Search Criteria: Research Area is "Research Tools: Apoptosis Research"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 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 | ||
| 007572 | B6.129P2(Cg)-Rorctm2Litt/J | Repository- Live |
| Mice homozygous for this Rorc(γtGFP (or RORγt)GFP) mutant allele are viable and fertile. While Rorcγ mRNA is detected in liver in Rorc(γ)tGFP homozygotes, mRNA and protein for the thymus-specific isoform (Rorcγt) encoded by the targeted allele are not detected in the thymus. EGFP expression reports Rorc(γt) transcription in the thymi of adult Rorc(γt)GFP mice. Homozygous mice exhibit abnormal lymph node, Peyer's patch, and lymphoid tissue inducer (LTi) cell development. Mice with Rorcγt-deficient T cells lack tissue-infiltrating proinflammatory T-helper cells (Th17 cells), and are protected from induced autoimmune disease (EAE) on this genetic background. The donating investigator also reports increased thymoma incidence with age in homozygotes. These RorcγtGFP mutant mice may be useful in studying immune system homeostasis, T cell repertoire selection, CD4/CD8 double positive (CD4+/CD8 For more information please see the full phenotype on the strain data sheet | ||
| 009088 | B6.129P2(SJL)-Myd88tm1.1Defr/J | Repository- Live |
| Homozygous mice are viable and fertile. The Myd88-deficient allele encodes a deletion of exon 3 of the myeloid differentiation primary response gene 88 locus. Myd88-deficiency is associated with a number of immune system abnormalities, as well as hematopoietic system, molecular signaling, and apoptotic abnormalities. | ||
| 005530 | B6.129S-Ddit3tm1Dron/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (MRNA or protein) is detected by Northern or Western blot analysis of toxin challenged mouse embryonic fibroblasts (MEFs). MEFs and renal proximal tubular epithelial cells have decreased apoptosis in response to endoplasmic reticulum stress induced by the toxin, tunicamycin. Pancreatic islets cells are more resistant to nitric oxide induced apoptosis. MEFs exhibit a delayed onset of unfolded protein response (UPR) target gene expression when treated with tunicamycin. This mutant mouse strain may be useful in studies of apoptosis and pathogenesis due to endoplasmic reticulum stress. | ||
| 006233 | B6.129S1-Casp3tm1Flv/J | Repository- Live |
| On this C57BL/6 congenic background, homozygotes are viable, fertile, and reach adulthood, but females reported display suboptimal mothering instincts. Functional endogenous protein and mRNA are absent from all tissues tested. Homozygous mice are resistant to in vivo cerebral ischemia/reperfusion and in vitro oxygen-glucose deprivation. Ovaries from female homozygotes show aberrant atretic follicles associated with a granulosa cell-intrinsic defect in apoptosis as well as defective corpus luteum regression. Homozygous mice are congenitally deaf with hair cell defects in the Organ of Corti. Optic lens formation/morphology also is abnormal with cataracts at the anterior lens pole. Of note, these mice lack the embryonic/perinatal-lethal brain pathology observed in mutant mice on the 129 and mixed B6;129 genetic backgrounds. These mutant mice may be useful in studies of apoptosis, ovarian follicle and corpus luteum development, and eye and ear development. | ||
| 006141 | B6.129S2-Thbs1tm1Hyn/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile, with an approximate 20% decrease in embryo/neonate viability and a mild and variable lordotic curvature of the spine apparent from birth. Homozygous mice have an abnormal, but no full length transcript in multiple tissues. Western analysis confirmed the absence of the protein in platelets. Homozygotes exhibit an increase in the number of circulating white blood cells. During the first four to ten weeks of life, homozygotes exhibit patches of acute and organizing pneumonia. At later time points, there is considerable hyperplasia of the various epithelial cell lineages. Mutant mice also have an increased number of retinal endothelial cells and inappropriate remodeling and maturation of retinal vasculature following injury. On the FVB/N background, spontaneous tumor growth and vasculature are significantly increased compared to wildtype. Mutant mice may be useful in studies of inflammatory responses in the lungs, eye, and ..... For more information please see the full phenotype on the strain data sheet | ||
| 007899 | B6.129S4-Casp2tm1Yuan/J | Repository- Live |
| Mice homozygous for this caspase-2 targeted mutation are viable and fertile. As the mutation deletes the QACRG active site and the caspase-2S sequence of the endogenous enzyme, this deletion was shown to inactivate both the long and short form of caspase-2. As such, homozygous mice exhibit defects in regulation of apoptosis; including an enlarged oocyte reserve attributed to a germ cell-intrinsic death defect during prenatal ovarian development (resistance to oocyte cell death following complete cytokine starvation or exposure to an anticancer drug), as well as accelerated motor neuron cell death and defective B lymphoblast apoptosis. In addition, caspase-2-deficient mice exhibit characteristics of premature aging (including shortened maximum lifespan, impaired hair growth, increased bone loss, reduced body fat content, and higher hepatic levels of oxidized proteins). As caspase-2 acts as an upstream regulator of cell death in many cell types, caspase-2-deficient mice may b ..... For more information please see the full phenotype on the strain data sheet | ||
| 006122 | B6.129S4-Mbl1tm1Kata Mbl2tm1Kata/J | Repository- Live |
| Mice homozygous for both mannose-binding lectin (MBL)-A and MBL-C targeted mutations (termed MBL-null) are viable, fertile, and normal in size with no obvious developmental defects. Histological examination of multiple organs from 6-10 week old mice shows no abnormalities. MBL-null mice have no endogenous gene expression in liver (the principal site of MBL synthesis) and no protein detectable in serum. While the classical complement pathway is unaffected in MBL-null mice, the lectin-dependent complement pathway is non-functional. MBL-null mice have increased mortality following intravenous injection of S. aureus associated with abnormal serum levels of TNFalpha and IL-6 (decreased at 2h, elevated at 24h post injection). Cyclophosphamide-induced febrile neutropenic MBL-null mice inoculated with S. aureus have greatly increased susceptibility to abscess formation in kidney, liver, and lung (but not spleen). These same treated mice also have persistent bacteremia despite a r ..... For more information please see the full phenotype on the strain data sheet | ||
| 006440 | B6.129S4-Ptentm1Hwu/J | Repository- Live |
| These mice possess loxP sites flanking exon 5 of the targeted gene. Mice homozygous for the"floxed" allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele.
For example, when crossed to a strain expressing Cre recombinase in astrocytes (see Stock No. 012887), this mutant mouse strain may be useful in studies of neurogenesis. When crossed to a strain expressing Cre recombinase in the central nervous system (see Stock No. 004600), this mutant mouse strain may be useful in studies of glia differentiation and cerebellar development. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to ..... | ||
| 006237 | B6.129S6-Casp7tm1Flv/J | Repository- Live |
| Homozygous mice are viable and fertile with normal appearance, organ morphology, and lymphoid development. Endogenous protein expression is absent in all tissues tested (including brain, thymus, heart, lung, liver, spleen, kidney, and skeletal muscle). Mouse embryonic fibroblasts (MEFs) from homozygotes exhibit a slight survival advantage when treated with apoptosis inducers, but other cell subsets undergo normal apoptosis (including activated T cells death following T cell receptor stimulation, thymocyte apoptosis, and Fas-mediated B cell and hepatocyte cell death). These mutant mice may be useful in studies of mitochondrial events of apoptosis, especially when paired with other executioner caspase mutant models. | ||
| 008240 | B6.129S6-Eif2ak4tm1.2Dron/J | Repository- Live |
| Mice homozygous for the GCN2.KO4 mutant locus (also called GCN2.KO4-, GCN2-, GCN2.KO4ex, or GCN2-KO) are viable, fertile and overtly indistinguishable from wild-type mice, with little if any mRNA expressed from the mutant locus. Homozygous GCN2-deficiency is associated with altered inflammatory responses and altered stress responses, including sensitivity to nutritional deficiencies and aberrant eating behavior. As GCN2 is a protein kinase that phosphorylates eIF2 (eukaryotic initiation factor 2) in response to environmental stresses (amino acid starvation, proteasome inhibition and UV irradiation) to reduce global translation and activate stress-related transcription factors (such as NF-kappaB) to alleviate cellular injury or alternatively induce apoptosis, these GCN2.KO4 mutant mice may be useful for such immunology, inflammatory, immunity cell biology, or neurobiology research.
Of note, mice with a conditional allele (loxP-flanked exon XII ..... | ||
| 013738 | B6.Cg-Tg(LCKprBCL2L1)12Sjk/J | Repository- Live |
| These lckpr-bcl-XL transgenic mice express a human B-cell leukemia/lymphoma 2 like, 1 (BCL2L1 or BCL-XL) cDNA sequence, under the control of a mouse lymphocyte protein tyrosine kinase proximal promoter (Lckpr). Mice that are heterozygous for this transgene are viable, fertile, and normal in size. Lckpr drives BCL-XL expression within all thymocyte subsets and protects thymocytes from a variety of apoptotic stimuli, including γ irradiation, glucocorticoids, and anti-CD3 treatment. This BCL-XL overexpression alters thymocyte maturation, resulting in an increase in CD3int/hi and a decrease in CD3lo thymocytes, along with an increase in intermediate CD4+8lo and CD4lo8+ thymocytes. They also exhibit an increase in single positive CD8 T cells in the spleen. Overexpression of BCL-XL causes down-regulation of B-cell leukemia/lymphoma 2 (BCL-2) an ..... 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 | ||
| 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 | ||
| 013101 | B6;129S6-Gadd45btm1Flv/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Isolated T cells exhibit increased proliferation with activation. Th1 cells from homozygotes are more resistant to activation induced apoptosis. 10 month old homozygotes exhibit mild splenomegaly. Homozygotes are more susceptible to experimental autoimmune encephalomyelitis, with longer duration and severity: 60% of homozygotes die when challenged with a higher dose of heat-inactivated Mycobacterium tuberculosis, compared to no deaths in controls. Immunocomplex deposits develop in the glomeruli of homozygotes. | ||
| 011067 | C57BL/6-Bbc3tm1Ast/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis of irradiated thymocytes from homozygotes and Northern blot analysis of thymus and spleen from homozygotes. MEFs and thymocytes from homozygous mice exhibit increased resistance to DNA-damage induced apoptosis after treatment by etoposide and gamma radiation. Neurons from homozygotes are more resistant to oxidative stress induced and endoplasmic reticulum (ER) stress induced apoptosis than wildtype controls. | ||
| 008517 | C57BL/6-Gt(ROSA)26Sortm3(CAG-MIR17-92,-EGFP)Rsky/J | Repository- Live |
| Mice homozygous for the "miR-17-92 transgene" conditional allele are viable and fertile, with a loxP-flanked Neo-STOP cassette preventing transcription of the downstream bicistronic sequences (human miR-17-92 cluster (encoding the precursor of seven miRNA molecules; miR-17-5p, miR-17-3p, miR-18a, miR-19a, miR-20a, miR-19b and miR-92) and EGFP). When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissue(s); resulting in expression of the human miR-17-92 cluster. Because the synthetic CAG promoter driven miR-17-92 transgene was targeted for insertion into the Gt(ROSA)26Sor locus, expression of the transgene is determined by which tissue(s) express Cre recombinase. EGFP fluorescence, however, is not reported following exposure to Cre recombinase (presumably due to RNaseIII excision of the stem-loop structures encoding individual miRNA destabilizing the EGFP portion of the primary transcript ..... For more information please see the full phenotype on the strain data sheet | ||
| 005070 | C57BL/6-Tg(Csf1r-EGFP-NGFR/FKBP1A/TNFRSF6)2Bck/J | Repository- Live |
| These Macrophage Fas-Induced Apoptosis (MAFIA) transgenic mice have an inducible Fas suicide/ apoptotic system driven by the mouse Csf1r, colony stimulating factor 1 receptor promoter. The transgene insert contains a mutant human FK506 binding protein 1A, 12kDa (FKBP12) which preferentially binds the dimerization drug AP20187. Enhanced Green Fluorescent Protein (EGFP) fluorescence and transgene expression is detected in 78% of isolated peritoneal cells. EGFP fluorescence is variable among tissues (B- and T-cells do not express EGFP). Administration of the dimerizing reagent, AP20187, induces apoptosis in macrophages and dendritic cells (intravenous injection of dimerizer is recommended, since the intraperitoneal route can elicit peritoneal adhesions). In treated mice, EGFP fluorescing peritoneal and bone marrow macrophage numbers are depleted by more than 90%, and macrophage numbers in blood, spleen, lung and thymus by more than 70%. 7 days after cessation of treatment, the EGFP ..... For more information please see the full phenotype on the strain data sheet | ||
| 006481 | C57BL/6J-Tg(ACTB-NOTCH1)1Shn/J | Repository- Live |
| Transgenic mice are viable, fertile and behaviorally normal. These "CALSL-NICD (H)" mice (or simply CALSL-NICD) reportedly carry 10-20 copies of the transgene inserted into a single genomic locus. Expression of the transgene-derived intracellular domain of human NOTCH1 is prevented by a "Lox-STOP-Lox" cassette. When transgenic mice are bred to a strain expressing Cre recombinase, the "floxed stop" cassette is excised in the resulting offspring, and human NOTCH1 expression is observed in the cre-expressing tissue(s). These transgenic mice may be useful in studying early neural progenitor cell development and apoptosis, and responses to tissue-specific Notch activation. For example, when crossed to a strain expressing Cre recombinase in the nervous system (see Stock No. 003771), this transgenic mouse strain may be useful in studies of notch signaling during apoptotic cell death. | ||
| 015823 | C57BL/6N-Pawrtm1Rang/J | Repository- Live |
| Mice homozygous for this Par4flox allele are viable and fertile, with loxP sites flanking exon 2 of the targeted PRKC, apoptosis, WT1, regulator (Pawr or Par-4) gene. Homozygotes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. PAR4 is a pro-apoptopic protein capable of inducing apoptosis in cancer cells and causing regression of tumors in animal models. PAR4 interacts with, and inhibit, atypical protein kinase C isoforms, functioning as a negative regulator of the NF-κB pathway. When these mutant mice are bred to mice that express Cre recombinase, the resulting offspring will have exon 2 deleted in the cre-expressing tissue, resulting in inactivation of Pawr gene function. Loss of PAR4 leads to a reduction in apoptosis by increased activation of NF-κB. These mutant mice may be useful in generating conditional mutations for studying tumor development and treatment. ..... For more information please see the full phenotype on the strain data sheet | ||
| 010543 | C;129-Hsf1tm1Ijb/J | Repository- Live |
| Mice that are heterozygous for this targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. A truncated gene product (mRNA) is detected by Northern blot analysis of embryonic cells. No gene product (protein) is detected by Western blot analysis of non-treated and heat shocked cells or brain, testis, heart and liver tissue. The prenatal lethal phenotype of homozygous mice is more severe on the 129 background than on BALB/c, C57BL/6, or ICR backgrounds. Surviving homozygotes have slowed growth with body weights approximately 78% of normal at eight weeks of age. Homozygotes exhibit abnormal chorioallantoic placenta (thinned spongiotrophoblast layer). Homozygous females are infertile due to impaired meiosis and zygotic cell division. Homozygotes are more resistant to experimentally induced skin tumors and exhibit a lower tumor burden than wild-type controls. Cultured MEFs from homozygotes are less sensitive to glucose depriv ..... For more information please see the full phenotype on the strain data sheet | ||
| 004597 | C;129S4-Ptentm1Hwu/J | Repository- Live |
| These mice possess loxP sites flanking exon 5 of the targeted gene. Mice homozygous for the "floxed" allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele.
For example, when crossed to a strain expressing Cre recombinase in astrocytes (see Stock No. 012887), this mutant mouse strain may be useful in studies of neurogenesis. When crossed to a strain expressing Cre recombinase in the central nervous system (see Stock No. 004600), this mutant mouse strain may be useful in studies of glia differentiation and cerebellar development. | ||
| 007079 | CByJ.B6-Prf1tm1Sdz/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice have normal numbers of CD8+ T cells and NK cells. CTL and NK cells are unable to lyse virus-infected or allogeneic fibroblasts in vitro. Homozygotes fail to clear lymphocytic choriomeningitis virus. Fibrosarcoma tumor cells are eliminated with reduced efficiency. This mutant mouse strain may be useful in studies of inflammatory response, susceptibility to infection, and susceptibility to multiple sclerosis. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 008232 | FVB/N-Tg(Ins2-IAPP)RHFSoel/J | Repository- Live |
| Mice homozygous for the RIPHAT transgene are viable and fertile, with expression of human islet amyloid polypeptide (h-IAPP) under the regulatory control of the rat insulin II promoter. While h-IAPP RNA from the transgene is observed in pancreas, kidney, and stomach, h-IAPP protein is reported only in pancreas tissues. Hemizygous mice show no symptoms of spontaneous disease. Homozygous males spontaneously develop diabetes mellitus due to beta-cell death, associated with impaired insulin secretion (hypoinsulinemia), hyperglycemia, and abnormal intracellular aggregates of h-IAPP (the donating investigator reports that extracellular aggregates are not found on this strain background). Homozygous male onset is between 4-8 weeks of age with death around 16 weeks of age. Homozygous females exhibit a less severe phenotype. These RIPHAT transgenic mice may be useful in studying the beta-cell destruction and islet amyloid deposition associated with non-insulin-dependent diabetes mellitus (NIDDM ..... For more information please see the full phenotype on the strain data sheet | ||
| 013072 | STOCK Atf4tm1Tow/J | Repository- Live |
| In this strain, a neomycin phosphotransferase resistance (neo) cassette replaces the entire coding region of the endogenous mouse activating transcription factor 4 (Atf4) gene, abolishing gene function. Mice homozygous for the Atf4 allele exhibit low viability, with delayed bone formation during embryonic development and low bone mass throughout postnatal life. They exhibit a reduction in oxidative stress-induced gene expression, resistance to oxidative death, and decreased consumption of the antioxidant glutathione. They also have decreased insulin sensitivity, smaller fat pads, and delayed hair growth as compared with control mice. Adults are severely microphthalmic, with no recognizable lens, anterior chamber, iris, or vitreous body. These mice may be useful for studying cell proliferation defects associated with blindness, osteoporosis, and stress responses. | ||
| 008882 | STOCK Bcl2tm1Irt/J | Repository- Live |
| Mice homozygous for this Bcl2flox conditional allele are viable and fertile, with a loxP-flanked neo cassette upstream of exon 2, as well as a loxP site downstream of exon 2 of the Bcl2 (B-cell leukemia/lymphoma 2) gene. When bred to mice that express Cre recombinase, the resulting offspring can have one of three resulting genotypes in the cre-expressing tissue(s); only the neo selection cassette deleted, only exon 2 deleted, or both the neo selection cassette and exon 2 deleted. The two latter genotypes result in loss of Bcl2 protein expression and are reported to confer the null phenotype. These Bcl2flox mutant mice may be useful in generating conditional mutations for studying apoptosis, mitochondrial permeability, cell survival signaling, cancer, neurological disorders, and immunity.
For example, when crossed to a strain expressing Cre recombinase in myeloid cell lineages (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 009340 | STOCK Eif2ak3tm1Dron/HotaJ | Repository- Live |
| These mice harbor a targeted mutation of the Eif2ak3 (eukaryotic translation initiation factor 2 alpha kinase 3 [also called Perk]) locus that abolishes endogenous gene expression. To date (Feb 2010), the donating investigator has not been able to generate homozygous mice on a C57BL/6J congenic background. The following phenotype describes mice on a mixed albino Swiss Webster;129/SvEv genetic background. Heterozygous mice are viable and fertile. Homozygous (Perk-/-) mice appear runty within a few days of birth and develop a rapid and progressive decline in endocrine and exocrine pancreatic function. This results in a complex pleiotropic phenotype including hyperglycemia, exocrine pancreatic insufficiency, diabetes, growth retardation, inability to breed, and early mortality. The phenotype of the Perk-/- mice is very similar to that observed in humans with Wolcott-Rallison syndrome; the consistent feature of which is severe diabetes mellitus developing in infancy. Heterozygous mi ..... For more information please see the full phenotype on the strain data sheet | ||
| 004301 | 129-Trp53tm1Holl/J | Cryopreserved - Ready for recovery |
| In this mutant mouse strain, the endogenous murine sequence for exons 4-9 of the targeted gene, which encode the DNA binding domain of the tumor suppressor protein, have been replaced with the homologous normal human sequence. Transcription is under the control of the endogenous mouse promoter. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous mutant mice exhibit normal expression and functional activity of the chimeric gene. Homozygous mutant mice have normal immunodetectable levels of p53 protein accumulation in nuclei in response to UV-induced DNA damage. Thymocytes from mutant mice are as susceptible to gamma-irradiation-induced and dexamethaxone-induced apoptosis as wildtype thymocytes. This mutant mouse strain may be useful in studies related to in vivo spontaneous and induced mutation of the human TRP53 gene sequence, and pharmacological agents for alt ..... For more information please see the full phenotype on the strain data sheet | ||
| 009443 | 129;B6-Hint1tm1Ibw/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of MEFs, cerebrum, cerebellum, colon, kidney, thymus, thyroid, stomach,
liver, pancreas, adrenal gland, testis, ovary, heart, lung, spleen, muscle, and skin tissues. No gene product (mRNA) is detected by RT-PCR of MEFs. Homozygotes have smaller thymuses. Homozygotes MEFs exhibit more rapid growth after 8 serial passages, and undergo spontaneous immortalization, as they can be cultured for more than 50 serial passages without morphological changes. Both early and late passage homozygotes MEFs are more resistant to ionizing radiation than wildtype controls. Irradiated MEFs have impaired DNA repair and exhibit chromosome aberrations, and genomic instability. Homozygotes are more sensitive to chemical carcinogens NMBA and DMBA and develop more tumors that are larger and ..... For more information please see the full phenotype on the strain data sheet | ||
| 003082 | 129S1/SvImJ-Bcl2tm1Mpin/J | Cryopreserved - Ready for recovery |
| Heterozygous mice exhibit expression of beta-galactosidase in populations of large sensory neurons. Mice homozygous for the Bcl2tm1Mpin targeted mutation do not produce either the a or b form of the Bcl2 protein. Bcl2 is a major regulator of programmed cell death, a critical process in shaping the developing nervous system. The absence of the Bcl2 does not significantly influence the development of motor neurons before or during the main period of physiological cell death. Rather, Bcl2 exerts its influence beyond this period, subsequent to the phase where the majority of neuronal loss normally takes place. Polycystic kidney disease is less severe in this strain compared to the Bcl2tm1Sjk targeted mutation (Stock No. 002265). | ||
| 008201 | B6.129-Sepp1tm1Rfb/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for this targeted mutation are viable and fertile. No RNA or selenoprotein P (Se-P) protein expression from the targeted gene is observed in plasma. Homozygous (Sepp1-deficient) mice are viable with altered selenium metabolism rendering them intolerant of low dietary selenium intake and resulting in significantly shortened life span. Homozygotes have lower brain selenium concentrations and develop progressive neurological dysfunction (impaired movement and coordination); the progression of which is preventable (but not reversible) with dietary selenium supplement. Homozygous females are fertile but have difficulty producing and raising pups. Homozygous males have sharply reduced fertility due to flagellar structural defects ("kinked sperm") which, unlike the neurological phenotype, are not prevented with dietary selenium supplement. Sepp1-deficient mice, supplemented with dietary selenium and infected with an African Trypanosomiasis parasite, exhibit increased ..... For more information please see the full phenotype on the strain data sheet | ||
| 002274 | B6.129S-Itga5tm1Hyn/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Itga5tm1Hyn targeted mutation die during embryonic development. Homozygous mutant embryos exhibit defects in the vasculature of the yolk sac and the embyro as well as severe defects in posterior and extraembryonic mesoderm. Implantation and initiation of gastrulation and neurulation is normal. There is normal development of notochord, somite and considerable development of brain, optic and otic anlagen and branchial arches. | ||
| 005517 | B6.129S4-Cyb5r4tm1Hfb/HfbJ | Cryopreserved - Ready for recovery |
| Mice heterozygous for the targeted mutation are viable and fertile, glucose tolerant, have normal blood sugar levels, serum lipid profiles and white adipose tissue mass. No protein from the targeted gene was detected by Western Blot analysis of mice homozygous for the allele. Homozygous mice consume more food, have decreased adipose tissue mass and are hyperlipidemic compared to wildtype controls post-weaning. At 4 weeks of age glucose levels are normal but insulin levels are 40% of wildtype controls. At 7 weeks of age clinical diabetes is present in both male and female of homozygous mice. Histological evaluation of pancreas from 21 week old homozygote animals revealed a significant reduction in the number of islets and decreased cytoplasmic to nuclear ratio in the islet cells and there was no insulitis nor phagocytosis of necrotic beta cell fragments. While there is a progressive loss of beta cells in aging homozygous mice, there is no loss of alpha, delta or PP cells. Electron m ..... | ||
| 006142 | B6.129S4-Ppargtm1Rev/J | Cryopreserved - Ready for recovery |
| All mice homozygous for this targeted mutation die after gestational day 9.5 from severe placental defects and myocardial thinning. Heterozygotes are viable and fertile. White adipose tissue from heterozygous mice display approximately half the mRNA expression compared to wildtype. Tracer-determined glucose disposal rates and hepatic glucose production show that peripheral tissues and livers from heterozygotes are more sensitive to the effects of insulin than wildtype. This mutation eliminates both DNA-binding and ligand-binding functions of the endogenous gene, concomitantly generating a lacZ reporter that faithfully recapitulates the endogenous expression pattern. Heterozygous mice or homozygous embryo-derived cells may be useful in studies of embryo and placental development, diabetes, atherosclerosis, inflammation, and for beta-galactosidase reporter function of the endogenous gene. | ||
| 008076 | B6.129S4-Traf1tm1Tsi/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the TRAF1 mutant allele (TRAF1-/-) are viable and fertile. No protein expression from the targeted gene is observed in CD40-stimulated splenocytes isolated from homozygous mice. Homozygous mice on a C57BL/6 congenic background (B6-TRAF1-/-) have abnormal memory T cell survival and impaired influenza virus CD8 T cell responses. Activated B6-TRAF1-/- T cells accumulate increased levels of proapoptotic BH3-only family member Bim, particularly the most toxic isoform, Bims. The donating investigator reports that B6-TRAF1 mutant mice may be difficult to breed and gain more weight than BALB/c-TRAF1 mutant mice. Homozygous mice on a BALB/c congenic background (BALB/c-TRAF1-/-) exhibit acute liver injury and elevated serum liver enzymes following intratracheal TNF-alpha treatment. Furthermore, activated TRAF1-/- T cells have significantly increased expression of Th2 cytokines (IL-4, IL-5 and IL-13) that el ..... | ||
| 003823 | B6.129S4-Ttpatm1Far/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Ttpa gene are viable, normal in size and do not display any gross physical abnormalities. The Ttpa protein product is required for the maintenance of proper alpha-tocopherol levels, the major form of vitamin E in plasma and tissues. The absence of Ttpa protein product in homozygous-null animals results in a corresponding 95% reduction in alpha-tocopherol. Low levels of alpha-tocopherol render female mice infertile, a condition that can be addressed with vitamin E supplements. Male fertility is unimpaired. These mice provide a viable model for studying vitamin E deficiency. | ||
| 006236 | B6.129S6-Casp6tm1Flv/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable and fertile with no gross morphological or behavioral abnormalities. These mutant mice may be useful in studies of mitochondrial events of apoptosis (especially when paired with other executioner caspase mutant models) and lens development. | ||
| 004197 | B6.129S6-Rac2tm1Mddw/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, and normal in size but exhibit phagocytic immunodeficiency. No endogenous gene product (mRNA or protein) was detected by Northern blot analysis, RT-PCR or Western blot analysis. The Rac proteins are a subclass of the Rho family of GTPases, and are involved in actin cytoskeletal organization in cell movement, cell proliferation, kinase signaling pathways, and in superoxide production in phagocytic cells. Neutrophils and mast cells derived from homozygous mice display abnormal actin-based functions: cytoskeleton remodeling ability, adhesion, migration, degranulation, and phagocytosis. Diminished superoxide production in response to some agonists, and reduced total number of leukocytes and neutrophils in peritoneal exudate is observed. As result of functional deficiencies in neutrophil and mast cell populations, these mutant mice are more vulnerable to invasive infection. Slowed growth of mast cells, accompanying redu ..... For more information please see the full phenotype on the strain data sheet | ||
| 008887 | B6.129X1-Bidtm1Sjk/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of spleen and thymus tissue. Most homozygotes survive injection of anti-Fas antibodies while wildtype mice succumb to acute liver failure within hours. Mutant mice are resistant to hypoxia-ischemia (HI) injury, experimentally induced apoptosis, and oxygen toxicity under hyperoxic conditions. Homozygotes exhibit reduced lysosome permeability and diminished reactive oxygen species generation. Isolated neurons are resistant to oxygen/glucose deprivation induced cell death. This mutant mouse strain may be useful in studies of mitochondiral activation in apoptosis, and ischemic cell injury and death. | ||
| 006072 | B6.129X1-Mcl1tm2Sjk/J | Cryopreserved - Ready for recovery |
| 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 are embryonic lethal. These mutant mice may be useful in studies of immune function, including apoptosis, B and T cell development, and bone marrow cell differentiation. When bred to a strain with loxP sites inserted into the same targeted allele (Stock No. 006088) and a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 004126), this mutant mouse strain may be useful in studies of lymphocyte development. When bred to a strain with loxP sites inserted into the same targeted allele (Stock No. 006088) and a strain expressing interferon inducible Cre recombinase in t ..... | ||
| 005642 | B6.Cg-Clutm1Jakh/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size, and do not display any behavioral abnormalities. No protein is detected in serum, liver, or brain and in situ hybridization shows no mRNA in heart. This mutant has been studied for different functions on different backgrounds. On the Swiss Black outbred background, aging homozygous mutant mice develop a progressive glomerulopathy characterized by deposition of tubulo-fibrillary immune complexes devoid of inflammation or necrosis. On the FVB/N background, homozygous null mice with chemically induced autoimmune myocarditis show severe and diffuse lesions with postinflammatory functional impairment. Induced skin carcinogenesis is more severe than wildtype. On the C57BL/6 background, homozygotes given a hypoxia-ischemia brain injury (modeling cerebral palsy) had 50% less brain injury compared to wild type. Conversely, mutants have less neuroprotective properties after permanent focal cerebral isc ..... For more information please see the full phenotype on the strain data sheet | ||
| 006200 | B6.Cg-Tnks2tm1.1Yjc/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of activated spleen lymphocytes. While neither telomere shortening nor chromosomal abnormalities (even across multiple generations) are observed, homozygous mice have significantly decreased body weight. These mutant mice may be useful in studies of both telomerase function and telomerase-independent pathways which affect development and metabolism. | ||
| 006329 | B6;129-Baxtm2Sjk Bak1tm1Thsn/J | Cryopreserved - Ready for recovery |
| Mice homozygous for both alleles (Baxfl and bak-) are viable and fertile with no reported abnormalities. Splenic and thymic tissues display no Bak1 protein expression. When bred to Cre recombinase expressing mice, the resulting offspring will have exons 2-4 of Bax deleted in the cre-expressing tissues (determined by promoter driving cre expression). The conditional deletion of Bax combined with the Bak1 null allele makes these mice useful in studies of apoptosis regulation, tissue homeostasis, and development in multiple cell lineages.
When bred to a strain with a Bak1 targeted null allele (Stock No. 004183) and to either a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 004126) or to a strain expressing interferon inducible Cre recombinase ( ..... | ||
| 004264 | B6;129-Cycstm1Wlm/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Cycstm1Wlm targeted-mutant allele die in utero by embryonic day 10.5, but cell lines established from early Cycs-null embryos are viable under conditions that compensate for defective oxidative phosphorylation. Cells lacking cytochrome c show reduced caspase 3 activation, and are resistant to the proapoptotic effects of UV irradiation, serum withdrawal, and staurosporine. Cells lacking cytochrome c, however, do demonstrate an increased sensitivity to cell death signals triggered by tumor necrosis factor, alpha. Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 004338 | B6;129-E2f2tm1Zubi/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable and normal in size. No gene product, mRNA or protein, was detected. At age 15 months mutant mice have a 27% survival rate due to diffuse autoimmune disease that resembles systemic lupus erythematosus (SLE). The phenotype includes splenomegaly by 8-12 weeks of age, glomerulonephritis, accumulated inflammatory infiltrates in the lung, liver, and skin abnormalities such as hair loss, skin wounds, erythema. Anti-dsDNA antibodies are detected in the serum. There are an increased number of mature CD8+ thymocytes and an abnormal accumulation of CD8+ Cd44high Cd69- T effector/memory cells that are autoreactive in peripheral lymphoid organs. E2F2 deficient mice appear to have normal negative selection of thymocytes but demonstrate defects in peripheral tolerance of T lymphoctes (especially Cd8+ T cells) leading to progressive autoimmune disease. This mutant mouse strain may be useful in studies of autoimmunity and may serve as model ..... For more information please see the full phenotype on the strain data sheet | ||
| 008452 | B6;129-Eif2ak4tm1.1Dron/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the GCN2.KO4conditional allele (also called GCN2.KO4c) are viable and fertile, with loxP sites flanking exon XII of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (containing amino acid residues 606-648 encoding the critical lysine 618 required for kinase activity) deleted in the cre-expressing tissue(s). GCN2 is a protein kinase that phosphorylates eIF2 (eukaryotic initiation factor 2) in response to environmental stresses (amino acid starvation, proteasome inhibition and UV irradiation) resulting in a reduction of global translation and activation of stress-related transcription factors (such as NF-kappaB). These GCN2.KO4conditional mice may be useful in studies related to eIF2 phosphorylation in response to environmental stresses. Of note, mice with a traditional "knockout" (deletion of exon XII) are also available (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 006088 | B6;129-Mcl1tm3Sjk/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator indicates that homozygous males have severely reduced fertility for unknown reasons, while females have normal fertility. Endogenous protein expression is unaffected by the inserted loxP sequences. When bred to mice with a cre recombinase gene under the control of a promoter of interest, exon 1 of the targeted gene is deleted in the tissue of interest. These mutant mice may be useful in studying global, temporal, or tissue-specific deletion of the endogenous gene, particularly in studies of immune function, including apoptosis, B and T cell development, and bone marrow cell differentiation. When bred to a strain with the targeted null allele (Stock No. 006072) and a strain with a Cd19 null allele and expressing Cre recombinase during th ..... | ||
| 002536 | B6;129S-Btktm1Wk/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Btktm1Wk targeted mutation are viable and fertile. Homozygous mutant mice show defects in B-cell maturation and activation. This strain has the same phenotype as the spontaneous X-linked immune deficiency mutation (CBA/CaHN-Btkxid/J; Stock No. 001011). See Inbred Strain listing. | ||
| 005937 | B6;129S4-Ucp3tm1Lowl/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable and fertile and do not express full length mRNA in skeletal muscle and brown adipose tissue. In skeletal muscle mitochondria, endogenous protein was undetectable. Skeletal muscle mitochondria from homozygous mice show decreased state 4 respiration. Further, skeletal muscle, but not liver, mitochondria produce more superoxide anions and reactive oxygen species both in vitro (lucigenin-derived chemiluminescence) and in vivo (aconitase activity). Skeletal muscle ATP synthesis under fasting conditions is approximately 4-fold greater in mutant mice. This mouse may be useful in studies of energy metabolism, thermogenesis, aerobic respiration (including mitochondrial respiration coupling), and age-related progressive deterioration of fatty acid homeostasis. | ||
| 008080 | B6;C3-Tg(CAG-SAC/EGFP)35Rang/J | Cryopreserved - Ready for recovery |
| Hemizygous SAC transgenic mice have normal fertility, viability, and aging. Widespread expression of the transgene is observed in all tested tissues (with some differential tissue-specific regulation of transgene expression or protein stability reported). The SAC-GFP fusion protein is composed of the cancer-specific proapoptotic effector domain (or SAC domain) of the Par-4 gene fused to an enhanced green fluorescent protein (EGFP). As a result, SAC-GFP transgenic mice have increased resistance to spontaneous liver/spleen and TRAMP-induced prostate tumor development. The protective nature of the transgene appears to be linked to inhibition of NF-kappaB activity and induction of apoptosis. Cells derived from SAC transgenic mice grow normally in short-term culture and presence of the SAC transgene prevents oncogene-mediated cellular transformation. The donating investigator reports that EGFP expression is appropriate for immunoblots, but not sufficient enough for fluorescence of flow cyto ..... For more information please see the full phenotype on the strain data sheet | ||
| 009685 | B6N.129S1(Cg)-Tnkstm1.1Yjc/J | Cryopreserved - Ready for recovery |
| Homozygous (TANK1-/-) mice are viable and fertile with no reported developmental or gross physical abnormalities. As exon 1 is deleted from the targeted allele, no full length protein (TANK1) is detected in thymus, testis or spleen tissues. Because the deletion does not encompass the potential alternative promoter between exons 4-5, an alternative transcript and subsequent low molecular weight protein (TANK1a) is expressed in testis (but not in other assayed tissues). These TANK1-mutant mice may be useful for studying the post-translational modification of proteins associated with cell cycle, mitosis, telomere length maintenance/aging, DNA replication/repair, cellular senescence, apoptosis, tumorigenesis, vesicle trafficking, and insulin responses. These TANK1-mutant mice may also be used along with TANK2-mutant mice (Stock No. 006200). | ||
| 005516 | C.129S4-Cyb5r4tm1Hfb/HfbJ | Cryopreserved - Ready for recovery |
| Mice heterozygous for the targeted mutation are viable and fertile, glucose tolerant, have normal blood sugar levels, serum lipid profiles and white adipose tissue mass. No protein from the targeted gene was detected by Western Blot analysis of mice homozygous for the allele. Homozygous mice consume more food, have decreased adipose tissue mass and are hyperlipidemic compared to wildtype controls post-weaning. At 4 weeks of age glucose levels are normal but insulin levels are 40% of wildtype controls. At 7 weeks of age clinical diabetes is present in both male and female of homozygous mice. Histological evaluation of pancreas from 21 week old homozygote animals revealed a significant reduction in the number of islets and decreased cytoplasmic to nuclear ratio in the islet cells and there was no insulitis nor phagocytosis of necrotic beta cell fragments. While there is a progressive loss of beta cells in aging homozygous mice, there is no loss of alpha, delta or PP cells. Electron m ..... | ||
| 008074 | C.129S4-Traf1tm1Tsi/TsiPryhJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the TRAF1 mutant allele (TRAF1-/-) are viable and fertile. No protein expression from the targeted gene is observed in CD40-stimulated splenocytes isolated from homozygous mice. Homozygous mice on a BALB/c congenic background (BALB/c-TRAF1-/-) exhibit acute liver injury and elevated serum liver enzymes following intratracheal TNF-alpha treatment. Furthermore, activated TRAF1-/- T cells have significantly increased expression of Th2 cytokines (IL-4, IL-5 and IL-13) that elicit enhanced Th2 responses in vivo. BALB/c-TRAF1-/- T cells exhibit elevated nuclear expression of NFAT-interacting protein (NIP45) and also induce significantly more intense pulmonary inflammation and higher airway hyper-responsiveness in OVA allergic inflammation models. Pulmonary leukocyte recruitment is attenuated following inhalation of lipopolysaccharide in BALB/c-TRAF1-/- mice. Homozygous mice on a C57BL/6 congenic background ( ..... | ||
| 012371 | C57BL/6-Bdkrb2/Bdkrb1tm1Mki/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation, commonly referred to as B1RB2R -/-, are viable, fertile and display no major defects. At 4 months of age non-manipulated B1RB2R -/- mice exhibit no significant differences in blood pressure or kidney function when compared to Bdkrb2 deficient mice (Stock No. 006860). Fasted B1RB2R -/- mice exhibit significantly lower levels of plasma nitrite/nitrate compared to Bdkrb2 deficient mice. Post-ischemic B1RB2R -/- mice exhibit significantly higher plasma levels of urea nitrogen and creatinine, higher levels of oxidative nuclear and mitochondrial DNA modification, and increased rates of apoptosis and mortality than either wildtype or Bdkrb2 deficient mice. Histological evaluation of the kidney indicates that post ischemic B1RB2R -/- mice exhibit more severe histological changes in the renal proximal tubules than either wildtype or Bdkrb2 deficient mice (Kakoki, et al, 2007). This Bdkrb1/Bdkrb2 targeted ..... | ||
| 012637 | C57BL/6-Gt(ROSA)26Sortm5(Map3k14)Rsky/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the NIK-wt allele are viable and fertile, with a loxP-flanked Neo-STOP cassette preventing transcription of the downstream bicistronic sequences (NIK [a wt form of the mouse NF-kappaB inducing kinase] and EGFP). When bred to mice that express Cre recombinase, offspring will have the STOP cassette deleted and subsequent expression of the NIK-wt molecule and EGFP fluorescence in the cre-expressing cells. Expression of NIK-wt leads to overexpression of NIK in mouse B lymphocytes, amplifying alternative NF-kappaB activation and peripheral B cell numbers, in a B cell-activating factor of the TNF family receptor (BAFF-R) dependent manner. BAFF-R binding is required to sustain the NIK p100 subunit processing needed for B cell survival, and is implicated in human multiple myeloma. Of note, breeding these mice to an FLP-expressing strain will result in removal of the frt-flanked IRES-EGFP cassette. When bred to a strain expre ..... | ||
| 012638 | C57BL/6-Gt(ROSA)26Sortm6(Map3k14*)Rsky/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the NIK-deltaT3 allele are viable and fertile, with a loxP-flanked Neo-STOP cassette preventing transcription of the downstream bicistronic sequences (NIKdeltaT3 [a constitutively active form of the mouse NF-kappaB inducing kinase] and EGFP). When bred to mice that express Cre recombinase, offspring will have the STOP cassette deleted and subsequent expression of the NIKdeltaT3 molecule and EGFP fluorescence in the cre-expressing cells. Expression of NIK-deltaT3 leads to uncoupling NIK from tumor necrosis factor receptor-associated factor 3 (TRAF3)-mediated control causing maximal p100 processing and dramatic hyperplasia of B cell-activating factor
of the TNF family receptor (BAFF-R)-independent B cells. BAFF-R binding is required to sustain the NIK p100 subunit processing needed for B cell survival, as implicated in human multiple myeloma.
Of note, breeding these mice to an FLP-expressing strain will result in removal of the | ||
| 011068 | C57BL/6-Pmaip1tm1Ast/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis of irradiated thymocytes from homozygotes and Northern blot analysis of testis, lung and spleen from homozygotes. Thymocytes from homozygous mice exhibit increased resistance to DNA-damage induced apoptosis after treatment by etoposide. NK cells from homozygotes survive better than wildtype controls when cultured without IL-15. | ||
| 008158 | C57BL/6-Serpinb9tm1Arp/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis of myeloid and lymphoid cells. After experimental viral infection, homozygous mice have lower (five to nine-fold reduction) numbers of virus specific cytotoxic T lymphocytes (CTLs) and increased apoptosis of virus specific CD8 T cells when compared to wildtype controls. Mutant mice have impaired Lymphocytic Choriomeningitis virus (LCMV) infection clearance. Granzyme A and granzyme B specific activity is reduced in cytotoxic granules and increased in CTL cytoplasm. Mutant CTLs have a three-fold increase in the number of granules lacking granzyme B. This mutant mouse strain may be useful in studies of viral immune response and inflammation, and the exocytosis pathway in CTL apoptosis. | ||
| 010800 | C57BL/6-Tg(Thy1-PTGS2)300Kand/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the human Thy-1-COX-2 transgene (hCOX-2 transgene) are viable and fertile, with expression of human COX-2 (PTGS2 or PGE2) directed primarily to neurons of the amygdala, striatum, cerebral cortex, and hippocampus by the murine Thy1.2 expression cassette. These moderate overexpressing C57BL/6J COX-2 transgenic line 300 mice have PGE2 levels that are ~10-12-fold greater than non-transgenic controls (compared to ~25-40-fold overexpression in line 303; see Stock No. 010703). At approximately 12 months of age, COX-2 transgenic mice develop an age-dependent deficit in spatial memory. Around 20 months of age, a less pronounced, but significant deterioration in performance of non-spatial memory tasks develops. Further progressive memory impairments are observed over time. These cognitive deficits are associated with parallel age-dependent increases in cortical neuronal apoptosis and glial activation. Transgenic m ..... For more information please see the full phenotype on the strain data sheet | ||
| 010703 | C57BL/6-Tg(Thy1-PTGS2)303Kand/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the human Thy-1-COX-2 transgene (hCOX-2 transgene) are viable and fertile, with expression of human COX-2 (PTGS2 or PGE2) directed primarily to neurons of the amygdala, striatum, cerebral cortex, and hippocampus by the murine Thy1.2 expression cassette. These overexpressing C57BL/6J COX-2 transgenic line 303 mice have PGE2 levels that are ~25-40-fold greater than non-transgenic controls (compared to ~10-12-fold overexpression in line 300; see Stock No. 010800). At approximately 12 months of age, COX-2 transgenic mice develop an age-dependent deficit in spatial memory. Around 20 months of age, a less pronounced, but significant deterioration in performance of non-spatial memory tasks develops. Further progressive memory impairments are observed over time. These cognitive deficits are associated with parallel age-dependent increases in cortical neuronal apoptosis and glial activation. Transgenic mice exhib ..... For more information please see the full phenotype on the strain data sheet | ||
| 008081 | CBy.129(B6)-Sirt1tm1Ygu/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted allele (SirT1co/co) are viable and fertile with a loxP-flanked neomycin cassette just upstream of, and a third loxP site just downstream of exon 4 of the targeted gene. The floxed mutation does not affect the protein expression of the targeted gene in MEF's or mammary tissue from homozygotes. When bred to mice that express Cre recombinase, the resulting offspring have exon 4 (encoding a conserved Sir2 motif) deleted in the cre-expressing tissue(s) (the donating investigator reports that they observe only one recombination event; complete removal of the neomycin cassette and exon 4, leaving a single loxp site remaining). These SirT1co/co mice may be useful in generating conditional mutations for studying the role of estrogen, insulin growth factor-1 (IGF-1), and transcription factors (including NF-kappaB) in mammary gland development, breast cancer, apoptosis, and metabolic diseases.
In an att ..... | ||
| 008660 | FVB.129S2(B6)-Hmox2tm1Poss/J | Cryopreserved - Ready for recovery |
| Homozygotes have reduced total heme oxygenase activity in brain and testes, diminished inflammatory pain response and are more susceptible to hyperoxia with attenuated hypoxic ventilatory response. Cultured neurons from homozygotes exhibit increased neurotoxicity and cell death. Neuronal and endothelial cell damage due to transient focal ischemia and glutamate induced cytotoxicity is increased. Olfactory epithelial neurons have decreased proliferation of neuronal precursors and increased apoptosis. Mutant pulmonary venous myocardium is hypertrophic. After hyperoxic exposure, total lung iron content increased 3.5 fold in homozygotes compared to wild-type. Homozygotes have a slower overall gastrointestinal transit time than wild-type. Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Although homozygous male animals exhibit ejaculatory abnormalities, both male and female homozygotes are fertile ..... For more information please see the full phenotype on the strain data sheet | ||
| 005076 | NOD.Cg-Tg(tetO-EGFP/FADD)1Doi/DoiJ | Cryopreserved - Ready for recovery |
| Mice hemizygous for this transgenic insert are viable, fertile, normal in size. Diabetes incidence and onset is similar to that observed in NOD inbred mice, but otherwise, the mice do not display any gross physical or behavioral abnormalities. These transgenic mutant mice may be mated to strains carrying either rtTA (reverse tetracycline trans-activator protein) or tTA (the tetracycline trans-activator) transgenes regulated by tissue specific promoters. In the bi-transgenic offspring of such crosses, tissue-specific expression of the EGFP/FADD fusion protein can be either induced (in rtTA transgenic mice) or suppressed (in tTA transgenice mice) by administration of the tetracycline analog, doxycycline (dox). Dox may be administered in the animals water supply.
Double transgenic mice generated by intercrossing Tg(tetO-EGFP/FADD)1Doi transgenic mice with NOD.Cg-Tg(Ins2-rtTA)2Doi/DoiJ (Stock No. 004602) transgenic mice express th ..... | ||
| 005115 | NOD.FVB-Tg(INS-MT2A,Tyr)1Pne/PneJ | Cryopreserved - Ready for recovery |
| Transgenic mice are viable, fertile, and normal in size, display accelerated spontaneous diabetes onset, especially in males, and have coat color pigmentation. Immunohistochemical staining with metallothionein specific antibodies confirms pancreatic islet cell specific expression of the INS-MT2A transgene. There is a 40-fold increase in metallothionein activity in transgenic islets when compared to wild-type controls. Insulin and DNA content, insulin staining and islet morphology in transgenic animals is essentially the same as in wild-type controls. Transgenic islets have a similar reactive oxygen species (ROS) level as wild-type controls in normal media. However, after exposure to cytokines there is a significant increase in ROS florescence in wild-type islets, but a very small increase in transgenic islets. Transgenic beta cells are diabetes resistant to diabetes when treated with streptozotocin. Transgenic beta cells generate less ROS fluorescence when treated with hydrogen peroxid ..... For more information please see the full phenotype on the strain data sheet | ||
| 005113 | NOD.FVB-Tg(INS-SOD2)3Pne/PneJ | Cryopreserved - Ready for recovery |
| Transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Immunohistochemical staining with mitochondrial superoxide dismutase specific antibody confirms INS-SOD2 transgene expression localized to the mitochondria of pancreatic islet cell. There is a significant increase in SOD2 activity in transgenic islets when compared to wild-type controls. There is no statistical difference in insulin and DNA content, insulin staining and islet morphology or diabetes development following cyclophosphamide treatment between mutant and wild type NOD mice. Transgenic mice are resistant to diabetes when treated with streptozotocin. Islet beta cells from transgenics generate less ROS when treated with peroxynitrite or superoxide. Untreated mutants do not display accelerated spontaneous diabetes. This model provides a tool for looking at the role of oxidative stress in diabetes. | ||
| 005114 | NOD.FVB-Tg(Ins1-Cat,Tyr)25Pne/PneJ | Cryopreserved - Ready for recovery |
| Transgenic mice are viable, fertile, and normal in size, display accelerated spontaneous diabetes onset in males, and have coat color pigmentation. Northern blot analysis and immunohistochemistry confirm pancreatic islet specific expression of the Ins1-Cat transgene. There is a 50-fold increase in catalase activity in transgenic islets when compared to wild-type controls, which approximates catalase activity normally found in the liver. Insulin and DNA content, insulin staining and islet morphology in transgenic animals is essentially the same as in wild-type controls. Transgenic islets have a similar reactive oxygen species (ROS) level as wild-type controls in normal media. However, after exposure to cytokines there is a significant increase of ROS florescence in control islets, but much smaller increase in transgenic islets. Transgenic mice are resistant to diabetes when treated with streptozotocin or alloxan. Transgenic beta cells generate less ROS fluorescence when treated with ..... | ||
| 005740 | STOCK Ppiftm1.1Mmos/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Brain architecture and cerebrovasculature are normal. No gene product (protein) is detected by immunoblot analysis of mitochondria isolated from liver tissue of mutant mice. Mitochondria from mutant mice have an increased capacity to retain calcium and fail to swell/rupture in response to CaCl2, suggesting abnormal permeability transition pore (PTP) function. Mouse embryonic fibroblasts (MEFs) derived from mutant mice are less susceptible to oxidative stress induced in vitro by exposure to hydrogen peroxide than MEFs derived from wildtype mice. In a model of ischemic brain injury employing a middle cerebral artery occlusion protocol, mutant mice exhibited a reduced infarct volume (37% in heterozygotes, and 62% in homozygotes) when compared to wildtype mice. This mutant mouse strain may be useful in studies investigat ..... For more information please see the full phenotype on the strain data sheet | ||
| 005737 | STOCK Ppiftm1Mmos/J | Cryopreserved - Ready for recovery |
| In this strain loxP sites flank exons 3-5 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. Cre-mediated recombination results in the deletion of the loxP-flanked region. This strain represents an effective tool for generating tissue-specific targeted mutants useful in studies examining the consequences of disrupting Ppif-dependent pathways. | ||
| 006085 | STOCK Rad9tm1Lieb/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Mouse embryo fibroblasts (MEFs) cannot be derived from homozygous embryos. Homozygous null mice have an embryonic lethal phenotype, failing to develop somewhere between embryonic days 9.5 and 12.5. Homozygous mutant embryonic day 8.5 and 9.5 embryos exhibit increased apoptosis and reduced cellular proliferation. This mutant mouse strain may be useful in studies of development, DNA damage and repair, and genomic stability. | ||
| 004510 | STOCK Rom1tm1Mci/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable and normal in size. When heterozygous mice are bred together, homozygous animals occur at a greatly reduced frequency (~6%). No gene product (protein) is detected in retinal tissue from homozygotes by Western blot analysis. Onset of progressive retinal degeneration occurs at 2 months of age beginning with a thinning of the outer nuclear layer of retinal cells. Rod outer segments in 2 month old mice display disorganized arrangement, irregular gaps and amorphous aggregates. At 4 months of age organization of rod outer segments improves. TUNEL assay of mutant retinal tissue show photoreceptor degeneration is due to apoptotic cell death. Ultra structural organization of rod outer segment disks is disorganized, often with patches of enlarged disks. Electroretinogram a-wave analysis of photoreceptor function reveals a diminished maximal photoreceptor response (50% lower than wildtype). This mutant mouse strain may be useful in stu ..... For more information please see the full phenotype on the strain data sheet | ||
| 014547 | FVB/N-Tg(tetO-Fasl)BDepa/J | Under Development - Now Accepting Orders |
| Mice hemizygous for the (tetOp)7-FasL transgene (TetOp-FasL transgenic mice) are viable and fertile with no reported phenotypic abnormalities. The (tetOp)7-FasL transgene has the Tet response element (TRE or tetO) upstream of a murine Fas ligand (FasL) coding sequence. When bred with other mice expressing tetracycline-controlled transactivator protein (tTA) or reverse tetracycline-controlled transactivator protein (rtTA), FasL overexpression in the resulting double mutant offspring can be regulated with tetracycline or its analog doxycycline (dox). FasL overexpression leads to Fas/FasL receptor-mediated death-signaling pathway activation and results in cell apoptosis.
The donating investigator reports that transgenic mice from founder line B (TetOp-FasL transgenic line B) exhibit very high FasL overexpression levels in the presence of rtTA and 0.01 mg/ml Dox (low FasL levels are achievable by titrating Dox even lower). The donating investigator rep ..... For more information please see the full phenotype on the strain data sheet | ||
(71 stocks) Back to Top
How to Register Interest
Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Awaiting Transfer
Select the strain name to link to the strain data sheet.
New Strains Awaiting TransferThe Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion.
- Receive periodic updates on the status of the colony AWAITING TRANSFER
- Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available
- Provide input affecting speed and quantity of availability
It is VERY IMPORTANT that you register interest in strains Awaiting Transfer. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.
Send questions to our Technical Support team using the Express Technical Support Form.
(5.1)