Search Criteria: Strain Type is "Mutant Stock"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 100410 | WBB6F1/J-KitW/KitW-v/J | Level 2 |
| 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. | ||
| 006494 | B6CBA-Tg(HDexon1)62Gpb/3J | Level 3 |
| This line is transgenic for the 5' end of the human HD gene carrying less than (CAG)150 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 cells develop
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| 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. | ||
| 003658 | STOCK Tg(TIE2GFP)287Sato/J | Level 4 |
| 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. | ||
| 006365 | 129-Cckartm1Kpn Cckbrtm1Kpn/J | Repository- Live |
| 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 | 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 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 | Repository- Live |
| 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. | ||
| 006830 | 129-Dysftm1Kcam/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable, fertile and show a normal growth rate. Mice develop a slowly progressive muscular dystrophy. By the age of 2 months, a few individual necrotic and centrally nucleated fibers can be detected throughout the muscle; the number increases with age. By 8 months, the muscle develops all of the pathological characteristics of muscular dystrophy (e.g. regenerating fibers, split fibers, muscle necrosis with macrophage infiltration and fat replacement). The severity of the pathology varies in different muscles. Muscle fibers are defective in Ca2+-dependent sarcolemma resealing/repair. No protein product from the targeted gene is detected in skeletal muscle microsomes. This mutant mouse strain represents a model that may be useful in studies of muscle disease and repair. | ||
| 006053 | 129-Gt(ROSA)26Sortm1Luo/J | Repository- Live |
| 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
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| 006067 | 129-Gt(ROSA)26Sortm2Luo/J | Repository- Live |
| 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 | ||
| 008349 | 129-Ptger3tm1Csml/J | Repository- Live |
| 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 | ||
| 007965 | 129S-Dvl1tm1Awb/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 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 | Repository- Live |
| 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. | ||
| 007664 | 129S-Efnb1tm1Sor/J | Repository- Live |
| 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. | ||
| 007205 | 129S-Myo1eGt(ROSA)74Sor/J | Repository- Live |
| 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 | Repository- Live |
| 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 | Repository- Live |
| 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. | ||
| 007209 | 129S-Schip1Gt(ROSA)77Sor/J | Repository- Live |
| 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 | Repository- Live |
| 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 | ||
| 006555 | A.129(B6)-Tg(APPSw)40Btla/J | Repository- Live |
| These R1.40 transgenic mice express all mRNA and protein isoforms of the human amyloid beta (A4) precursor protein APP containing the Familial Alzheimer's Disease (FAD) Swedish mutation K670N/M671L. Transgene expression (mRNA and full-length protein) is 2 to 3 fold the endogenous mouse App expression level in the hemizygous state in brain tissue as revealed by RT-PCR and Western Blot analysis. Transgene expression pattern mimics endogenous mouse gene expression patterns. The donating investigator reports increased mortality in young homozygous animals (higher incidence in females). These R1.40 transgenic mice may be useful in studying the pathogenesis of Familial Alzheimer's Disease and possible therapeutic treatments.
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. It should be noted that the phenotype could va
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| 000578 | B6 x STOCK Tyrc-ch Bmp5se +/+ Myo6sv/J | Repository- Live |
| 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
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| 003916 | B6(Cg)-Col2a1sedc/J | Repository- Live |
| 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). | ||
| 003046 | B6(FVB)-MitfMi-Mee/J | Repository- Live |
| 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. | ||
| 006336 | B6.129-Selplgtm1Rpmc/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 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 | Repository- Live |
| 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 | ||
| 004595 | B6.129P2-Htttm2Detl/J | Repository- Live |
| Mice homozygous for the targeted allele are viable and fertile. At 15-40 weeks of age mice carrying this allele on a segregating C57BL/6 and 129P2 background exhibit an abnormal gait, clasping behavior and diminished exploratory activity. Infrequent tonic-clonic like seizures may also be observed. Mice with a higher percentage of C57BL/6 in their genetic background develop behavioral and neurological phenotypes at a much later age (70-100 weeks). (Heng MY et al. 2007) Mutant mice may be noticeably smaller than wild-type littermates. Increased glial fibrillary acidic protein immunoreactivity is present in the striatum and ubiquititin- and huntingtin-positive neuronal intranuclear inclusions (NIIs) are detected throughout the dorsal striatum, nucleus accumbens and to a lesser extent other regions of the brain. Onset of symptoms occurs earlier for homozygotes than for heterozygotes.This mutant mouse strain represents a model that may be useful in studies related to Huntington's di
..... 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. | ||
| 007671 | B6.129S4-Fgfr1tm5.1Sor/J | Repository- Live |
| 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. | ||
| 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/ESR1,-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 | ||
| 005738 | B6.FVB-Tg(tetO-EGFP,-Tgfbr2)8Mcle/J | Repository- Live |
| 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 | ||
| 005650 | B6129-Tg(Myh6-cre/Esr1)1Jmk/J | Repository- Live |
| Mice that are homozygous for the transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre 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, this double fusion protein has substantially greater Cre recombinase activity with less promiscuity compared with a single CreMer fusion protein. Inducible expression of cre in cardiac cells makes this strain suitable for creating bitransgenic mice for use in studies of temporally regulated deletion of loxP-flanked targeted genes. | ||
| 006394 | B6;129-Apba2tm1Sud Apba3tm1Sud Apba1tm1Sud/J | Repository- Live |
| 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 | ||
| 006329 | B6;129-Baxtm2Sjk Bak1tm1Thsn/J | Repository- Live |
| 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 (
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| 006382 | B6;129-Casktm1Sud/J | Repository- Live |
| 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
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| 002711 | B6;129-Gabrb3tm1Geh/J | Repository- Live |
| The gamma-Aminobutyric acid type A receptors mediate the majority of rapid inhibitory synaptic transmission in the CNS. The beta3 subunit is an essential component of these receptors in many brain regions, especially during development, and is implicated in several pathophysiologic processes. The majority of mice homozygous for the Gabrb3tm1Geh mutation (or beta3-/-) die at birth with ~60% displaying cleft palate and the remaining ~35% die for unidentified reasons. Homozygous females that survive are fertile but do not care for their pups. Survivors have frequent myoclonus and occasional epileptic seizures, are hypersensitive to external stimuli and handling, have a lack of coordination and display altered responses to certain anesthesias. In addition, the observed behavioral deficits (especially regarding social behaviors) indicate that mutant mice may be a useful model of autism spectrum disorders. Of note, several strains bearing gamma-aminobutyric acid (GABA-A)
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| 004847 | B6;129-Gt(ROSA)26Sortm1(cre/Esr1)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. | ||
| 003504 | B6;129-Gt(ROSA)26Sortm1Sho/J | Repository- Live |
| Mice with the Gtrosa26tm1Sho targeted mutation are similar to the B6;129-Gtrosa26tm1Sor from Dr. Philippe Soriano, but reported in the literature to be an improved reporter strain for monitoring cre-mediated excisions. The B-galactosidase-neomycin phosphotransferase fusion gene (Bgeo)-trapped reverse orientation splice acceptor Bgeo line 26 (ROSA26) locus was modified by gene targeting such that Bgeo is expressed only after Cre-mediated excision of loxP-flanked DNA sequences. Bgeo from the excised ROSA26 allele is expressed ubiquitously in embryos and adult mice. When mating the reporter strain with cre-expressing transgenic mice, one can see that the loxP-flanked ROSA26 allele is accessible to cre during early embryogenesis, as well as in a specific hematopoietic lineage (T lymphocytes). These mice may prove useful in the study of cell fate and cell migration during embryogenesis through recombinase-activated taggi
..... 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. | ||
| 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. | ||
| 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. | ||
| 006894 | B6;129-Mgat4atm1Jxm/J | Repository- Live |
| Mice homozygous for this floxed targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. When bred to cre transgenic strains, the loxP-flanked exon is deleted by cre expression to produce a null allele. | ||
| 006904 | B6;129-Msctm1Eno/J | Repository- Live |
| Mice homozygous for this MyoR mutant allele are viable and fertile with no obvious abnormalities. These mice may be useful in studying muscle development, specifically craniofacial muscles. For example, when these mice are bred with capsulin-mutant mice, the resulting double mutant offspring have significant abnormalities in craniofacial (and other) muscle development and MyoD-family transcription factor gene expression. 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. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 006933 | B6;129-Mycntm1Psk/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 exons 2 and 3 deleted in the cre-expressing tissue(s). | ||
| 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 | ||
| 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 | ||
| 007608 | B6;129-Smad1tm1Sor/J | Repository- Live |
| Homozygotes for the Smad1tm1Sor (also called Smad1C) allele have an embryonic lethal phenotype and do not survive past ED9.5. These mice carry a mutation (the C-terminal SSVS motif was changed to AAVA) in exon 7, which effects transcriptional activity. Homozygous embryos display posterior truncation, abnormal turning, allantois malformations (failure of the allantois to connect to the chorionic plate), anterior truncation of the head with only one brachial arch, and enlarged pericardium. At ED7.5 homozygous embryos do not have any detectable primordial germ cells. Western blot analysis of ED9.5 homozygotes showed that protein levels were not affected. Heterozygotes for this mutant allele 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 homeostasis and BMP and MAPK signaling pathways during development and in the adult. | ||
| 007613 | B6;129-Smad1tm2Sor/J | Repository- Live |
| Homozygotes for the Smad1tm2Sor (also called Smad1L) allele are viable and fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mice carry a mutation in exon 3, which effects MAPK-mediated phosphorylation of the protein. Western blot analysis of MEFs from homozygotes showed that similar protein levels compared to wildtype. Homozygous embryos have fewer primordial germ cells than wildtype controls. Homozygous mice display abnormal gastric mucosa cell population ratios with fewer zymogenic cells and more parietal cells. The cytoskeleton of MEFs from homozygotes exhibit a loss of adhesion zippers, decreased stress fibers, and an accumulation of actin in the cortical regions with an increase in beta-catenin immunostaining localized to the cell membranes. This mutant mouse strain may be useful in studies of stomach development, gastic mucosal homeostasis and BMP and MAPK signaling pathways during development and in the adult. | ||
| 006390 | B6;129-Sncatm1Sud Sncbtm1.1Sud/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. No protein product from these targeted genes is detected in brain tissue. Overall brain morphology and structure appears normal. No significant changes in the ultrastructure, short- or long-term synaptic plasticity, or in the pool size or replenishment of recycling synaptic vesicles is detected. Dopamine levels in the double targeted mice are decreased by approximately 20%, but dopamine uptake and release from isolated nerve terminals is normal. Serotonin levels are unchanged. This mutant mouse strain represents a model that may be useful in studies of synaptic function and neurodegenerative disease. | ||
| 008294 | B6;129-Syt11tm1Sud/J | Repository- Live |
| These transgenic animals carry a FLAG-(C)4-FLAG insertion in exon 2 of the gene. Homozygotes are viable and have no obvious phenotype. Mutant protein expression levels are similar to those of the wildtype protein. Expression is brain-specific and localized in the neuronal soma and dendrites (presumably on cargo vesicles). Protein can be recognized using FLAG antibody by Western blot analysis, but not in histological sections or labeled cultures. No significant N-ethyl-maleimide-sensitive factor attachment protein receptor (SNARE) binding is observed in immunoprecipitation (IP) assays. Exon 2 is flanked by loxP sites. When crossed with a Cre recombinase-expressing strain, tissue-specific expression can be eliminated by deletion of exon 2. This strain may be useful in studies of neurotransmitter release mechanisms. | ||
| 006388 | B6;129-Syt7tm1Sud/J | Repository- Live |
| Homozygotes are viable, fertile, and have normal body weight. There is no obvious neuronal phenotype. Western analysis indicates that no protein product is produced. | ||
| 006389 | B6;129-Syt7tm2Sud/J | Repository- Live |
| Homozyogotes are viable, fertile and have normal body weight. This strain was created by excision of a neomycin cassette from the targeted mutation line (see Stock No. 006388 ) and wildtype levels of expression are restored for all splice variants. These mice have no obvious neuronal phenotype. | ||
| 008295 | B6;129-Syt9tm1Sud/J | Repository- Live |
| Mice homozygous for this targeted knock-in are viable and fertile and do not display any gross physical or behavioral abnormalities.Synaptotagmin IX knock-in mice contain GFP "emerald" fused to the first exon of the targeted gene, and exon 2 is flanked by loxP sites. GFP expression is primarily localized in the limbic system and striatum of the brain. When crossed with a Cre recombinase-expressing strain, offspring are produced with tissue-specific deletion of Syt9 and which lack GFP expression, suggesting this creates a null allele. This strain may be used to study Ca2+ sensors involved with fast neurotransmitter release. Synaptotagmin IX knock-in mice contain GFP " | ||
| 006251 | B6;129-Tor1atm1Wtd/J | Repository- Live |
| Homozygous mutant mice have a perinatal lethal phenotype. They fail to feed or vocalize at birth, and typically die within 48 hours. No protein is detected by immunoblot analysis in tissues (liver, brain, spinal cord, mouse embryonic fibroblasts (MEFs)) from homozygous mutant animals. Microscopic and ultrastructural examination of central nervous system neurons from embryonic day 18 homozygous embryos reveals abnormalities including dysmorphic ventral horn neuron nuclei, vesicles in the neuronal nuclear envelope and enlarged endoplasmic reticulum. Neurons within homozygotes appear normal when migrating, but develop nuclear membrane abnormalities upon maturation.
In contrast to homozygous mutant mice, heterozygotes are viable, fertile, normal in size, and do not manifest any gross physical or behavioral abnormalities. Torsin A (TOR1A) protein levels in heterozygous mice are approximately 50% of wildtype levels. This mutant mouse strain may be useful in studies of torsion dystonia 1
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| 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 | ||
| 006980 | B6;129-Trp53tm2Xu/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile. They carry two phosphorylation site disruptions: Ser18 to Ala (S18A), and Ser23 to Ala (S23A). Trp53-dependent apoptosis is essentially abolished in thymocytes. These mice develop spontaneous tumors at approximately 1.5 years of age and a range of malignancies that are distinct from those found in animals carrying either a single S23A mutation or a complete knockout of the gene. This mutant mouse strain may be useful in studies of phosphorylation events in cancer development and apoptosis. | ||
| 006495 | B6;129-Trp53bp1tm1Jc/J | Repository- Live |
| Homozygous "53BP1"-deficient mice are viable and fertile, but exhibit retarded growth and generate reduced litter sizes. Protein from the targeted gene is not detected in the testes (by immunoblot) or in mouse embryonic fibroblasts (MEFs) (by immunofluorescence). Homozygotes are immunocompromised, hypersensitive to whole-body irradiation, and develop thymic lymphomas with higher frequency (8%) compared to wildtype by 4-7 months of age. MEFs from homozygous mutant mice have a defective DNA damage response with impaired Chk2 activation. These mutant mice may be useful in studies of the immune system, cancer, tumor suppression, and DNA damage response pathways. | ||
| 007605 | B6;129P-Psen1tm1Vln/J | Repository- Live |
| These mice possess loxP sites on either side of exon 7 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 "floxed" mice are bred to mice that express Cre recombinase, resulting offspring can have one of three resulting genotypes (only exon 7 deleted, only the neo selection cassette deleted, or both exon 7 and the neo selection cassette deleted) in the cre-expressing tissue(s). These PS1-floxed mice may be useful in generating conditional knockouts of Presenilin 1 for studying Alzheimer's Disease. | ||
| 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. | ||
| 005323 | B6;129P2 Pemttm1J-tnyw/J | Repository- Live |
| 008042 | B6;129P2-Adam2tm1Dgm/J | Repository- Live |
| Mice homozygous for this fertilin b (Adam2) mutant allele are viable with no gross phenotypic abnormalities reported. Both precursor and processed fertilin b proteins were absent from spermatogenic cells and mature sperm isolated from homozygous males. While homozygous females are fertile with normal egg activation, homozygous males exhibit sperm deficiencies in sperm-egg membrane adhesion, sperm-egg fusion, migration from the uterus into the oviduct, and binding to the egg zona pellucida, rendering them infertile. These fertilin b (Adam2) mutant mice may be useful in reproductive biology studies; specifically to determine the role of ADAM (A Disintegrin And Metalloprotease) family proteins in sperm-egg interactions, fertilization, and spermatogenesis. These mice may also be useful in conjunction with other ADAM family mutant mice, including the cyritestin (Adam3)-deficient strain (
..... For more information please see the full phenotype on the strain data sheet | ||
| 008043 | B6;129P2-Adam3tm1Pmkf/J | Repository- Live |
| Mice homozygous for this cyritestin (Adam3) mutant allele are viable with no gross phenotypic abnormalities reported. No protein product is detected from the targeted gene in sperm isolated from homozygous males. While homozygous females are fertile, homozygous males exhibit sperm deficiencies in adhesion to the egg zona pellucida and to the egg plasma membrane rendering them infertile. These cyritestin (Adam3) mutant mice may be useful in reproductive biology studies; specifically to determine the role of ADAM (A Disintegrin And Metalloprotease) family proteins in sperm-egg interactions, fertilization, and spermatogenesis. These mice may also be useful in conjunction with other ADAM family mutant mice, including the fertilin b (Adam2)-deficient strain (see Stock No. 008042). | ||
| 002782 | B6;129P2-Ccr5tm1Kuz/J | Repository- Live |
| At birth, mice homozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No transcript is detected in splenocytes or peritoneal macrophages. Thioglycollate-elicited peritoneal macrophages from homozygotes exhibit a delayed period before reaching peak mobilization (72 hours vs. 36 for wild type mice). | ||
| 008333 | B6;129P2-Dldtm1Ptl/J | Repository- Live |
| Mice heterozygous for the Dld (dihydrolipoamide dehydrogenase or E3 component) targeted mutation are viable and fertile. Heterozygous mice exhibit approximately half of wild-type enzymatic activity levels for E3 and all affected mitochondrial multienzyme complexes. Heterozygotes (on a C57BL/6;129P2 genetic background) exhibit increased vulnerability to treatments with MPTP (dopaminergic neurotoxin used to induce Parkinson's disease-like lesions), malonate (inhibitor of cellular respiration used to mimic Huntington's disease features), and 3-NP (mitochondrial toxin used to mimic Huntington's disease features). Homozygous mice exhibit normal development and metabolism during the preimplantation period, explained by the persistence of E3 enzyme from the oocyte. Homozygotes exhibit developmental delays shortly after implantation (7.5 to 8.5 days postcoitum (dpc)) and cease development within the subsequent two days. These Dld mutant mice may be useful to study early murine em
..... For more information please see the full phenotype on the strain data sheet | ||
| 006704 | B6;129P2-Gucy2dtm2Mom/MomJ | Repository- Live |
| 006849 | B6;129P2-Mecp2tm2Bird/J | Repository- Live |
| These mice possess a loxP-flanked STOP cassette in intron 2 of the targeted gene on the X chromosome. Western blot and hybridization analysis confirm the absence of wildtype protein from the targeted allele. Hemizygous (Mecp2lox-Stop/y) males do not breed and develop Rett syndrome symptoms (reduced mobility, hindlimb clasping) at approximately 6 weeks of age, with death occurring at approximately 11 weeks of age. Heterozygous females are fertile until developing Rett syndrome characteristics at 4-12 months of age. This Rett syndrome-like phenotype is similar to that observed for the traditional knock-out allele (see Stock No. 003890). Cre recombinase-mediated removal of the floxed-STOP cassette restores transcription from the targeted allele and MECP2 protein activity to normal, and reverses the Rett syndrome-like neurological defects. This mutant mouse strain may be bred to a strain expressing tamoxi
..... | ||
| 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 | ||
| 006648 | B6;129P2-Olfr151tm22Mom/MomJ | Repository- Live |
| The coding region of GFP was fused to the C-terminus of the olfactory receptor Olfr151. Olfactory sensory neurons that express the mutated locus can be revealed by the intrinsic fluorescence of GFP, or by immunofluorescence with anti-GFP antibodies. | ||
| 006675 | B6;129P2-Olfr151tm25Mom/MomJ | Repository- Live |
| Olfactory sensory neurons that express the olfactory receptor Olfr151 also co-express the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. | ||
| 006676 | B6;129P2-Olfr151tm26Mom/MomJ | Repository- Live |
| Olfactory sensory neurons that express the olfactory receptor Olfr151 also co-express the tauGFP fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by the intrinsic fluorescence of GFP, or by immunofluorescence with anti-GFP antibodies. | ||
| 006596 | B6;129P2-Olfr160tm4Mom/MomJ | Repository- Live |
| Olfactory sensory neurons that express the olfactory receptor Olfr160 also co-express the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. | ||
| 006595 | B6;129P2-Olfr17tm1Mom/MomJ | Repository- Live |
| Olfactory sensory neurons that express the olfactory receptor Olfr17 also co-express the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. | ||
| 006667 | B6;129P2-Omptm3Mom/MomJ | Repository- Live |
| The coding region and part of the 3' non-translated region of the Omp gene was replaced by GFP. The targeted mutation results in a knockout. Mature olfactory sensory neurons express GFP at high levels. These neurons can be revealed by the intrinsic fluorescence of GFP, or by immunofluorescence with anti-GFP antibodies. Homozygous mice are subfertile. | ||
| 006668 | B6;129P2-Omptm4(cre)Mom/MomJ | Repository- Live |
| The coding region and part of the 3' non-translated region of the Omp gene was replaced by Cre. The targeted mutation results in a knockout. Mature olfactory sensory neurons express the Cre recombinase at high levels. Homozygous mice are subfertile. As an example, when crossed to a strain with widespread expression of GFP and a loxP-flanked Bgeo reporter (see Stock No. 004178), this mutant mouse strain may be useful in lineage tracing. | ||
| 002466 | B6;129P2-Prkcctm1Stl/J | Repository- Live |
| Mice homozygous for the Prkcctm1Stl targeted mutation are viable and develop normally. Homozygous mice show diminished long-term potentiation (LTP) in the hippocampus, but two other types of synaptic plasticities are normal, namely long-term depression and paired-pulse facilitation. Despite this diminished LTP capacity homozygotes can learn to do hippocampus-dependant tasks, such as the Morris water maze and context-dependent fear conditioning, with only slight deficits. | ||
| 006383 | B6;129P2-Sv2atm1Sud Sv2btm1Sud/J | Repository- Live |
| Approximately half of the double homozygous targeted mutation mice die within days of birth. The surviving mice are subject to severe seizures that start in the second postnatal week then die within the following 2 weeks. Nissl staining of brain tissues revealed no structural abnormalities. No changes were found in the levels of selected synaptic proteins. Neurons experience sustained increases in Ca2+-dependent synaptic transmission when two or more action potentials are triggered in succession. Electrophysiological recordings from cultured hippocampal cells exhibit no detectable abnormalities. No protein products from the targeted genes are detected in brain tissue. This mutant mouse strain represents a model that may be useful in studies of synaptic vesicle trafficking in neurons. | ||
| 006568 | B6;129P2-Terf2tm1Tdl/J | Repository- Live |
| These mice possess loxP sites on either side of exons 1 and 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 used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele that can result in acute telomere dysfunction.
For example, when crossed to a strain expressing interferon inducible Cre recombinase (see Stock No. 003556), this mutant mouse strain may be useful in studies of telomere damage response. | ||
| 006380 | B6;129P2-Vamp2tm1Sud/J | Repository- Live |
| Mice homozygous for this targeted mutation die shortly after birth. Heterozygotes suffer no apparent morbidity or premature mortality. Newborn homozygotes exhibit a rounded appearance with a shoulder hump that may be caused by excess brown fat in the upper back. No developmental changes were noted. Analysis of brain sections did not detect any abnormalities or neurodegeneration. No changes are observed in the expression of a series of synaptic proteins. Spontaneous synaptic vesicle fusion and fusion induced by hypertonic sucrose are decreased approximately 10-fold, and fast Ca2+-triggered fusion was decreased more than 100-fold. No protein product from the targeted gene is detected in forebrain tissue. This mutant mouse strain represents a model that may be useful in studies of synaptic fusion mechanisms. | ||
| 006790 | B6;129P2-Del(14)3Mom/MomJ | Repository- Live |
| The H element was identified by the high homoology of this non-coding DNA between mouse and human. In hemizygotes, the Del(14)3Mom deletion of the H element abolishes expression of Olfr1507 (MOR28) and Olfr1508 (MOR10) genes in cis from the 129P2/OlaHsd chromosome, while expression of Olfr1507 and Olfr1508 genes from the wildtype C57BL/6J chromosome persists. In homozygotes, Olfr1507, Olfr1508, and Olfr1509 (MOR83) genes are not expressed, and there is a graded, distance-related decrease in the numbers of cells expressing more distal olfactory receptor genes, Olfr1510 (MOR29A), Olfr1511 (MOR29B), Olfr1512 (MOR30A), and Olfr1513 (MOR30B). The expression of other olfactory receptor genes on Chromosome 14 such as Olfr1514 (MOR205-1), Olfr749 ((S1), and Olfr221 (MOR205-1) is not affected in an obvious way by the Del(14)3Mom deletion. Expression of olfactory receptor genes loc
..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 006470 | B6;129S-Hopxtm1Eno/J | Repository- Live |
| Homozygous mice are viable and fertile on this mixed genetic background. Absence of the targeted protein is confirmed in heart and brain tissues from homozygotes. The lacZ expression pattern is similar to that of the endogenous gene. Homozygous heart tissues show altered serum response factor (SRF)-associated gene expression. Mice homozygous for this null allele segregate into two phenotypic classes characterized by an excess or deficiency of cardiac myocytes. These mutant mice may be useful in studying cardiac growth and development. | ||
| 006958 | B6;129S-Nkd1tm1Kwha/J | Repository- Live |
| Mice homozygous for this nkd1lacZ mutant allele are viable and fertile with slightly reduced mean litter sizes. Northern blot of lung tissue, as well as western blot of embryonic tissue, confirms that the deleted exons (encoding the Dvl-binding domain) are not expressed in homozygous mutants. However, the endogenous promoter directs expression of the internal ribosome entry site-β-galactosidase (IRES-lacZ) fusion gene in a manner that closely mimics the patterns of the endogenous gene mRNAs. Because the naked cuticle (NKD) genes are considered targets for Wnt/β-catenin signaling, these nkd1lacZ mutant mice (as well as the similar nkd2lacZ mutant strain; Stock No. 006960) may be useful as a reporter for Wnt/β-catenin-dependent transcriptional activity during embryonic development or in adult mice. | ||
| 006960 | B6;129S-Nkd2tm1Kwha/J | Repository- Live |
| Mice homozygous for this nkd2lacZ mutant allele are viable and fertile with slightly reduced mean litter sizes. RT-PCR analysis of homozygous brain tissue confirms that the deleted exons (encoding the Dvl-binding domain) are not expressed in homozygous mutants. However, the endogenous promoter directs expression of the internal ribosome entry site-β-galactosidase (IRES-lacZ) fusion gene in a manner that closely mimics the patterns of the endogenous gene mRNAs. Because the naked cuticle (NKD) genes are considered targets for Wnt/β-catenin signaling, these nkd2lacZ mutant mice (as well as the similar nkd1lacZ mutant strain; Stock No. 006958) may be useful as a reporter for Wnt/β-catenin-dependent transcriptional activity during embryonic development or in adult mice. | ||
| 006381 | B6;129S-Stxbp1tm1Sud/J | Repository- Live |
| Mice homozygous for this targeted mutation die immediately after birth, probably due to respiratory failure. Predicted Mendelian genotypic ratios are demonstrated in progeny of heterozygous crosses. Homozygotes show a complete loss of neurotransmitter secretion from synaptic vesicles throughout development. Postsynaptic receptors are functional and spontaneous action potentials are occasionally observed, however. Ion channels show normal properties. Normal brain assembly, including formation of layered structures, fiber pathways and morphologically defined synapses occurs. After assembly is completed, neurons undergo apoptosis, leading to widespread neurodegeneration. No protein product from the targeted gene is detected in E18 embryos or perinatal pups. This mutant mouse strain represents a model that may be useful in studies of synaptic vesicle exocytosis and neurodegeneration. | ||
| 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. | ||
| 007001 | B6;129S-Tg(UBC-cre/ESR1)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 | ||
| 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. | ||
| 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. | ||
| 002263 | B6;129S2-Alox5tm1Fun/J | Repository- Live |
| Mice homozygous for the Alox5tm1Fun targeted mutation are viable and fertile. In general, homozygous mutant mice are selectively resistant to inflammatory insults. They are resistant to the lethal effects of platelet activating factor but reaction to endotoxin shock is normal. Phorbol ester induced inflammation is normal but arachidonic acid induced inflammation is reduced. Commonly referred to as 5-LO. | ||
| 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 | ||
| 006594 | B6;129S2-Omptm1Mom/MomJ | Repository- Live |
| The coding region and part of the 3' non-translated region of the Omp gene was replaced by taulacZ, a fusion protein of the microtubule-binding protein tau (from bovine origin) and beta-galactosidase. The targeted mutation results in a knockout. Mature olfactory sensory neurons express beta-galactosidase at high levels. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. Homozygous mice are subfertile. | ||
| 005250 | B6;129S2-Relnrl-4J/J | Repository- Live |
| 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 | ||
| 007204 | B6;129S4-2610005L07RikGt(ROSA)73Sor/J | Repository- Live |
| Mice homozygous for this mutant allele (called BC058969 in the primary publication) are viable and fertile, with greater than 50% embryonic lethality observed in homozygous embryos. Homozygotes occur at a lower than Mendelian ratio (9%) from heterozygote x heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects (sternum and calvarial bones). Notably, 100% incidence of calvarial bones defects is reported. Additionally, homozygotes are reported to have low β-galactosidase activity; in situ hybridization or other sensitive methods may be necessary to detect expression of the lacZ-neo reporter fusion gene. These BC058969-mutant (2610005L07Rik-mutant) mice may be useful in studying cellular signal
..... For more information please see the full phenotype on the strain data sheet | ||
| 006258 | B6;129S4-Apoa2tm1Bres/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile. Homozygous mice have no detectable transcripts in liver tissues and the high density lipoprotein (HDL) particle size is reduced. Homozygotes have decreased plasma levels of HDL cholesterol and free fatty acids in both fed and fasted states. In addition, the plasma concentration of fasting glucose and insulin is decreased. These mice may be useful in studies of lipid metabolism, atherosclerosis, heart disease, insulin resistance and diabetes. | ||
| 006404 | B6;129S4-Apoa4tm1Bres/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile with no protein detectable in plasma, liver, or intestinal tissues. Homozygotes have decreased plasma levels of cholesterol, free fatty acids, and high density (HDL) and very low density lipoprotein (VLDL). These mice may be useful in studies of lipid metabolism, atherosclerosis, heart disease, appetite regulation, intestinal lipid absorption, or inflammatory bowel disease. | ||
| 007200 | B6;129S4-Arid5bGt(ROSA)75Sor/J | Repository- Live |
| Mice homozygous for this mutant allele have reduced size and weight gains after birth, occur at lower than Mendelian ratio (16%) and 46% die within 3 weeks of age. Homozygotes are fertile when they survive to adulthood. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit kidney defects (abnormally high blood urea nitrogen level, mutant kidney size smaller than wildtype, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells in glomeruli), and abnormalities in palate bone fusion. These Arid5b-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. | ||
| 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. | ||
| 007843 | B6;129S4-Efnb2tm2Sor/J | Repository- Live |
| These mice express the histone 2B and Green fluorescent protein, H2BGFP, fusion gene under the control of the endogenous Efnb2 promoter. Homozygotes die at E10.5 due to cardiovascular defects. Homozygous embryos exhibit defects in cardiovascular and somite development, cranial and trunk neural crest cell populations. These mutant mice may be useful in studies of embryonic development. | ||
| 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. Spontaneous bleeding into joints or soft tissues, a trait associated with human patients afflicted with hemophilia A is not observed. 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. | ||
| 002848 | B6;129S4-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. | ||
| 007670 | B6;129S4-Gt(ROSA)26Sortm3(phiC31*)Sor/J | Repository- Live |
| These mutant mice express a site-specific recombinase, PhiC31o, that has been targeted to the endogenous Gt(ROSA)26Sor locus and codon-optimized for expression in mouse tissues. PhiC31o mediates irreversible DNA recombination at specific nonidentical pairs of sequence sites, attB and attP. When crossed with a strain containing a sequence of interest flanked by attB and attP sites, PhiC31o-mediated recombination results in tissue-specific deletion of the targeted sequence. Recombination efficiency is similar to that of Cre recombinase. This strain represents an effective tool for generating tissue specific-targeted mutants. | ||
| 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. | ||
| 007672 | B6;129S4-Man1a2tm1.1Ahe/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. Homozygous mice have a perinatal lethal phenotype and die within hours of birth due to respiratory distress (cyanosis and alveolar hemorrhage). No gene product (mRNA) is detected by RT-PCR analysis of total RNA from homozygous embryonic tissues. At embryonic day 18.5 homozygous embryos exhibit reduced alveolar air space, thickened alveolar walls, small atelectactic areas and delayed lung development. This mutant mouse strain may be useful in studies of lung development and pulmonary physiology. | ||
| 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. | ||
| 007845 | B6;129S4-Myf5tm3(cre)Sor/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Myf5 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 skeletal muscle and the dermis, and in several ectopic locations. Homozygotes for this allele have a perinatal lethal phenotype and die at birth. Homozygotes display abnormal rib development and some fusions of the cervical or thoracic vertebrae. This mutant mouse strain represents a model that may be useful in studies of skeletal development. | ||
| 007201 | B6;129S4-Plekha1Gt(ROSA)82Sor/J | Repository- Live |
| 25% of homozygotes die by 2 weeks of age. Homozygous males are infertile and, after 3 weeks of age, exhibit higher than normal (wildtype) weight gain. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Plekha1-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. | ||
| 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
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| 008078 | B6;129S4-Tcfe2atm5Zhu/J | Repository- Live |
| These mice contain an Enhanced Green Fluorescent Protein (EGFP) gene inserted into the endogenous Tcfe2a, transcription factor E2a, locus. The Donating Investigator reports that this allele produces modified E12 and E47 proteins with their carboxyl ends fused to the EGFP protein. Function of the fusion proteins were confirmed by their ability to rescue viability, fertility, and B cell development. This strain serves as a reporter strain, with functional Tcfe2a, transcription factor E2a, expression indicated by EGFP expression. Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 006238 | B6;129S4-Thbs2tm1Bst/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile. Multiple analyses has confirmed the absence of protein in embryonic and adult tissue of homozygous mice. Homozygotes exhibit skin disorders (abnormal collagen fiber patterns, reduced tensile strength, increased fragility) and skin fibroblasts have attachment defects. Mice also exhibit an increase in total density/cortical thickness of the long bones, abnormally long bleeding times, and a significant increase in blood vessel density. Homozygous mice exhibit accelerated wound healing after biopsy and accelerated/increased tumor formation following chemically-induced skin carcinogenesis. Mutant mice may be useful in studies of collagen fibrillogenesis in skin and tendons, angiogenesis and vascular pathophysiology, wound healing, chemically-induced tumor progression, and as a potential model for Ehlers Danlos syndrome. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are fre
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| 007206 | B6;129S4-TiparpGt(ROSA)79Sor/J | Repository- Live |
| 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); kidney defects (blood urea nitrogen level abnormally high, kidney size smaller than wildtype, swollen blood filled, degraded glomeruli are often observed, increased number of vascular smooth muscle cells partially filling the glomeruli space); and abnormalities in palate bone fusion. Homozygotes occur at lower than Mendelian ratio (22%), and 32% die by age 2 week. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Tiparp-mutant mice may be useful in studying kidney development, vascular development, hematopoiesis and cellular signaling during development and in adult mice; specifically receptor tyrosine
..... For more information please see the full phenotype on the strain data sheet | ||
| 007203 | B6;129S4-Zfand5Gt(ROSA)72Sor/J | Repository- Live |
| Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Histological examination of E18.5 homozygous embryos reveals thin blood vessel walls, hemorrhages and lung edema. There are fewer vascular smooth muscle cells (vSMCs) in blood vessels as indicated by immunohistochemistry for desmin and alpha-smooth muscle actin. Skeletal defects are observed in 20% of animals in the sternum and calvarial bones. Homozygotes die a few hours after birth due to difficulty breathing and bruising is visible beneath the skin. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Zfand5-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. | ||
| 007202 | B6;129S4-Zfp826Gt(ROSA)76Sor/J | Repository- Live |
| At age E11.5 to E18.5, homozygous embryos exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At six 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); kidney defects (abnormally high blood urea nitrogen level, kidney size smaller than wild-type, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells in glomeruli); abnormalities in palate bone fusion and abnormal neural crest derived and thoracic skeleton development. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes occur at lower than Mendelian ratio (18%) and 8% die by age one week. Surviving homozygotes and heterozygotes are viable and fertile. These Zfp826 (BC055757)-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (R
..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 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
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| 005939 | B6;129S6-Insig1tm1Mbjg Insig2tm1Mbjg/J | Repository- Live |
| Mice homozygous for both targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This double mutant has normal expression of Insig1 and no Insig2 gene expression or protein in liver. As the Insig1 mutant locus contains a loxP, frt-flanked exon 1, Cre-mediated deletion of exon 1 (encoding amino acids 1-113) terminates gene function. Double homozygous mutant mice die in utero some time after embryonic day 18.5. These mice may be useful in studies of cholesterol synthesis and feedback suppression, sterol regulatory element-binding protein (SREBP) processing pathways, liver metabolism and storage functions, and may have use in insulin-related topics such as diabetes and endocrine/exocrine function. | ||
| 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. | ||
| 006208 | B6;129S6-Pdzk1tm1Dls/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile. Liver tissue from homozygous mutant mice lacks endogenous protein expression. Homozygotes, but not heterozygotes, have significantly decreased (~85-95%) hepatic high density lipoprotein (HDL) receptor scavenger receptor B-I (SR-BI) levels. This decrease is further exacerbated following diet supplementation with the PPAR-alpha activator fenofibrate. These mice may be useful in studies of cardiovascular health and atherosclerosis, lipid metabolism, SR-B1 regulation, kidney function, as well as kidney transporter (e.g. urate transporter) regulation and liver organic anion transport. | ||
| 002641 | B6;129S7-Bdkrb2tm1Jfh/J | Repository- Live |
| Mice homozygous for the Bdkrb2tm1Jfh targeted mutation are viable and fertile and display no major defects. Homozygous mutant tissue from the ileum, uterus, and superior cervical ganglia all failed to respond to pharmacological doses of bradykinin. This finding supports the existance of only one type of B2 receptor. B2 deficient mice also display a greater hypert | ||