nox3het mice retract, rather than extend, their limbs; they also flex ventrally, instead of dorsally as wild type mice do. When lowered quickly by the tail, Nox3het/Nox3het mice fail to extend their forelimbs in a normal manner and have difficulty righting themselves if dropped vertically from a short distance. Morphological assessment of the inner ear of homozygotes r ..... For more information please see the full phenotype on the strain data sheet | ||
| 001518 | B6 x STOCK T tf/th45 tf/J | Cryopreserved - Ready for recovery |
| 000578 | B6 x STOCK Tyrc-ch Bmp5se +/+ Myo6sv/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Snell's waltzer spontaneous mutation (Myo6sv) show to a marked degree the typical circling, head-tossing, deafness, and hyperactivity of other mutant mice of this type. Homozygous mutant mice are recognizable by the age of 1 week. The abnormalities of the inner ear consist of degeneration of the entire neuroepithelium comprising the organ of Corti, the saccular and utricular maculae, and the cristae of all three semicircular canals. Although viability of homozygotes is nearly normal, breeding ability is reduced and males are more reliable breeders than females.
Specific cytoskeletal components are critical for specific cellular structures. The microvilli of intestinal brush border cells in Myo6sv homozygotes are shorter than normal. While myosin 6 is not critical for the development of hair cell stereocilia, it is essential for their maintenance. At birth the stereocilia appear nearly normal with only occasional stereocil ..... | ||
| 000577 | B6 x STOCK a Oca2p Hps5ru2 Ednrbs/J | Cryopreserved - Ready for recovery |
| 000601 | B6 x STOCK a/a T(7;18)50H/J | Cryopreserved - Ready for recovery |
| 001962 | B6 x STOCK In(10)17Rk/J | Cryopreserved - Ready for recovery |
| 002022 | B6 x STOCK In(2)58Rk/J | Cryopreserved - Ready for recovery |
| 000610 | B6 x STOCK Rb(6.15)1Ald/J | Cryopreserved - Ready for recovery |
| 000951 | B6 x STOCK T(10;18)18H/J | Cryopreserved - Ready for recovery |
| 000597 | B6 x STOCK T(2;16)28H/J | Cryopreserved - Ready for recovery |
| 000961 | B6 x STOCK T(2;3)24H/J | Cryopreserved - Ready for recovery |
| 000592 | B6 x STOCK T(2;4)13H a/J | Cryopreserved - Ready for recovery |
| 000950 | B6 x STOCK T(2;8)26H/J | Cryopreserved - Ready for recovery |
| 000595 | B6 x STOCK T(2;9)11H/J | Cryopreserved - Ready for recovery |
| 001820 | B6 x STOCK T(2D;11B5)4Dn/J | Cryopreserved - Ready for recovery |
| 003916 | B6(Cg)-Col2a1sedc/J | Cryopreserved - Ready for recovery |
| Newborn homozygotes are smaller than normal, have a shortened trunk, and often display head bobbing. Decreased body weight persists into adulthood, and the noses, trunks, tails, skulls, and long bones of adults are shortened relative to those of normal siblings. Abnormal epiphyses, with dysplasia of the vertebrae, femora, and tibias are found. Although light microscopy failed to detect any abnormalities in the inner ear, the head bobbing characteristic accompanying this mutation is usually associated with inner ear defects. Auditory brainstem response threshold analysis of 10-15 week old homozygotes does show hearing impairment. Clefts develop between the inner and outer aspects of the inner nuclear layer of the retina (retinoschisis). | ||
| 004608 | B6(Cg)-Htra2mnd2/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the recessive Htra2mnd2 mutation have a basal ganglia disorder initially described as an early onset motor neuron disease. This is first outwardly evident by 21 to 24 days of age as an unsteady gait with extended hind limbs, repetitive movements and episodes of sudden arrests. This progresses to include severe muscle atrophy, hunched posture, increased imbalance, chorea, dystonia, and progressive akinesis. A failure to gain weight becomes evident shortly after the onset of the other symptoms and by 35 days of age wildtype littermates are twice as heavy as the mutants. Body fat is not detectable at necropsy. Both the spleen and the thymus drop from normal weights at 23 days of age to 10% of normal at 30 days of age and the thymic corticomedullary junction is lost. Death usually occurs within two weeks of disease onset, by 40 days of age. The growth retardation is not the primary cause since disease is not delayed by intragastric feeding. For more information please see the full phenotype on the strain data sheet | ||
| 003046 | B6(FVB)-MitfMi-Mee/J | Cryopreserved - Ready for recovery |
| On the C57BL/6 background, homozygotes have a white coat color while heterozygotes have a black coat. Clinically, heterozygotes have variable amounts of pigment in the retina with a normal optic cup and retinal vessels. Homozygotes have an iris coloboma, a large optic cup and poor or no retinal vessels. Homozygotes show some pigment in the iris, which does not dilate. | ||
| 006893 | B6.129-Mgat3tm1Jxm/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. The mice exhibit normal developmental and physiologic parameters. No alterations are apparent in the neural system, circulating leukocytes, erythrocytes or in serum metabolite levels that reflect kidney function. | ||
| 008619 | B6.129-Opn1mwtm1(OPN1LW)Nat/J | Cryopreserved - Ready for recovery |
| A portion of the X-linked mouse opsin 1 (medium-wave-sensitive) "green pigment" gene was replaced by a human opsin 1 (long-wave-sensitive) "red pigment" cDNA in these targeted mutant mice. Heterozyguous female mice are endowed with a unique ability to make chromatic discriminations at long wavelengths. Hemizygous males and homozygous females have greater sensitivity to long wavelength light than normal mice. Heterozygotes, hemizygotes, and homozygotes are normal in size, viability, and fertility. Expression is observed in retinal cone photoreceptors as determined by immunostaining. The knocked-in coding sequences are expressed normally. | ||
| 006336 | B6.129-Selplgtm1Rpmc/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by flow cytometry analysis of leukocytes. Homozygotes have elevated total leukocyte counts, with increased numbers of neutrophils, lympohcytes and eosinophils. Leukocytes isolated from homozygotes exhibit abnormal tethering and rolling (adhesion and migration) due to impaired attachment. This mutant mouse strain represents a model that may be useful in studies of leukocyte adhesion and migration in the inflammatory response. This strain was transferred from the collection of the Consortium for Functional Glycomics. | ||
| 008313 | B6.129P2-Hlxtm1Rph/J | Cryopreserved - Ready for recovery |
| Homozygous null mice have an embryonic lethal phenotype. Homozygous mice on the C57BL/6 and B6;129 mixed background fail to develop past embryonic days 15.5 due to impaired fetal hematopoiesis (anemia, hypoplastic and abnormal development of the liver, hypoplastic gut). Homozygous mice on the FVB/N background survive through embryonic day 18.5 and dead homozygote newborn pups are observed. Late gestation homozygous embryos on the FVB/N background are smaller than wildtype littermates, pale, hydropic (subcutaneous fluid ballooning skin), and have impaired neural crest cell and enteric neuron migration from the stomach to intestine. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Naive CD4 T cells from heterozygotes exhibit increased responsiveness to IL-4, resulting in differentiation of more Th2 cells. This mutant mouse strain may be useful in studies of liver and gastrointe ..... For more information please see the full phenotype on the strain data sheet | ||
| 007671 | B6.129S4-Fgfr1tm5.1Sor/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exon 4 of the targeted gene. Exon 4 is the first exon found in all reported Fgfr1 splice variants. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 4 and the neomycin selection cassette deleted in the cre-expressing tissue(s). This mutant mouse strain may be useful in studies of fibroblast growth factor (Fgf) cellular signaling during embryonic development. | ||
| 007583 | B6.129S4-Slc17a6tm1Rpa/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exon 2 in the targeted gene. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. They show ~30% less expression of the targeted gene than wildtype mice, however. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in eliminating expression in a tissue-specific manner (widespread deletion of expression is lethal). | ||
| 006566 | B6.129S6-Ppt1tm1Hof/SopJ | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by immunoassay. Palmitoyl-protein thioesterase activity in the brain of the mutant is reduced to background levels. Although healthy at birth, by age four to five months, mutant mice display lack of grooming and an abnormal gait that progresses to hind limb paralysis. By six to eight months of age mutant mice have a low body weight and display an abnormal clasping behavior. Aggressive behavior results in fighting and dermatitis due to bite wounds. By seven months of age, mortality is 50% with very few mice surviving beyond ten months of age. Myoclonic jerks and seizures manifest at age three to four months. Strong rapid hind limb seizures ("popcorn" seizures) that propel mice several feet also occur. Brain size of the mutant mice is reduced. Histologically, mutant brains show neuronal loss and apoptosis in ..... For more information please see the full phenotype on the strain data sheet | ||
| 004994 | B6.129X1-Camk4tm1Tch/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis. Synaptic plasticity, as assayed by long-term potentiation (LTP) and long-term depression (LTD), in mutant mice is deficient. Homozygotes exhibit diminished contextual and auditory fear memory. Cyclic AMP-responsive element binding protein (CREB) activation by fear conditioning is absent in the amygdala and decreased in the hippocampus. Thymocyte maturation is impaired. Both CD4+ and CD8+, single positive, thymocyte levels are reduced. This mutant mouse strain may be useful in studies examining learning and memory or related to thymocyte development. | ||
| 005251 | B6.129X1-Htr3atm1Jul/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis of the dorsal root ganglia. Quantitative autoradiography ligand binding assays of solitary tract nucleus, area postrema and trigenimal nucleus caudalis and electrophysiological tests of isolated nociceptor neurons do not detect functional receptor activity. Mutant mice have an impaired response to persistent pain caused by inflammatory tissue injury. This mutant mouse strain may be useful in studies of nociceptive processing, pain response behavior, and peripheral neurogenic inflammation. | ||
| 006429 | B6.Cg-Dwh/GrsrJ | Cryopreserved - Ready for recovery |
| Mice carrying the dominant mutation dispersed white hair on this predominantly C57BL/6J background have white hairs dispersed throughout the normally black coat along with patches of white hairs on the back or belly. | ||
| 013110 | B6.Cg-Uchl1gad-2J/GrsrJ | Cryopreserved - Ready for recovery |
| Homozygotes are normal in appearance until 6 or 7 weeks of age when weakness of the hindlimbs begins to present through limb grasping or dragging or splaying of the hindlimbs when walking. A progressive decrease in body weight begins at 12 weeks of age and the hind limb atrophy progresses to paralysis and premature death. Homozygotes are not able to breed. | ||
| 006851 | B6.Cg-Tg(Per1-luc)025Jt/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the "mPer1-Luc" transgene are viable and fertile, with luciferase (luc) expression driven by the mouse Per1 promoter and 5'-UTR elements. Expression of luc RNA is highly specific to the suprachiasmatic nuclei (SCN) with a clear circadian rhythm that correlates with endogenous Per1. Slice cultures taken from hemizygous mice maintain a circadian rhythm of luminescence for at least 5 days after culturing. A prolonged (6 hour) light pulse treatment during the subjective night rapidly induces both mPer1-luc and endogenous mRNA expression; while the endogenous mRNA level decreased to baseline during the 6 hour period, the mPer1-luc mRNA levels remain higher. These mPer1-luc transgenc mice may be useful in studying circadian rhythms and as a real-time reporter of Per1 expression.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from ..... | ||
| 008210 | B6.D1-Pde10atm1Pfi/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the phosphodiesterase 10A (PDE10A) targeted mutation are viable and fertile with no gross abnormalities, although breeding homozygotes together produces reduced liter sizes. The targeted gene generates a truncated transcript. A small amount of functionally inactive protein is detected in striatum, cortex and cerebellum. Homozygous mice on the C57BL/6N genetic background (PDE10AC57) exhibit multiple behavioral abnormalities; decreased locomotor activity when placed in a novel environment, delayed acquisition of conditioned avoidance response, blunted response to the NMDA receptor antagonist MK-801 (but not PCP), altered locomotor responses to both amphetamine and methamphetamine, and increased striatal dopamine utilization. These PDE10AC57 mutant mice may be useful in neurobiological studies including metabolic inactivation of intracellular signal transduction pathways by cyclic phosphodiesterases (PDEs), regulation of information processing by ..... For more information please see the full phenotype on the strain data sheet | ||
| 003095 | B6.D2-Vac14ingls/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the recessive Vac14ingls mutation are significantly smaller than their littermates, and their coat color is dilute with white underfur both dorsally and ventrally (Sweet 1991; Samples 2003). Most develop hydrocephalus with onset by one week of age. Homozygotes are weak and uncoordinated and have difficulty righting themselves. They fail to gain weight during the second week of life, and most die by three weeks of age. (Bronson et al. 2003) Length of survival appears to correlate with the severity of hydrocephalus, which varies from absent to severe; however, all homozygotes die by four weeks, whether or not they are hydrocephalic (Samples et al. 2003).
Hydrocephalus affects the lateral ventricles most severely; serial sections reveal an intact cerebral aqueduct. Diffuse astrocytic hypertrophy and hyperplasia are observed in brains and spinal cords of mutant mice. A few mutants develop status spongiosis, and a few exhibit gliosis a ..... | ||
| 005738 | B6.FVB-Tg(tetO-EGFP,-Tgfbr2)8Mcle/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Enhanced Green Fluorescent Protein (EGFP) and a truncated dominant-negative mouse transforming growth factor, beta receptor II (Tgfbr2) under the control of a bidirectional tetracycline transactivator responsive promoter (TRE; tetO). No fluorescence is observed in the tissues of this mutant. Primary cultures derived from ear biopsies exhibit green fluorescence when transfected with a tetracycline transactivator (tTA; "Tet-off") vector. When these transgenic mice are bred with other transgenic mice expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), tissue-specific EGFP and dominant-negative Tgfbr2 transgene expression can be regulated with the tetracycline analog, doxycycline. This mutant mouse strain may be useful in studies of TGF-beta signali ..... For more information please see the full phenotype on the strain data sheet | ||
| 007733 | B6;129-4930579C15Riktm1Gar/J | Cryopreserved - Ready for recovery |
| Female mice that are homozygous for the targeted mutation are healthy and fully fertile. Male homozygous mice do not display any gross physical or behavioral abnormalities, however they are subfertile. No RNA message is detected by Northern blot analysis of testis tissue from homozygotes. The mechanism for sub-fertility is unknown. This mutant strain may be useful in the study of sperm biology. | ||
| 008514 | B6;129-Amphtm1Pdc/J | Cryopreserved - Ready for recovery |
| In addition to ablated activity of the targeted gene, these mice show a parallel dramatic reduction in amphiphysin 2 selectivity in the brain due to its enhanced degradation in the absence of amphiphysin 1. Defects in synaptic vesicle recycling that are unmasked by stimulation suggest impairments at multiple stages of the cycle. These defects correlate with increased mortality due to rare irreversible seizures. Due to such seizures, animals die mainly between two and five months of age without other noticeable health problems. Approximately 50% of homozygotes survive to 10 months of age. Homozygotes exhibit major learning deficits as demonstrated by the Morris water maze task, and show very mild fear responses in both the context test and the auditory cue test compared to their wild-type littermates. Viable homozygotes reportedly breed until about three months of age and produce small litters of just two to three pups. | ||
| 006394 | B6;129-Apba2tm1Sud Apba3tm1Sud Apba1tm1Sud/J | Cryopreserved - Ready for recovery |
| Triple homozygous knock-in mice are viable and fertile and and do not display any gross physical or behavioral abnormalities. Expression of all three proteins is normal. When crossed with a cre deleter strain that eradicates protein expression, Apba1/Abcba2 (Apba1/2) double knockout and Apba1/2/3 triple knockout mice exhibit a high percentage of postnatal lethality (only ~20% of the mice survive). Apba1/2 mice are visually indistinguishable from their littermates and display no major alterations in breathing, movements or reaction to stimuli several hours after birth, but fail to nurse and die within 24 hours. Their brains are morphologically and structurally normal. Quantitation of 18 neuronal proteins fails to reveal significant changes. Surviving mice show reduced weight gain and exhibit movement dysfunction. Cultured neurons from triple knock-in neonates show impairments in presynaptic neurotransmitter release after treatment with lentiviral cre. Apba1/3 ..... For more information please see the full phenotype on the strain data sheet | ||
| 002878 | B6;129-Apobtm1Sgy Apoetm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Apobtm1Sgy and Apoetm1Unc targeted mutations do not express the apolipoproteins B100 or E. They do retain the ability to express apolipoprotein B48. They have the highest total cholesterol (392 mg/dl vs 341 for Apobtm1Unc/Apoetm1Unc); highest LDL cholesterol (APOB48 is not a ligand for LDLR), and atherosclerotic lesions more extensive than Apoetm1Unc/Apoetm1Unc homozygotes. The extent of atherosclerosis correlated significantly with plasma cholesterol levels. | ||
| 002879 | B6;129-Apobtm2Sgy Apoetm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Apobtm2Sgy and Apoetm1Unc targeted mutations do not express the apolipoproteins B48 or E, they do express APOB100. Homozygotes are viable and fertile with no overt abnormalities. Compared to the APOB48 APOE deficient mice and the APOE deficient mice, they have the lowest total cholesterol (247mg/dl), lowest LDL cholesterol, and the least extensive Atherosclerotic lesions. The extent of atherosclerosis correlated significantly with plasma cholesterol levels. | ||
| 002245 | B6;129-Apoetm1Unc Ldlrtm1Her/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Apoetm1Unc and Ldlrtm1Hertargeted mutations on a normal chow diet show cholesterol levels corresponding to those seen in the Apoetm1Unc targeted mutant strain. The lipoprotein pattern in homozygous mice also resembles that seen in the Apoetm1Unc targeted mutant strain (VLDL & chylomicron remnants). The double targeted mice have a marked increase in both APOB48 and APOB100. In addition, APOAIV is increased. | ||
| 006329 | B6;129-Baxtm2Sjk Bak1tm1Thsn/J | Cryopreserved - Ready for recovery |
| Mice homozygous for both alleles (Baxfl and bak-) are viable and fertile with no reported abnormalities. Splenic and thymic tissues display no Bak1 protein expression. When bred to Cre recombinase expressing mice, the resulting offspring will have exons 2-4 of Bax deleted in the cre-expressing tissues (determined by promoter driving cre expression). The conditional deletion of Bax combined with the Bak1 null allele makes these mice useful in studies of apoptosis regulation, tissue homeostasis, and development in multiple cell lineages.
When bred to a strain with a Bak1 targeted null allele (Stock No. 004183) and to either a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 004126) or to a strain expressing interferon inducible Cre recombinase ( ..... | ||
| 009077 | B6;129-C3tm1Crr Man2a1tm1Jxm/J | Cryopreserved - Ready for recovery |
| 006382 | B6;129-Casktm1Sud/J | Cryopreserved - Ready for recovery |
| Homozygous floxed mice are viable and fertile, but females do not thrive. The body size of mutants is significantly smaller than littermate controls and they exhibit a slightly increased mortality. Knock-in mice are hypomorphs and protein is expressed at less than 30% of normal levels. Crossing of the floxed mutants with mice expressing cre recombinase in the male germline excises the floxed exon and a neomycin resistance gene cassette to create a complete knockout of the gene. Knockout homozygotes die within a few hours of birth. They exhibit a partially penetrant cleft palate syndrome and increased apoptosis in the thalamus, but display no other major developmental changes or deficits in basic electrical properties of their neurons.
When bred to a strain expressing Cre recombinase in the male germline (see Stock No. 003328 or 007252 for example), this mutant mouse str ..... | ||
| 004177 | B6;129-Cd3etm1Lov/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for this targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Although a shortened transcript lacking exon 5 and 6 sequence is generated in the thymus, no protein product is detected. Thymocyte development is arrested resulting in a significant reduction in the number of thymocytes (10% of wild type). Residual thymocytes are immature, consisting entirely of double negative cells (CD4+CD8- or CD4- CD8+ thymocytes are absent). The development of intestinal intraepithelial T lymphocytes also appears to be arrested. These mice provide a source of T lymphocyte-depleted splenocytes and are suitable for use as hosts in studies utilizing adoptive T lymphocyte transfer techniques. | ||
| 008821 | B6;129-Cd79btm1Gzmn/J | Cryopreserved - Ready for recovery |
| Cytoplasmic tyrosines 195 and 206, associated with immune receptor tyrosine activation motifs (ITAMs), were replaced with alanine in this Ig beta targeted mutant strain. The only reported reproducible differences in developing B cells in these Igβ AA mutant mice is a higher level of surface IgM and IgD on immature and recirculating B cells. Igβ AA mice also show a five-fold reduction in the number of B1a B cells in the peritoneal cavity. This strain may be useful in studies of B cell receptor signaling. | ||
| 008822 | B6;129-Cd79btm3Mnz/J | Cryopreserved - Ready for recovery |
| The cytoplasmic domain of the targeted Igβ gene was replaced with the cytoplasmic domain of the Igα gene. Mutant B cells are able to complete all stages of development, but fail to differentiate into B1a cells. Igβc-α cells are anergic to T-independent and T-dependent antigens in vivo. This strain may be useful in studies of B cell development. | ||
| 008616 | B6;129-Cdhr1tm1Nat/J | Cryopreserved - Ready for recovery |
| Homozygous protocadherin 21 targeted mutation mice are viable and fertile and are normal in size and viability. They exhibit a slow retinal degeneration in which the outer segments of both rods and cones are disorganized and fragmented. Light responses of both rods and cones is only modestly compromised and phototransduction proteins appear to be correctly localized. This strain may be useful in studies of sensory neurons/photoreceptors, and retinal degeneration. | ||
| 003536 | B6;129-Cdk5tm1Kul/J | Cryopreserved - Ready for recovery |
| Cdk5 is an important molecule for brain development and neuronal differentiation. Cdk null mice exhibit unique lesions in the central nervous system associated with perinatal mortality. The brains of mutant mice lack cortical laminar structure and cerebellar foliation. The large neurons in the brain stem and in the spinal cord show chromatolytic changes with accumulation of neurofilament immunoreactivity. They also exhibit neuronal migration abnormalities, cerebellar defoliation, NF accumulation neuronal bodies, and degenerated motor neurons. | ||
| 011064 | B6;129-Cnga4tm1Reed/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by in situ hybridization analysis of olfactory receptor neurons from homozygotes. Beta-galactosidase expression is faintly detected in an incomplete mimic of the endogenous gene expression pattern, by histochemical analysis of olfactory epithelium and olfactory bulb. Olfactory receptor neuron channels from homozygotes have reduced desensitization rate and decreased affinity for cAMP. Homozygotes exhibit defective odor detection ability and reduced rate of odor adaptation due to impaired Ca2+-calmodulin mediated channel desensitization. | ||
| 004454 | B6;129-Crhr1tm1Klee/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical abnormalities. No gene product (mRNA) is detected in cerebellum tissue. No gene product receptor function is seen in treated cultured pituitary cells. Pups from homozygote crosses die within 48 hours after birth of lung dysplasia due to insufficient maternal glucocorticoid during fetal development. When corticosterone is administered by drinking water or in utero to homozygous females from embryonic day 12 through postnatal day 14, offspring have normal lung maturation. There is a reported 15% mortality in male mutant mice between 3 -12 weeks of age. Mutants have very low plasma corticosterone levels, and no diurnal rise in levels. Histological analysis reveals reduced zona fasciculata layer of the adrenal gland in mature animals. Homozygous mice display reduced anxiety response behavior. Hormonal response to stress, as measured by circulating ACTH and corticoste ..... For more information please see the full phenotype on the strain data sheet | ||
| 008157 | B6;129-Cst7tm1Ayr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. Expression is eliminated in dendritic cells, macrophages and B cells. No overt phenotype has as yet been identified, despite a broad analysis of immune cell populations. | ||
| 004604 | B6;129-Ctnna1tm1Efu/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exon 2 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
When bred to a strain expressing Cre recombinase in the female germline (see Stock No. 003551 for example), this mutant mouse strain may be useful in studies of mammary epithelium. When bred to a strain expressing Cre recombinase in the mammary gland (see Stock No. 003552 for example), this mutant mouse strain may be useful in studies of mammary epithelium. When bred to a strain expressing Cre recombinase in the nervous system (see Stock No. 003771 for example), this mutant mouse strain may be useful in studies of the cerebral cortex and the hedgehog signalling pathway. | ||
| 004264 | B6;129-Cycstm1Wlm/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Cycstm1Wlm targeted-mutant allele die in utero by embryonic day 10.5, but cell lines established from early Cycs-null embryos are viable under conditions that compensate for defective oxidative phosphorylation. Cells lacking cytochrome c show reduced caspase 3 activation, and are resistant to the proapoptotic effects of UV irradiation, serum withdrawal, and staurosporine. Cells lacking cytochrome c, however, do demonstrate an increased sensitivity to cell death signals triggered by tumor necrosis factor, alpha. Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 009688 | B6;129-Dbhtm2(Th)Rpa Thtm1Rpa/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for both targeted mutations are viable and fertile. Dopamine-deficient (DA-deficient, DA-/-, or DD) mice are homozygous for the TH mutant allele and heterozygous for the DBH-TH mutant allele (Th-/-; DbhTh/+). While no expression from the TH mutant allele is observed in any tissues (resulting in deficiency of both dopamine (DA) and norepinephrine (NE)), the DBH-TH mutant allele contains the TH coding sequence under the control of the endogenous DBH promoter region and restores TH expression in noradrenergic neurons. DD mice become hypoactive and hypophagic around two weeks of age and usually die before four | ||