JAX Mice Database - Apoptosis Research

Search Criteria: Research Area is "Apoptosis Research"

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
002818	B6.129-Tnfrsf1a^tm1Mak/J	Level 4
	Mice homozygous for the Tnfrsf1a^tm1Mak targeted mutation (formerly Tnfr1^tm1Mak) have normal thymocyte development, lymphocyte populations and clonal deletion of potentially self-reactive T cells. TNF signaling is largely abolished, with no TNF induction of NF-kB. Homozygous mutant mice are resistant to lethal dosages of either lipopolysaccharides or S. aureus enterotoxin but succumb to L. monocytogenes infection. TNFRSF1an may also protect against atherosclerotic lesion development in mice fed an atherogenic diet.
000482	B6.MRL-Fas^lpr/J	Level 4
	Mice homozygous for the lymphoproliferation spontaneous mutation (Fas^lpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Onset and severity of symptoms associated with the Fas^lpr allele is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Fas^lpr/Fas^lpr at a 24 fold increase over control lymph node weight, MRL/Mp-Fas^lpr/Fas^lpr at 75 fold and congenic strain C3H/HeJ-Fas^lpr/Fas^lpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Fas^lpr/Fas^lpr at 4 to 7 months to negligible at 14 to 16 months in mice with C57BL/6J and C3H/HeJ backgrounds and homozygous for Fas^lpr> ..... For more information please see the full phenotype on the strain data sheet
003008	B6;129S-Tnf^tm1Gkl/J	Level 4
	Mice homozygous for the Tnf^tm1Gkl 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-Tnfrsf1a^tm1Imx Tnfrsf1b^tm1Imx/J	Level 4
	Mice homozygous for both the Tnfrsf1a^tm1Imx and Tnfrsf1b^tm1Imx 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.
001021	B6Smn.C3-Fasl^gld/J	Level 4
	Mice homozygous for the Fasl^gld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasl^lpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. 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. The Cryaa ..... For more information please see the full phenotype on the strain data sheet
002407	C57BL/6-Prf1^tm1Sdz/J	Level 4
	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. Also known as perforin.
000485	MRL/MpJ-Fas^lpr/J	Level 4
	Mice homozygous for the lymphoproliferation spontaneous mutation (Fas^lpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Starting at about three months of age, levels of circulating immune complexes rise greatly in the MRL-lpr/lpr mouse but not the MRL normal (Hewicker 1990). Onset and severity of symptoms associated with the Fas^lpr gene is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Fas^lpr/Fas^lpr at a 24 fold increase over control lymph node weight, MRL/Mp-Fas^lpr/Fas^lpr at 75 fold and congenic strain C3H/HeJ-Fas^lpr/Fas^lpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Fas^lpr> ..... For more information please see the full phenotype on the strain data sheet
008215	(C57BL/6-Tg(TRAMP)8247Ng/J x FVB/NJ)F1/J	Repository- Live
	Mice carrying the TRAMP (Transgenic Adenocarcinoma of Mouse Prostate) transgene develop progressive forms of prostate cancer with distant site metastasis, primarily to the lymph nodes and lungs. These transgenic mice express the simian virus 40 (SV40) large tumor T antigen (Tag) under the control of the rat probasin promoter. Expression of the transgene is specific to the prostate epithelium. Transgenic mice exhibit various forms of disease from mild intraepithelial hyperplasia to large multinodular malignant neoplasia. The median survival time for these F1 transgenic mice is 19 weeks, very few mice survive past 33 weeks of age, which is significantly shorter than the lifespan of transgenic mice on the C57BL/6 background. Comparative histological analysis of tumors from these F1 transgenic mice and from transgenic mice on the C57BL/6 background reveals that the tumors found in these F1 mutants arise from the dorsolateral and ventral lobes of the prostate and are more spherical, hig ..... For more information please see the full phenotype on the strain data sheet
006050	129-Sirt6^tm1Fwa/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
002779	129S-Parp1^tm1Zqw/J	Repository- Live
	Mice that are homozygous null for the targeted gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Although a shortened transcript is generated, no enzymatic activity is detected in tissues. Proliferation of homozygous-null fibroblasts and thymocytes is impaired following gamma-radiation in comparison to cells derived from wild-type mice. Older mice are susceptible to spontaneous development of skin disease. A significant portion of older mice ( ~30%) can be expected to exhibit epidermal hyperplasia. Null mice are also less susceptible to damage induced by the neurotoxin MPTP.
007572	B6.129P2(Cg)-Rorc^tm2Litt/J	Repository- Live
	Mice homozygous for this Rorc(γt^GFP (or RORγt)^GFP) mutant allele are viable and fertile. While Rorcγ mRNA is detected in liver in Rorc(γ)t^GFP 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)-Myd88^tm1.1Defr/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-Ddit3^tm1Dron/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.
005540	B6.129S-Tnf^tm1Gkl/J	Repository- Live
	Mice homozygous for the 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 not affect the degree of obe ..... For more information please see the full phenotype on the strain data sheet
004525	B6.129S1-Bcl2l11^tm1.1Ast/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No full length gene product (protein) is immunodetected in spleen cells from homozygous mutant mice. Homozygous mice have lympho-myeloid hyperplasia and reduced platelet number. Lymphocytes are insensitive to certain apoptotic stimuli. Both homozygous and heterozygous mice exhibit progressive systemic autoimmune disease. This mutant mouse strain may be useful in studies of apoptosis, degenerative and autoimmune diseases, including lupus erythematosus and autoimmune kidney disease.
006233	B6.129S1-Casp3^tm1Flv/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-Thbs1^tm1Hyn/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
002620	B6.129S2-Tnfrsf1b^tm1Mwm/J	Repository- Live
	Mice homozygous for a Tnfrsf1b^tm1Mwm targeted mutation (formerly Tnfr2^tm1Mwm, p75 deficient) are viable and fertile. Homozygous mutant mice show normal T-cell development and activity, but are resistant to TNF-induced cell death. Subcutaneous injections of TNF into homozygotes elicit much less tissue necrosis.
002101	B6.129S2-Trp53^tm1Tyj/J	Repository- Live
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and sarcomas) at three to six months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
002266	B6.129S4-Bdnf^tm1Jae/J	Repository- Live
	Mice heterozygous for the Bdnf^tm1Jae mutation show about half normal levels of Bdnf mRNA, but appear normal. Mice homozygous for the Bdnf^tm1Jae mutation are smaller than normal siblings and most die within the second postnatal week. They have defective coordination of movements and balance. They also exhibit head bobbing and spinning during periods of hyperactivity. There are rare survivors to adulthood. There is excessive degeneration in all sensory ganglia examined, including the vestibular ganglion. Motor neurons are not affected. BDNF can prevent death of central motor neurons and other neurons in vitro, but does not affect these in vivo.
007899	B6.129S4-Casp2^tm1Yuan/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-2_S 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
002213	B6.129S4-Ngfr^tm1Jae/J	Repository- Live
	Mice homozygous for the Ngfr^tm1Jae mutation are viable and fertile. They display a decreased cutaneous innervation by calcitonin gene-related peptide- and substance P-immunoreactive sensory fibers. Because of this decreased innervation they develop ulcers on their toes by four months of age. The toes become inflamed and progressively infected. There is also reduced sensitivity to heat in the extremities of these mice. Pineal glands lack sympathetic innervation and innervation to sweat glands on foot pads is either reduced or absent. Deficits in the peripheral nervous system were examined by looking at cellular responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. p75-deficient DRG and SCG neurons displayed a two- to three-fold decreased sensitivity to NGF at embryonic day 15 and postnatal day three, respectively. These ages coincide with the peak of naturally occurring cell death. p75-deficient ..... For more information please see the full phenotype on the strain data sheet
006440	B6.129S4-Pten^tm1Hwu/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 ..... For more information please see the full phenotype on the strain data sheet
006237	B6.129S6-Casp7^tm1Flv/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-Eif2ak4^tm1.2Dron/J	Repository- Live
	Mice homozygous for the GCN2.KO4 mutant locus (also called GCN2.KO4^-, GCN2^-, GCN2.KO4^ex, 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 ..... For more information please see the full phenotype on the strain data sheet
002994	B6.129X1-Bax^tm1Sjk/J	Repository- Live
	Mice homozygous for the Bax^tm1Sjk mutation are viable but display lineage-specific aberrations in cell death. Thymocytes and B cells from homozygous mutant mice display hyperplasia. Ovaries contain unusual atretic follicles with excess granulosa cells while Bax-deficient males are infertile. There is an accumulation of atypical premeiotic germ cells and no mature haploid sperm found in seminiferous tubules. Multinucleated giant cells and dysplastic cells accompany massive cell death. Used in conjunction with strain B6.129-Bak1^tm1Thsn/J (see Stock No. 004183), to generate the double knock-out Bak/Bax, a model for demonstrating severe defects in the regulation of apoptosis during development and tissue homeostasis. *Coat color of Bax^tm1Sjk* mice** The coat color loci tyrosinase (Tyr) and pink-eyed dilution (p) are linked to the Bcl2-associated X pr ..... For more information please see the full phenotype on the strain data sheet
016882	B6.Cg-Tg(CMV-CASP3)14Edge/J	Repository- Live
	Mos-iCsp3 transgenic mice have a CMV promoter directing expression of a floxed-lacZ-STOP cassette followed by two tandem FK506-binding sites (Fvs) and a downstream human Caspase 3 (Casp3) gene. Hemizygous Mos-iCsp3 mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Caspase 3 is a member of the cysteine-aspartic acid protease family of enzymes which are integral to apoptosis pathways. Inactive until cleaved by an initiator enzyme, Caspase 3 is processed at conserved aspartic residues and is activated by the formation of dimers. In this transgenic strain, a STOP cassette is present, flanked by a loxH site and a loxP site, preventing inducible Caspase 3 expression and allowing for widespread lacZ staining. LacZ staining in founder line 14 is seen in the eye, kidney, pancreas, skin, thymus, and portions of the brain. The presence of both a loxH site and a loxP site causes reduc ..... For more information please see the full phenotype on the strain data sheet
016908	B6.Cg-Tg(CMV-CASP3)17Edge/J	Repository- Live
	Mos-iCsp3 transgenic mice have a CMV promoter directing expression of a floxed-lacZ-STOP cassette followed by two tandem FK506-binding sites (Fvs) and a downstream human Caspase 3 (Casp3) gene. Hemizygous Mos-iCsp3 mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Caspase 3 is a member of the cysteine-aspartic acid protease family of enzymes which are integral to apoptosis pathways. Inactive until cleaved by an initiator enzyme, Caspase 3 is processed at conserved aspartic residues and is activated by the formation of dimers. In this transgenic strain, a STOP cassette is present, flanked by a loxH site and a loxP site, preventing inducible Caspase 3 expression and allowing for widespread lacZ staining. LacZ staining in founder line 17 is seen in the spinal cord, muscle, pancreas, skin, and portions of the brain and skull. The presence of both a loxH site and a loxP site cau ..... For more information please see the full phenotype on the strain data sheet
016221	B6;129-Ip6k2^tm1Dlin/J	Repository- Live
	In this strain, a floxed-neo cassette replaces the first 202 nucleotides of exon 2 of the inositol hexaphosphate kinase 2 (Ip6k2) gene, abolishing gene expression. Homozygotes are viable, fertile, and normal in size. IP6K2 suppresses growth and increases apoptosis during cell stress by catalyzing the synthesis of inositol polyphosphates. These compounds are involved in the regulation of telomere length, protein phosphorylation, and cell growth and movement. After chronic exposure to the carcinogen 4-nitroquinoline 1-oxide (4-NQO) these mice exhibit a four-fold increase in the incidence of invasive squamous cell carcinoma (SCC) formation in the tongue, oral cavity, and esophagus. They also display relative resistance to ionizing radiation and exhibit increased survival following total body irradiation. Cells from these mice are relatively resistant to growth-suppression by interferon-β (IFN-β). These mice may be useful for studying the mechanisms of IP6K2-dependent ..... For more information please see the full phenotype on the strain data sheet
011122	B6;129-Mertk^tm1Grl/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. In response to endotoxin, homozygotes exhibit an increase in spleen size and a decrease in monocyte response. Retinal photoreceptor epithelial cells fail to phagocytose outer segment membranes resulting in complete photoreceptor degeneration and blindness. When combined with the mutations Tyro3^tm1Grl (Stock No. 007937) and Axl^tm1Grl (Stock No. 011121) mice exhibit a lymphoproliferative disorder, autoimmunity, increased apoptosis in multiple tissues, abnormal spermatogenesis and reduced (in females) fertility or infertility (in males). This mutant mouse strain may be useful in studies of autoimmunity, germ cell development homeostatic regulation and apoptosis.
009071	B6;129-Ppif^tm1Jmol/J	Repository- Live
	Mitochondria isolated from the livers, hearts, and brains of homozygous targeted mutant mice are resistant to swelling and permeability transition in vitro. Hepatocytes and fibroblasts are largely protected from Ca²⁺-overload and oxidative stress-induced cell death. Mice are protected from ischaemia/reperfusion-induced cell death in vivo. This strain may be useful in studies of mitochondrial-driven cell death.
008045	B6;129-Trp53^tm2Holl/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-Trp53^tm1Holl/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
003244	B6;129S-Tnfrsf1a^tm1Imx Il1r1^tm1Imx/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.
002785	B6;129S4-E2f1^tm1Meg/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.
013101	B6;129S6-Gadd45b^tm1Flv/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.
009069	B6;129X1-Dusp6^tm1Jmol/J	Repository- Live
	Homozygous targeted mutant mice have larger hearts than wild-type mice at every age examined. They show greater rates of myocyte proliferation during embryonic development and in the early postnatal period, resulting in cardiac hypercellularity. This lends protection against decompensation and hypertrophic cardiomyopathy following long term pressure overload and myocardial infarction injury in adult mice. Embryonic fibroblasts derived from these mice also show reduced apoptosis rates as compared to wildtype. Homozygotes are viable, fertile and otherwise overtly normal. This strain may be useful in studies of heart function and disease.
000501	B6CBACa A^w-J/A-Aifm1^Hq/J	Repository- Live
	Harlequin mice exhibit paucity of fur resulting in near baldness in hemizygous males and homozygous females. Heterozygous females have a patchy absence of hair that is not always obvious, since the degree of hair loss is notably less than 50%. Homozygotes and hemizygous males weigh less than heterozygous or wild type controls. Ataxia is noticeable by 5 months and progresses as the mice age. Initially the ataxia manifests itself as a side-to-side, unsteady gait with a lateral tremor visible at rest. A delayed cerebellar cortical atrophy has been characterized in these mutants, with an apoptotic loss of granule cells beginning at 4 months of age and a necrotic loss of Purkinje cells occurring subsequently. The granule cells re-enter the cell cycle, but the Purkinje cells do not, supporting the postulate that inappropriate cell cycle re-entry of terminally differentiated neurons can induce apoptosis. Cell loss is greater in the caudal lobules of the cerebellum and is extensive by 9 to 11 ..... For more information please see the full phenotype on the strain data sheet
000480	C3.MRL-Fas^lpr/J	Repository- Live
	Mice homozygous for the lymphoproliferation spontaneous mutation (Fas^lpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Onset and severity of symptoms associated with the Fas^lpr allele is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Fas^lpr/Fas^lpr at a 24 fold increase over control lymph node weight, MRL/Mp-Fas^lpr/Fas^lpr at 75 fold and congenic strain C3H/HeJ-Fas^lpr/Fas^lpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Fas^lpr/Fas^lpr at 4 to 7 months to negligible at 14 to 16 months in mice with C57BL/6J and C3H/HeJ backgrounds and homozygous for Fas^lpr> ..... For more information please see the full phenotype on the strain data sheet
011067	C57BL/6-Bbc3^tm1Ast/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)26Sor^{tm3(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
003242	C57BL/6-Tnfrsf1a^tm1Imx/J	Repository- Live
	Mice homozygous for the Tnfrsf1a^tm1Imx targeted mutation (formerly Tnfr1^tm1Imx, p55 deficient) show defects in resistance to intracellular pathogens and are resistant to the lethal effects of LPS administration in conjunction with D-galactosamine. Pulmonary inflammatory responses are diminished in p55 deficient mice. There are also defects in Peyer's patch development, splenic architecture, formation of germinal centers, and liver regeneration. TNFRSF1 deficient mice display increased susceptibility to atherosclerosis when maintained on a high fat diet.
003135	C57BL/6-Tg(TRAMP)8247Ng/J	Repository- Live
	These mice harbor the Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP); PB-Tag Line 8247 transgene. Mice hemizygous for the TRAMP transgene develop progressive forms of prostate cancer with distant site metastasis and exhibit various forms of disease from mild intraepithelial hyperplasia to large multinodular malignant neoplasia. TRAMP hemizygotes can exhibit prostatic epithelial neoplasia (PIN) by 12 weeks of age. Tumors, appearing as well differentiated adenocarcinoma, can arise by 24 weeks of age, mostly in the dorsal and lateral lobes of the prostate. By 30 weeks of age, most hemizygous mice will display evidence of metastatic spread to the lymph nodes and/or lungs, phylloides appearance of some tumors, and seminal vesicle invasion. Tumors exhibit elevated levels of nuclear TRP53 and decreased androgen receptor expression. Note that pure C57BL/6 TRAMP hemizygotes may live to 52 weeks of age or longer. TRAMP mice are also available on a mixed C57BL/6 x FVB/N genet ..... 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-Pawr^tm1Rang/J	Repository- Live
	Mice homozygous for this Par4^flox 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-Hsf1^tm1Ijb/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-Pten^tm1Hwu/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.
010822	CByJ(Cg)-dde/GrsrJ	Repository- Live
	dde homozygotes have disproportionate dwarfing evident at birth by shortened limbs, although the axial skeleton appears normal. The back feet have fused toes. Retinal dysplasia presents as white lines in the retina and electroretinaograms show abnormal rod and cone function. Males are sterile and females are poor breeders and poor mothers, often requiring foster mothers to rear the pups. The lifespan of homozygotes varies with some dying shortly after wean and others surviving to approximately one year of age. Ailments identified in homozygotes include emphysema, stomach polyp, apoptitic cells of the tesis, thyroid cysts, holes in the thoracid chord white matter, and holes in the skeletal muscle fibers in the leg. While it has been proposed that dde may offer a model for Walker-Wardburg syndrome, this has not yet been proven.
007082	CByJ.129S(B6)-Tnf^tm1Gkl/J	Repository- Live
	Mice homozygous for the Tnf^tm1Gkl 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
007079	CByJ.B6-Prf1^tm1Sdz/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.
002932	CPt.C3-Fasl^gld/J	Repository- Live
	Mice homozygous for the Fasl^gld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fas^lpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. 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.
005564	FVB(Cg)-Tg(Ins2-CALM1)26Ove Tg(Cryaa-TAg)1Ove/PneJ	Repository- Live
	Transgenic mice are viable, display small eyes with cataracts and are hyperglycemic within 24 hours of age. S1 Nuclease protection assays indicate expression of calmodulin in the pancreas of 40-60 day old transgenic mice. Immunofluorescence analysis of the pancreas indicates increased levels of camodulin in B-cells of the pancreas. Camodulin fluorescing cells were not detected in the pancreatic acinar cells or any other tissue. Digital image scanning indicates the concentration of camodulin in transgenic B-cells is 5-fold higher than in wild type controls. Pancreatic insulin is 28% of control levels by 15 days of age. Insulin mRNA levels were also reduced in the transgenic animals. Transgenic mice experience hypoalbuminemia, elevated blood pressure, impaired cardiomyocytes and late stage diabetic nephropathy. Although transgenic mice are hyperglycemic within 24 hours of age, they are able to survive over a year without insulin treatment. This stock is useful for studying systemic c ..... For more information please see the full phenotype on the strain data sheet
013591	FVB-Tg(C3-1-TAg)cJeg/JegJ	Repository- Live
	Male transgenic mice develop prostatic hyperplasia in early life that progresses to adenoma or adenocarcinoma in about half of the animals which survive longer 7 months of age. Female animals generally develop mammary intraepithelial neoplasia with similarities to DCIS by 3 months of age with subsequent development of mammary adenocarcinoma by 6 months of age in 100% of the animals. About 10 - 15% of female mice develop lung metastases, although lung metastases from prostate cancer is extremely rare. Bone metastases have not been observed. The phenotype for this transgene has been most extensively studied in the FVB/N background.
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
006825	MRL/MpJ-Fas^lpr/2J	Repository- Live
	The current colony (as of fall 2006) of MRL/MpJ-Fas^lpr/J has experienced a progressive loss of lymphoproliferative phenotype over the past several years, as reported by some of our customers and as observed by our technical staff. This loss of phenotype has been manifested by reduced enlargement of brachial and mesenteric lymph nodes, and poor splenomegaly. Also, the life spans of the mice in the current colony have also been found to be much longer than the historically observed and reported 17 weeks for females and 22 weeks for males. However, genotyping continues to show that all the mice in the colony remain homozygous for the Fas^lpr mutation, and the SNP profile in the region of the mutation on Chromosome 19 has not changed. In an effort to regenerate the desired phenotype, we recovered mice from our embryo archive cryopreserved in 1993. The sixteen-week old cryo-recovered mice have lymph nodes that were 4.5 (females) to 10.1 times (male) la ..... For more information please see the full phenotype on the strain data sheet
008659	NOD.Cg-Rag1^tm1Mom Ins2^Akita Prf1^tm1Sdz/SzJ	Repository- Live
	Like NOD.Cg-Rag1^tm1Mom Prf1^tm1Sdz/J (004848), this strain lacks mature T and B cells. NK cells, although present, lack cytotoxic activity. Both sexes develop spontaneous hyperglycemia as early as three weeks of age, however, the phenotype is predominantly exhibited by males. Pancreatic islets have reduced insulin staining and exhibit an altered morphology with age. Human islet transplantation at doses of 4000 IEQ is successful in returning hyperglycemic males to a euglycemic state. This strain may useful in studies of human islet and beta stem and progenitor cell function.
004848	NOD.Cg-Rag1^tm1Mom Prf1^tm1Sdz/SzJ	Repository- Live
	Mice that are homozygous for both targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities when housed under specific pathogen free conditions. These double homozygote mutant mice have no mature T or B lymphocytes, no detectable NK cell cytotoxic activity, and lack serum immunoglobulin. The number of nucleated spleen cells is significantly reduced in double mutant mice, when compared to the single homozygote, NOD.129S7(B6)-Rag1^tm1Mom/J (Stock No. 003729). Although an increased number of DX5⁺CD122⁺ NK cells are found in the spleens of double mutants, these NK cells have impaired cytotoxic activity. The disruption of Prf1 ablates NK cell cytotoxic activity resulting in increased engraftment levels over that observed with Stock No. 003729. All mutant mice develop thymic lymphomas. This double mutant mouse strain may be useful in studies involving engraftment of human hematolympho ..... For more information please see the full phenotype on the strain data sheet
011121	STOCK Axl^tm1Grl/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When combined with the mutations Tyro3^tm1Grl (Stock No. 007937) and Mertk^tm1Grl (Stock No. 011122), mice exhibit a lymphoproliferative disorder, autoimmunity, increased apoptosis in multiple tissues, blindness, abnormal spermatogenesis and reduced (in females) fertility or infertility (in males). This mutant mouse strain may be useful in studies of autoimmunity, germ cell development and apoptosis.
008882	STOCK Bcl2^tm1Irt/J	Repository- Live
	Mice homozygous for this Bcl2_flox 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 Bcl2_flox mutant mice may be useful in generating conditional mutations for studying apoptosis, mitochondrial permeability, cell survival signaling, cancer, neurological disorders, and immunity. For example, when crossed to a strain expressing Cre recombinase in myeloid cell lineages (see Stock No. For more information please see the full phenotype on the strain data sheet
004339	STOCK Bdnf^tm3Jae/J	Repository- Live
	These mice possess loxP sites on either side of exon 5 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to a strain expressing Cre recombinase under the control of a tetracycline-responsive promoter element (see Stock No. 006224, 006234, 006244) and a strain expressing a tetracycline-controlled activator protein in brain tissues (see Stock No. 003763), this mutant mouse strain may be useful in studies of hippocampal-dependent learning and long-term potentiation. When bred to a strain expressing Cre recombinase in neuronal cells (see Stock No. 003966 for example), this ..... For more information please see the full phenotype on the strain data sheet
009340	STOCK Eif2ak3^tm1Dron/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
006616	129(B6)-Ccni^tm1Jro/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. No protein product from the targeted gene is detected in the tissues tested. Distinct lacZ staining is seen in the glomerulus of podocytes in the kidney. Weaker and variable expression of lacZ is seen in tubular cells. Increased susceptibility to apoptosis both in vitro and in vivo is observed. Following induction of experimental glomerulonephritis, podocyte apoptosis was increased 4-fold in homozygotes, which is associated with dramatically decreased renal function. This mutant mouse strain represents a model that may be useful in studies of apoptosis, renal impairment and glomerulosclerosis.
002497	129-Ntf5^tm1Jae/J	Cryopreserved - Ready for recovery
	Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice lose sensory neurons in the nodose-petrosal and geniculate ganglia. However, they do not show loss of facial nucleus motor neurons, sympathetic neurons of the superior cervical ganglion, or dopaminergic neurons in the substantia nigra.
004301	129-Trp53^tm1Holl/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
002080	129-Trp53^tm1Tyj/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and sarcomas) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
009443	129;B6-Hint1^tm1Ibw/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
002082	129S-Rb1^tm1Tyj/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age.
008652	129S-Trp53^tm2Tyj/J	Cryopreserved - Ready for recovery
	These mice carry a conditional point-mutant allele of the transformation related protein 53 gene (p53R172H; structural mutant homologous to human p53 codon 175). The conditional allele is functionally equivalent to a null mutation. Mice have all the phenotypic issues of p53 knockout mice and therefore have some decreased viability of homozygotes. Cre-mediated recombination leads to deletion of a transcriptional termination sequence (Lox-Stop-Lox) and expression of the oncogenic protein.
008651	129S-Trp53^tm3Tyj/J	Cryopreserved - Ready for recovery
	These mice carry a conditional point-mutant allele of the transformation related protein 53 gene (p53R270H; contact mutant homologous to human p53R273H). The conditional allele is functionally equivalent to a null mutation. Mice have all the phenotypic issues of p53 knockout mice and therefore have some decreased viability of homozygotes. Cre-mediated recombination leads to deletion of a transcriptional termination sequence (Lox-Stop-Lox) and expression of the oncogenic protein.
003082	129S1/SvImJ-Bcl2^tm1Mpin/J	Cryopreserved - Ready for recovery
	Heterozygous mice exhibit expression of beta-galactosidase in populations of large sensory neurons. Mice homozygous for the Bcl2^tm1Mpin 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 Bcl2^tm1Sjk targeted mutation (Stock No. 002265).
003079	B6.129-Calb1^tm1Mpin/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Calb1^tm1Mpin targeted mutation are viable and fertile. Homozygous mutant mice show severe impairment in tests of motor coordination and exhibit ataxia when challenged on a runway. These results suggest functional deficits in cerebellar pathways. Confocal calcium imaging of cerebellar Purkinje cells reveals marked changes of synaptically-evoked postsynaptic calcium transients.
006860	B6.129-Ins2^Akita Bdkrb2^tm1Jfh/SmiJ	Cryopreserved - Ready for recovery
	Mice homozygous for the targeted mutation and heterozygous for the Ins2^Akita spontaneous mutation are viable and fertile. Similar to mice only heterozygous for the Ins2^Akita mutation, the double mutant mice are severely diabetic: their body weights are 70% of wildtype, they consume over 3-fold the normal amount of food, and their urinary output is approximately 20-fold more than that of wildtype mice. Double mutant mice have markedly enlarged kidneys. Urinary albumin excretion in double mutants is almost 4-fold that of either single mutant, and double mutants experience more severe nephropathy than mice that are heterozygous for the Akita mutation alone. Megsin and nephrin expression is markedly increased in double mutant mice when compared to wildtype or to mice with either single mutation alone. By 12 months of age, double mutant mice experience hair loss due to a reduction in hair follicle numbers and thinning of the dermis. Double mutants ..... For more information please see the full phenotype on the strain data sheet
008201	B6.129-Sepp1^tm1Rfb/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
003233	B6.129P2-Fas^tm1Osa/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Tnfrsf6^tm1Osa targeted mutation mice show hyperplasia in the liver in an age-dependent manner. Hepatocytes contain enlarged nuclei characteristic of senescent cells. Lymphadenopathy and splenomegaly in FAS deficient mice are evident at 8 weeks of age. The lymphnodes and spleen become progressively larger, becoming about 10 and 40 times larger than those of wildtype or heterozygotes at 16 weeks of age, respectively.
011026	B6.129S-Bcl2l11^tm3Rjd/J	Cryopreserved - Ready for recovery
	These mice express a mutated Bim (Bcl2l11, BCL2-like 11 (apoptosis facilitator)) protein in which JNK phosphorylation site Thr112 is replaced with Ala. This mutation suppresses JNK-mediated Bim-induced apoptosis. This mutation does not affect expression of Bim in the spleen.
008382	B6.129S1-Map2k6^tm1Flv/J	Cryopreserved - Ready for recovery
	Thymocytes from homozygous targeted mutation mice are partially protected from anti-CD3 mAb-mediated deletion in vivo and in vitro. No obvious abnormalities in the lymphoid compartments have been observed. No expression was detected in splenocytes assayed by Western blot. Homozygotes are viable, fertile and have no breeding difficulties. This strain may be useful in studies of T-cell apoptosis.
004322	B6.129S1-Mapk10^tm1Flv/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. No gene product, mRNA or protein, is detected in brain tissue. Histological and immunohistological examination of the brains of homozygous mutant mice reveal normal development and cellular organization. Mutant mice are resistant to seizures and neuronal apoptosis caused by administration of excitotoxic glutamate-receptor agonist kainic acid. With higher doses of kainic acid, mutant mice display severe tonic-clonic convulsions, but survive the treatment while wildtype mice have 60% mortality. This mutant mouse strain represents a model that may be useful in studies related to neurotoxicity of excitatory amino acids and induced models of Parkinson's disease and stroke.
002248	B6.129S2-Gzmb^tm1Ley/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Gzmb^tm1Ley mutation are viable and fertile. Lymphopoiesis and peripheral lymphoid tissue development is normal. T cell responses to mitogenic (Con A and IL2) and allogeneic (mixed lymphocyte culture) stimulation are unaffected. There is a 10-fold reduction in condensation of chromatin resulting in nuclear crescents and pyknosis when Gzmb^tm1Ley CTL are used as effectors. Thus, activated CTL from homozygous mice are deficient in the early induction of DNA fragmentation and apoptosis in allogeneic target cells. Formerly called Ctla1.
004372	B6.129S2-Mad2l1^tm1Sorg/J	Cryopreserved - Ready for recovery
	Mice that are heterozygous for the Mad2l1^tm1Sorg targeted allele are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Homozygous null mice are embryonic lethal; they fail to develop past embryonic days 6-7 due to catastrophic chromosome missegregation and apoptosis. Histological analysis of heterozygous mutant mice reveal increased germinal center formation in spleen and a higher incidence of lung carcinomas when compared to the wildtype. This mutant mouse strain represents a model that may be useful in studies of the role cell-division checkpoints in tumorogenesis.
002102	B6.129S2-Rb1^tm1Tyj/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. 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 this strain. 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.
002275	B6.129S4-Ntf3^tm1Jae/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Ntf3^tm1Jae targeted mutation are smaller than their normal littermates and most die shortly after birth. Survivors die prior to weaning. They display limb ataxia, an inability to position the limbs properly when attempting to move, and there is a tendency for all four limbs to intermittently stiffen in an extensor posture. Autopsy showed all peripheral ganglia markedly smaller in the mutant. Spinal proprioceptive afferents and their peripheral sense organs are completely absent. Heterozygous mice appear normal; however, the number of muscle spindles in heterozygotes is half that of normal wildtype siblings. There is approximately a 50% reduction in the sympathetic superior cervical ganglion (SCG) neurons caused by excessive apoptosis of sympathetic neuroblasts during neurogenesis.
003541	B6.129S4-Ntf3^tm2Jae/J	Cryopreserved - Ready for recovery
	This strain has loxP sites located on either side of the Ntf3 exon 2. Mice homozygous for this allele are viable, fertile and without behavioral abnormalities. If this strain is crossed with a transgenic strain bearing Cre recombinase, expression of the Ntf3 gene in offspring can be blocked in a tissue-specific manner depending on the promoter controlling the recombinase. Strains under the control of the rat nestin promoter block expression in the central nervous system; see strains 002275 and 002276. When bred to a strain expressing Cre recombinase in skeletal muscle (see Stock No. 007893 for example), this mutant mouse strain may be useful in studies of muscle spindle development
008076	B6.129S4-Traf1^tm1Tsi/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, Bim_s. 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 ..... For more information please see the full phenotype on the strain data sheet
011028	B6.129S6-Bcl2l11^tm1Rjd/J	Cryopreserved - Ready for recovery
	This strain carries a single loxP site in intron 4 of the Bim (Bcl2l11, BCL2-like 11 (apoptosis facilitator)) gene and serves as a control strain for mutant strains Bim3SA (Stock No. 11025) , BimT112 (Stock No. 11026), and BimDeltaEL (Stock No. 11027).
011025	B6.129S6-Bcl2l11^tm2Rjd/J	Cryopreserved - Ready for recovery
	These mice express a mutated Bim (Bcl2l11, BCL2-like 11 (apoptosis facilitator)) protein that lacks three sites of phosphorylation by MAP kinases. Ser55, Sere65, and Ser73 were replaced with Ala. The mutated protein (Bim3SA) is not subject to MAP kinase-induced ubiquitination and degradation. This causes a gain-of-function and increased apoptosis. The mutation does not affect the expression of mRNA in the spleen or thymocytes, as determined by immunoblot.
011027	B6.129S6-Bcl2l11^tm4Rjd/J	Cryopreserved - Ready for recovery
	These targeted mutation mice lack exon 3 of the Bim (Bcl2l11, BCL2-like 11 (apoptosis facilitator)) gene. Alternative splicing to include exon 3 is required for expression of the BimEL isoform, lacking in these mice. Other isoforms, including BimL and BimS, are expressed however. These mice represent a model for the analysis of BimEL loss-of-function.
011021	B6.129S6-Bmf^tm1Rjd/J	Cryopreserved - Ready for recovery
	Homozygous Bmf (BCL2 modifying factor) targeted mutant mice lack expression of its protein which bears only the pro-apoptotic BH3 domain. Expression in brain, spleen, thymus and lymph node tissues is eliminated. Female homozygotes exhibit an imperforate vagina and hydrometrocolpos (22% penetrance). Male and female mice exhibit increased numbers of B cells.
011022	B6.129S6-Bmf^tm2.1Rjd/J	Cryopreserved - Ready for recovery
	These mice express Bmf (BCL2 modifying factor) with a targeted Ser74Ala mutation. They provide a model for defects in JNK(Mapk8)-induced apoptosis mediated by Bmf phosphorylation. This mutation does not affect expression in the spleen.
011023	B6.129S6-Bmf^tm3.1Rjd/J	Cryopreserved - Ready for recovery
	These mice express Bmf (BCL2 modifying factor) with a targeted gain-of-function Ser74Asp mutation in the JNK (Mapk8) phosphorylation site. This mutation does not affect expression in the spleen.
011024	B6.129S6-Bmf^tm4.1Rjd/J	Cryopreserved - Ready for recovery
	This targeted mutation strain may be used as a control for Bmf S74A (see Stock No. 11022) and S74D (see Stock No. 11023) mutant mice in studies of JNK phosphorylation-induced apoptosis.
006236	B6.129S6-Casp6^tm1Flv/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.
004069	B6.129S6-Crebbp^tm1Dli/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Crebbp gene are embryonic lethal, dying at about embryonic day 10.5 exhibiting open neural tube defects. Heterozygous mice though viable and fertile, are subject to early growth retardation, craniofacial abnormalities and often fail to thrive. Heterozygous mice are also subject to age-dependent splenomegaly and irregular hematopoiesis. By three months of age, the abundance of all hematopoietic cell types is significantly diminished. Older mice (10-21 months) are more prone to develop hematologic malignancies than wildtype mice.
007666	B6.129S6-Jmjd6^tm1Flv/J	Cryopreserved - Ready for recovery
	Homozygotes are defective in removing apoptotic cells, which accumulate in the lung and brain, causing abnormal development and neonatal lethality. Approximately 15% of the homozygotes manifest a hyperplastic brain phenotype resembling that of mice deficient in other cell death-associated genes. The absence of expression in homozygous mice has been confirmed by Northern blot analysis of embryonic fibroblasts. This strain may be useful in studies of mammalian organogenesis, respiratory distress syndromes and congenital brain malformations.
004197	B6.129S6-Rac2^tm1Mddw/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
007218	B6.129S6-Trp53^tm2Xu/J	Cryopreserved - Ready for recovery
	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 also develop 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, cancer development and apoptosis. 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.
003246	B6.129S7-Tnfrsf1b^tm1Imx/J	Cryopreserved - Ready for recovery
	Mice homozygous for a Tnfrsf1b^tm1Imx targeted mutation (formerly Tnfr2^tm1Imx, p75 deficient) are viable and fertile. T cells from homozygous mutant mice display defects in activation induced cell death in vitro and dramatically elevated levels of circulating Tnf following systemic challenge with LPS. Pulmonary neutrophil influx is exacerbated in p75 deficient mice in a model of hypersensitivity pneumonitis.
008887	B6.129X1-Bid^tm1Sjk/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-Mcl1^tm2Sjk/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 ..... For more information please see the full phenotype on the strain data sheet
004853	B6.C3-Tg(KRT14-Birc5)19Gros/J	Cryopreserved - Ready for recovery
	These transgenic mice express the mouse baculoviral IAP repeat-containing 5, Birc5 (survivin), gene under the direction of the human keratin 14 promoter. Transgene expression is specific to epidermal and follicular keratinocytes. Mice hemizygous for the transgenic insert are resistant to chemical (DMBA)- and UVB-induced keratinocyte apoptosis in vivo. Although hemizygotes were less susceptible to DMBA-induced papilloma formation, spontaneous papilloma regression was not observed and there was enhanced conversion of papillomas to carcinomas. This mutant mouse strain represents a model that may be useful in studies of keratinocyte apoptosis and skin cancer development.
005089	B6.Cg-Qk^qk-2J/GrsrJ	Cryopreserved - Ready for recovery
	Qk^qk-2J homozygotes display rapid tremors by approximately 2 weeks of age. Histological examination at 3 weeks of age reveals holes in the striatum of the cortex and cerebellum and in the myelin of the spinal cord. Vision and hearing appear normal.
000567	B6.Cg-T^2J +/+ Qk^qk-v/J	Cryopreserved - Ready for recovery
	Mice homozygous for the quaking spontaneous mutation (Qk^qk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS. In this strain the brachyury 2 Jackson mutation (T^2J) is maintained in repulsion with the quaking mutation.
006200	B6.Cg-Tnks2^tm1.1Yjc/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.
000518	B6.Cg-Usp14^ax-J/J	Cryopreserved - Ready for recovery
	The first outward sign of homozygosity for the recessive mutation Usp14^ax-J is an unsteady gait, particularly in the hind quarters, that can be detected by approximately 2 weeks of age. These pups often show difficulty in righting themselves when turned on their backs. They have a rapid tremor that is most apparent when they are active. Extensor paralysis progresses and wasting of the hind quarters ensues until the hind quarters are not functional and the mouse can not sit upright or move except through the use of onlyits front limbs. Although death is premature, viability in the first two to three weeks is not diminished. At 18 days of age these mutants weigh an average of 15% less than wildtype controls and by 45 days this difference is increased such that they weigh 50-60% less than wildtype controls. Homozygotes do not breed. The lumbar vertebrae are slightly shorter than normal with shorter spinous processes and more elongate foramen. These homozygotes have defec ..... For more information please see the full phenotype on the strain data sheet
002319	B6.Cg-Tg(BCL2)22Wehi/J	Cryopreserved - Ready for recovery
	Expression of the human BCL2 transgene is restricted to B cell lineage (no T cell expression) in which it enhances cell survival. Hemizygotes show increased numbers of B lymphocytes, Ig-secreting cells and serum Ig, as well as a heightened and prolonged antibody response to immunization. This phenotype is somewhat greater on the BALB/c than on the C57BL/6 background. Hemizygotes on a mixed B6,SJL background (but not on the BALB/c background) develop autoimmune disease characterized by immune complex glomerulonephritis, anti-nuclear antibodies, lymphadenopathy and myocardial infarction. These mice serve as a robust source for the production of B cells and antibodies. Although mice bearing this allele exhibit a mild increase in spontaneous lymphoma and plasmacytoma occurrence (<10% to 18 months) on a (C57BL/6 x SJL)F2 background, on the BALB/c and C57BL/6 backgrounds tumor incidence is insignificant. When this transgene is crossed with an Emu-myc transgene bearing strain (Stock ..... For more information please see the full phenotype on the strain data sheet
002320	B6.Cg-Tg(BCL2)25Wehi/J	Cryopreserved - Ready for recovery
	Expression of the human BCL2 transgene restricted to the T cell lineage (no B-cell expression). Thymocytes, peripheral T-cells and activated T cells from these mice withstand prolonged culture in the absence of growth factors. Cells are resistant to killing by gamma-radiation, glucocorticoids, ionomycin, PMA and sodium azide but NOT complement, cytotoxic T cells or Fas ligand. Hemizygotes have a normal total T-cell count and thymic involution rate but show an enhanced response to immunization. This transgenic line displays no detectable autoimmunity. These mice serve as a robust source for the production of T-cell lines or hybridomas. Also known as 25Wehi or Emu-bcl-2-25.
002321	B6.Cg-Tg(BCL2)36Wehi/J	Cryopreserved - Ready for recovery
	Expression of the human BCL2 transgene in both T cell and B cell lineages. This transgenic line combines the characteristics of both Tg(BCL2)22Wehi and the Tg(BCL2)25Wehi lines. Hemizygotes show increased numbers of B lymphocytes, Ig-secreting cells and serum Ig, as well as a heightened and prolonged antibody response to immunization. T-cells withstand prolonged culture in the absence of growth factors and are resistant to killing by gamma-radiation, glucocorticoids, ionomycin, PMA and sodium azide but NOT complement, cytotoxic T cells, or Fas ligand. Hemizygotes have a normal total T-cell count and thymic involution rate but show an enhanced response to immunization. These mice serve as a robust source for the production of B-cells, antibodies T-cell lines or hybridomas. Although mice bearing this allele exhibit a mild increase in spontaneous lymphoma and plasmacytoma occurrence (<10% to 18 months) on a (C57BL/6 x SJL)F2 background, on the BALB/c and C57BL/6 backgrounds tumor incid ..... For more information please see the full phenotype on the strain data sheet
008247	B6.Cg-Tg(Ela1-TAg*)289Mjt/J	Cryopreserved - Ready for recovery
	Hemizygous T1-147 transgenic mice (harboring the E1-T147 transgene) are viable and fertile, with high-level expression of an N-terminal, truncated (1-147 amino acid), and mutant (does not express the small t antigen) form of simian virus 40 large T antigen (TAg) directed to pancreatic acinar cells by the rat elastase 1 (Ela1 or E1) upstream control region. Hemizygous T1-147 transgenic mice exhibit pancreatic dysplasia in the embryonic pancreas, with cancer progression after birth to primary pancreatic acinar cell tumor formation (100% penetrance). These mice have microadenomas and acinar cell carcinomas present as early as 10 weeks of age, and become moribund or show clear evidence of abdominal distention around 20-30 weeks of age. T1-147 transgenic mice with large tumors develop metastatic disease to the liver and mesenteric lymph nodes. The donating investigator reports that the cancer phenotype of these T1-147 transgenic mice is identical to that of their similar T1-127 trans ..... For more information please see the full phenotype on the strain data sheet
006329	B6;129-Bax^tm2Sjk Bak1^tm1Thsn/J	Cryopreserved - Ready for recovery
	Mice homozygous for both alleles (Bax^fl 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 ( ..... For more information please see the full phenotype on the strain data sheet
004264	B6;129-Cycs^tm1Wlm/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Cycs^tm1Wlm 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-E2f2^tm1Zubi/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-Eif2ak4^tm1.1Dron/J	Cryopreserved - Ready for recovery
	Mice homozygous for the GCN2.KO4^conditional 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.KO4^conditional 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-Mcl1^tm3Sjk/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 ..... For more information please see the full phenotype on the strain data sheet
006980	B6;129-Trp53^tm2Xu/J	Cryopreserved - Ready for recovery
	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.
008678	B6;129-Ubb^tm1Rrk/J	Cryopreserved - Ready for recovery
	Mice heterozygous for the targeted allele are viable and fertile. This polyubiquitin B (Ubb) mutation is characterized by a GFP-puro^r fusion protein "knock-in" allele that also abolishes endogenous gene function. Direct visualization of GFP fluorescence is observed in ovaries, testes, hypothalamus (arcuate nucleus) and cerebral cortex. Homozygotes have no Ubb mRNA observed in the various tissues tested, and are viable but sterile due to failure of germ cells to progress through meiotic prophase I and hypogonadism. Homozygotes also exhibit a complex metabolic phenotype initially characterized by dysfunction of neurons within the central nervous system accompanied by retarded perinatal growth that progresses to adult-onset obesity linked to selective hypothalamic neurodegeneration. Homozygotes also develop adult-onset hyperleptinemia (but normal levels of circulating glucose and insulin) as a consequence of increased fat content. These Ubb-mutant mice may be useful in studyin ..... For more information please see the full phenotype on the strain data sheet
002265	B6;129S2-Bcl2^tm1Sjk/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Bcl2^tm1Sjk targeted mutation appear normal at birth; however, growth retardation is evident by one week of age with considerable heterogeneity in weight compared to normal wildtype siblings (30% to 90%). There is some pre-weaning loss. Homozygotes succumb to renal failure as a result of polycystic kidney disease. Hematopoiesis, including lymphocyte differentiation is initially normal but the thymus and spleen decrease in size due to increased apoptosis. The coat color of homozygotes turns grey with the second hair follicle cycle.
002247	B6;129S2-Gzmb^tm1Ley/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Gzmb^tm1Ley mutation are viable and fertile. Lymphopoiesis and peripheral lymphoid tissue development is normal. T cell responses to mitogenic (Con A and IL2) and allogeneic (mixed lymphocyte culture) stimulation are unaffected. There is a 10-fold reduction in condensation of chromatin resulting in nuclear crescents and pyknosis when Gzmb^tm1Ley CTL are used as effectors. Thus, activated CTL from homozygous mice are deficient in the early induction of DNA fragmentation and apoptosis in allogeneic target cells. Formerly called Ctla1.
008191	B6;129S2-Trp53^tm1Tyj Nf1^tm1Tyj/J	Cryopreserved - Ready for recovery
	These mice carry Trp53 and Nf1 targeted mutations (in cis) on chromosome 11. These mutations are approximately 10 Mbp apart and may segregate independently of one another. Double homozygotes are embryonic lethal. Double heterozygotes survive an average of five months and exhibit a significant increase in the percentage of soft tissue sarcomas compared with mice of other genotypes (Nf1 +/-, 5%; p53, 57%; Nf1/Trp53 trans, 36%; Nf1/Trp53 cis, 81%). Furthermore, although Nf1/Trp53 trans mice exclusively develop osteo-, fibro-, rhabdomyo-, and hemangiosarcomas, about 30% of tumors from the Nf1/Trp53 cis animals stain positively for S100 (consistent with glial cell origin) and exhibit classic histological features of malignant peripheral nerve sheath tumors (MPNSTs). This strain may be useful in studies of astrocytomas/glioblastomas and tumor suppressor genes.
002103	B6;129S2-Trp53^tm1Tyj/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and sarcomas) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
011031	B6;129S4-Shh^tm1.1Rseg/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile and do not exhibit patterning defects found in Shh null mutants. The R34A and K38A mutations are targeted to the conserved Cardin Weintraub motif and reduce SHH high-affinity proteoglycan binding. Homozygous mice exhibit reduced body weight, small eyes, hypoplasia of the cerebellum and olfactory bulb, reduced precursor cell proliferation in the cerebellar granule cell layer, the spinal cord, the subventricular zone and the hippocampal subgranular layer. This mutant mouse strain may be useful in studies of cell proliferation and SHH-signaling.
012715	B6;129S6-Sun1^tm1Mhan/J	Cryopreserved - Ready for recovery
	Homozygous female and male Sun1 (Sad1 and UNC84 domain containing 1) targeted mutation mice are sterile due to massive apoptotic events that are induced in the gonads. The testes of homozygous males are much smaller than those of wildtype and heterozygous animals. Spermatids and spermatozoa are completely absent and only abnormal spermatocyte-like cells accumulate in some tubules. Ovaries of homozygous females are much smaller than those of their littermates and ovarian follicles are completely absent. No oocytes are detected in day 5 neonatal mice. Docking of chromosomal telomeres at the nuclear envelope is disrupted in both spermatocytes and oocytes of homozygous animals. Efficient chromosomal homolog pairing and synapsis formation in meiosis are disrupted. These mice otherwise develop normally into adults and live for more than a year with no overt differences in physical appearance compared to wildtype littermates. This strain may be useful in studies of meiosis, reproduct ..... For more information please see the full phenotype on the strain data sheet
002968	B6;129S7-Mdm2^tm1Bay/J	Cryopreserved - Ready for recovery
	Mice homozygous for a null mutation in Mdm2 die early in gestation, but are rescued in the absence of Trp53. Mdm2/Trp53-double null mice share the same phenotype as Trp53 mice.
003240	B6;B10.A-H2^a-Tg(H2KmPCC)2939Stoe/J	Cryopreserved - Ready for recovery
	PCC transgenic mice are viable and fertile. Pigeon cytochrome c was engineered for expression in lymphoid tissues of transgenic mice in two forms: one in which it is expressed as a type II plasma membrane protein (mPCC), and a second in which it was targeted to the mitochondria after cytoplasmic synthesis (ePCC). This strain carries the mPCC construct. (For mice carrying the ePCC construct, see strain 003221.) PCC is expressed in thymus, spleen and LPS stimulated B cells in both strains of mice. mRNA expression levels are higher in mPCC mice than in ePCC mice. However, tolerance is induced in the thymus of both strains, regardless of antigen compartmentation.
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
004187	B6;SJL-Tg(MCL1)8Caig/J	Cryopreserved - Ready for recovery
	These transgenic mice express the human MCL1 under the direction of the human MCL1 promoter. Expression of the human MCL1 protein was immunodetectable. Mice hemizygous for the transgene exhibited human MCL1 in bone marrow, lymph node, thymus and spleen (both B- and T-cell populations). Low levels of transgene expression was found in kidney, small intestine, uterus, lung and liver. The majority of the transgenic mice had enlarged spleens, with an increased total splenocyte number (both B- and T-cell). Transgenic mice displayed an increase of myeloid cells relative to lymphoid cells in bone marrow, and an enhanced viability of hematopoietic and lymphoid cells (B, T and myeloid) at immature and mature stages of development. In transgenic mice from 6 to 11 months of age, 27% displayed lymph node enlargement. Transgenic mice had an 88% probability of developing pathologic lymph node disease, and a 60% probability of developing disseminated disease from 6 months to 2 years of a ..... For more information please see the full phenotype on the strain data sheet
000506	B6C3Fe a/a-Qk^qk-v/J	Cryopreserved - Ready for recovery
	Mice homozygous for the quaking spontaneous mutation (Qk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS.
000207	B6C3Fe a/a-Edaradd^cr/J	Cryopreserved - Ready for recovery

000624	B6C3Fe a/a-anx/J	Cryopreserved - Ready for recovery
	Compared with their wildtype siblings, anx/anx homozygotes are characterized by a thinning in the neck and tail at 5 days of age, lower body weight detectable by 9 days of age, and death by 22 days of age on the B6C3H-a/a background. Outbreeding to CAST/Ei modifies the phenotype such that homozygotes live to approximately 5 weeks of age. Evaluation of stomach content shows that anx/anx mice ingest less than their siblings. They show headweaving, body tremors, uncoordinated gait, and hyperactivity along with diminished adipose tissue and reduced serum leptin levels. (Maltais et al., 1984; Johansen et al., 2000) Intraperitoneal injection of 20 day old pups with 5,7-dihydroxytryptamine, a seratonin antagonist, reduces the severity of the neurological phenotypes. Homozygotes have extensive serotonergic hyperinnervation in normal target fields including the hippocampus, frontal cortex, olfactory bulb, and cerebellum, yet they have normal catecholamine ..... For more information please see the full phenotype on the strain data sheet
002622	B6Ei.Cg-pwk/J	Cryopreserved - Ready for recovery
	Homozygous patchwork mice have hairs that are either totally white or totally pigmented, but no diluted coloration of the hair. On a nonagouti background this produces a salt-and-pepper appearance from white hairs juxtaposed with black hairs. This occurs throughout the coat and does not vary by anatomic region. The absence of pigment in the white hairs is due to an absence of melanocytes in the hair follicles of the white hairs; functioning melanocytes are present in the hair follicles of the black hairs. The absence of melanotyes in the follicles of the white hairs results from premature death of melanoblasts during development. TUNEL staining indicates that this melanoblast death is apoptotic and begins around embryonic day 18.5. This suggests that patchwork melanoblasts can survive and function if enough survive, but fail to survive when adequately reduced in number. Analysis of aggregation chimeras between patchwork and albino donors revealed gray hairs at the boundaries bet ..... For more information please see the full phenotype on the strain data sheet
009685	B6N.129S1(Cg)-Tnks^tm1.1Yjc/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).
003221	BALB/cAnBr-Tg(H2KePCC)2403Stoe/J	Cryopreserved - Ready for recovery
	PCC transgenic mice are viable and fertile. Pigeon cytochrome c was engineered for expression in lymphoid tissues of transgenic mice in two forms: one in which it is expressed as a type II plasma membrane protein (mPCC), and a second in which it was targeted to the mitochondria after cytoplasmic synthesis (ePCC). This strain carries the ePCC construct. (For mice carrying the ePCC construct, see strain 003240). PCC is expressed in thymus, spleen and LPS stimulated B cells in both strains of mice. mRNA expression levels are higher in mPCC mice than in ePCC mice. However, tolerance is induced in the thymus of both strains, regardless of antigen compartmentation.
011114	C(TSJ)-Rpl38^Ts/GrsrJ	Cryopreserved - Ready for recovery
	Homozygosity for the tail short mutation causes early embryonic lethality. Heterozygotes are smaller than normal and have variably shortened tails with flexures. Skeletal abnormalities are found with varying expressivity including vertebral fusions, bilateral asymmetry of the length of the humerus and tibia, triphalangy of digit 1 of the forefoot, an extra pair of ribs, and craniofacial defects. Embryonic anemia and reduced fertility are also found.
013539	C.129(B6)-Mapk9^tm1.1Rjd/J	Cryopreserved - Ready for recovery
	In this strain, codon 108 in exon 6 of the endogenous mitogen-activated protein kinase 9 (Mapk9 or c-Jun N-terminal kinase 2 (Jnk2)) gene was mutated from a Methionine (ATG) to a Glycine (GGG). Homozygous mice are viable, fertile, and normal in size. Jnk2 exhibits widespread expression and is involved in the regulation of cellular proliferation, transformation, and apoptosis, and has been implicated in some neurodegenerative diseases, diabetes, and arthritis. Phosphorylation of JNK2 by other MAPK kinases is required for activation. This mutation in JNK2^MG/MG mice expands the size of the ATP pocket of JNK2, increasing sensitivity to inactive small molecule inhibition by PP1, allowing for specific reversible JNK2 inhibition. These mice exhibit a loss of JNK2 signaling while maintaining expression, and show an increase in cellular proliferation, motility, and survival. These mice may be useful for studying MAP kinase signaling pathways, JNK activatio ..... For more information please see the full phenotype on the strain data sheet
002526	C.129S2(B6)-Trp53^tm1Tyj/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and sarcomaa) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors. 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.
008074	C.129S4-Traf1^tm1Tsi/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 ( ..... For more information please see the full phenotype on the strain data sheet
000225	C3FeLe.B6 a/a-Ptpn6^me/J	Cryopreserved - Ready for recovery
	Mice homozygous for the motheaten spontaneous mutation (Ptpn6^me) develop severe autoimmune disease. Characteristics include by granulocytic skin lesions, pneumonitis, impaired humoral and cell-mediated immune responses, decreased responses to T cell and B cell mitogens and deficient cytotoxic T cell and NK cell activity. B cells are LY-1+. Homozygous mutant mice also exhibit hyperimmunoglobulinemia, and express multiple autoantibodies. Macrophages show increased proliferative capacity. In addition to defects in the immune system, motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The lifespan of homozygous motheaten mice is approximately 3 weeks with death attributed to an autoimmune pneumonitis.
002427	C3H/He-Tg(LCKprBCL2)36Sjk/J	Cryopreserved - Ready for recovery
	Hemizygotes carrying the human LCKprBCL2 transgene display normal architecture of all lymphoid organs to 10 weeks of age. They show an increased percentage of CD3^hi/TCR^hi and CD4^-8⁺ thymocytes with a decreased percentage in CD3^lo T cells. CD8⁺ cells and the total percentage of T cells are increased in the spleen and lymph nodes. Mice are resistant to apoptosis induced by glucocorticoid treatment, by radiation treatment, or by anti-CD3 treatment. Malignant lymphoma develop in hemizygotes at approximately 18 months of age.
000784	C3H/HeJ-Fasl^gld/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Fasl^gld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasl^lpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks.
002547	C3Ou.129S2(B6)-Trp53^tm1Tyj/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and sarcomas) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
002546	C3Ou.129S2-Rb1^tm1Tyj/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. 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 this strain. 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.
012371	C57BL/6-Bdkrb2/Bdkrb1^tm1Mki/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 ..... For more information please see the full phenotype on the strain data sheet
011068	C57BL/6-Pmaip1^tm1Ast/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.
010711	C57BL/6-Ptrh2^tm1Eruo/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. This mutant mouse strain may be useful in generating conditional mutations to study anoikis /apoptosis.
008158	C57BL/6-Serpinb9^tm1Arp/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
010825	C57BL/6J-Ptpn6^me/SzJ	Cryopreserved - Ready for recovery
	Mice homozygous for the motheaten spontaneous mutation (Ptpn6^me) develop severe autoimmune disease. Characteristics include granulocytic skin lesions, pneumonitis, impaired humoral and cell-mediated immune responses, decreased responses to T cell and B cell mitogens and deficient cytotoxic T cell and NK cell activity. B cells are LY-1+. Homozygous mutant mice also exhibit hyperimmunoglobulinemia, and express multiple autoantibodies. Macrophages show increased proliferative capacity. In addition to defects in the immune system, motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The lifespan of homozygous motheaten mice is approximately 3 weeks with death attributed to an autoimmune pneumonitis.
002226	C57BL/6J-Tg(Alb1HBV)44Bri/J	Cryopreserved - Ready for recovery
	This strain is referred to as "50-4" or "Tg(Alb1-HBV)Bri44" in the primary reference.
003445	C57BL/6J-Tg(Amy1TAg)354Knw/J	Cryopreserved - Ready for recovery
	C57BL/6-TgN(Amy1TAg)354Knw mice are viable and fertile. They express the SV40 tumor antigen under control of the liver promoter of the mouse alpha-amylase gene (Amy-1^a). This transgenic strain develops malignant tumors of the brown adipose tissue at about 18 months of age. The tumors have high metastatic potential, with metastases commonly occurring in liver, lung, spleen, heart and adrenal glands. Note: This line, '354', contains the same trangene construct as line '501' (Stock No. 003446). Divergent tumor development between these lines is reported to be a result of different transgene integration sites.
003446	C57BL/6J-Tg(Amy1TAg)501Knw/J	Cryopreserved - Ready for recovery
	C57BL/6-TgN(Amy1TAg)501Knw mice are viable and fertile. They express the SV40 tumor antigen under control of the liver promoter of the mouse alpha-amylase gene (Amy1^a). This transgenic strain develops metastatic osteosarcomas at about 13 months of age. Note: This line, '501', contains the same trangene constuct as line '354' (Stock No. 003445). Divergent tumor development between these lines is reported to be a result of different transgene integration sites.
003477	C57BL/6J-Tg(SV)419Bri/J	Cryopreserved - Ready for recovery
	Transgenic mice overexpressing the SV40 enhancer and large-T antigen develop brain tumors in the choroid plexus as well as thymomas and kidney tumors (usually polycystic kidney tumors). The mice die at 24 months of age.
003476	C57BL/6J-Tg(SV)427Bri/J	Cryopreserved - Ready for recovery
	Transgenic mice overexpressing the SV40 enhancer and large-T antigen develop brain tumors in the choroid plexus beginning at seven months of age.
002233	C57BL/6J-Tg(SV)7Bri/J	Cryopreserved - Ready for recovery
	Transgenic mice overexpressing the SV40 enhancer and large-T antigen develop brain tumors in the choroid plexus beginning at three to four months of age.
003189	C57BL/6J-Tg(WAPTAg)3Knw/J	Cryopreserved - Ready for recovery
	Multiparous females of the WapTag3 lineage have hyperplastic mammary glands and occasionally develop mammary adenocarcinomas by 6 months of age. At this age, both males and females of this lineage develop osteosarcomas arising from the ospetrosium and renal adenocarcinomas. WAPTag3 females do not suckle their pups.
003188	C57BL/6J-Tg(WapTAg)1Knw/J	Cryopreserved - Ready for recovery
	Multiparous female mice of the WapTag1 lineage develop mammary adenocarcinomas with an average latency of 13 months. The histopathological phenotype is heterogeneous; papillary, ductal, tubular, and sometimes solid phenotypes are observed. Those tumors with a papillary morphology closely resemble human papillary carcinomas. Tumors arise adjacent to morphologically normal mammary epithelium or hyperplastic lesions. Mammary carcinomas are extremely rare in virgin female mice. Male mice, and those female mice that do not develop mammary carcinoma develop undifferentiated soft tissue sarcomas. Multiparous females of the WapTag3 lineage have hyperplastic mammary glands and occasionally develop mammary adenocarcinomas by 6 months of age. At this age, both males and females of this lineage develop osteosarcomas arising from the os petrosum and renal adenocarcinomas.
002124	C;129S-Ngfr^tm1Jae/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Ngfr^tm1Jae mutation are viable and fertile. They display a decreased cutaneous innervation by calcitonin gene-related peptide- and substance P-immunoreactive sensory fibers. Because of this decreased innervation they develop ulcers on their toes by 4 months of age. The toes become inflamed and progressively infected. There is also reduced sensitivity to heat in the extremities of these mice. Pineal glands lack sympathetic innervation and innervation to sweat glands on foot pads is either reduced or absent. Deficits in the peripheral nervous system were examined by looking at cellular responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. p75-deficient DRG and SCG neurons displayed a 2- to 3-fold decreased sensitivity to NGF at embryonic day 15 and postnatal day 3, respectively. These ages coincide with the peak of naturally occurring cell death.
001876	CBA/KlJms-Fas^lpr-cg/J	Cryopreserved - Ready for recovery
	Mice homozygous for the lymphoproliferation complementing gld spontaneous mutation (Fas^lpr-cg) are viable and fertile. Homozygous mutant mice are characterized by massive lymphadenopathy. Fas^lpr-cg complemented both Fas^lpr and the Fasl^gld mutation in that double heterozygotes with either mutation had lymphadenopathy. However, further crosses showed the new mutation to be an allele at Fas^lpr. Like Fas^lpr and Fasl^gld homozygotes, CBA/KlJms-Fas^lpr-cg homozygotes produce antibodies to some nuclear antigens, such as dsDNA, ssDNA, and poly(ADP-ribose); however, they do not produce anti-erythrocyte antibodies. Although they exhibit lymphoid cell infiltration around blood vessels in lung, liver, and kidney, they lack the immune-complex glomerulonephritis, vasculitis, and interstitial pneumonia characteristic of Fas^lpr homozygotes.
002900	FVB.129S2(B6)-Rb1^tm1Tyj/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation die in utero. Homozygous embryos are morphologically indistinguishable from normal embryos at 12.5 days post coitum, but then die between 13.5 d.p.c and 14.5 d.p.c. Defects are seen in fetal liver hematopoiesis as well as in lens and nervous system development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. 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 this strain. 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.
002899	FVB.129S2(B6)-Trp53^tm1Tyj/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and sarcomas) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
002455	MRL-Fas^lpr.129P2(B6)-B2m^tm1Unc	Cryopreserved - Ready for recovery
	Mice homozygous for both the lymphoproliferation spontaneous mutation (Fas^lpr) and the B2m^tm1Unc targeted mutation are viable and fertile. Class I molecule-deficient B2m^tm1Unc mice were backcrossed to MRL/MpJ-Fas^lpr to study the role of MHC class I molecules in the development of systemic autoimmune disease. Double homozygous mutant mice demonstrated a substantial reduction in CD4^-CD8^- T cells and a diminution of autoimmune disease. Specifically, hypergammaglobulinemia; autoantibodies including anti-DNA, anti-Smith antigen, and rheumatoid factor; and glomerulonephritis were significantly reduced compared to MRL/MpJ-Fas^lpr homozygous mice. Moreover, the pattern of hypergammaglobulinemia suggests that the requirement for MHC class I proteins is restricted temporally to later stages of the disease.
003234	MRL.129P2(B6)-Fas^tm1Osa/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Tnfrsf6^tm1Osa targeted mutation mice show hyperplasia in the liver in an age-dependent manner. Hepatocytes contain enlarged nuclei characteristic of senescent cells. Lymphadenopathy and splenomegaly in FAS deficient mice are evident at 8 weeks of age. The lymphnodes and spleen become progressively larger, becoming about 10 and 40 times larger than those of wildtype or heterozygotes at 16 weeks of age, respectively.
002983	MRL.CBAJms-Fas^lpr-cg/J	Cryopreserved - Ready for recovery
	Mice homozygous for the lymphoproliferation complementing gld spontaneous mutation (Fas^lpr-cg) are viable and fertile. Homozygous mutant mice are characterized by massive lymphadenopathy. Fas^lpr-cg complemented both Fas^lpr and the Fasl^gld mutation in that double heterozygotes with either mutation had lymphadenopathy. However, further crosses showed the new mutation to be an allele at Fas^lpr. Like Fas^lpr and Fasl^gld homozygotes, CBA/KlJms-Fas^lpr-cg homozygotes (Stock No. 001876) produce antibodies to some nuclear antigens, such as dsDNA, ssDNA, and poly(ADP-ribose); however, they do not produce anti-erythrocyte antibodies. Although they exhibit lymphoid cell infiltration around blood vessels in lung, liver, and kidney, they lack the immune-complex glomerulonephritis, vasculitis, and interstitial pneumonia characteristic of Fas^lpr<> ..... For more information please see the full phenotype on the strain data sheet
003896	MRL/MpJ Fas^lpr-Foxq1^sa-J/J	Cryopreserved - Ready for recovery
	MRL/MpJ, and one of its ancestral strains LG/J, display heightened wound healing relative to a panel of other inbred strains. At 4 weeks post-injury, 2mm ear punch wounds healed to 0-0.4mm in MRL/MpJ mice but were still 1.2-1.6mm in C57BL/6 mice. At 15 days post-injury C57BL/6 showed a maximal closure of 30% reduction in ear hole size while MRL showed 85% reduction. The process of healing in MRL/MpJ mice was faster, more complete, showed increased swelling, angiogenesis, fibroblast migration, extracellular matrix deposition, and decreased scarring and fibrosis. Additionally, hair follicles and accompanying sebaceous glands were regenerated to a much greater degree. The other ancestral strains of MRL/MpJ (C3H, C57BL/6, and AKR) do not display this enhanced healing. Bone marrow transplantation showed that the MRL/MpJ healing phenotype did not readily transfer with bone marrow and did remain in the irradiated host tissues. Enhanced healing of cardiac wounds has also been reported in MRL/M ..... For more information please see the full phenotype on the strain data sheet
003505	NOD.B6-Prf1^tm1Sdz/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Prf1^tm1Sdz targeted mutation are viable and fertile. Homozygous mutant mice on an autoimmune type 1 diabetes prone NOD background have normal numbers of CD4^- CD8⁺ T cells in the spleen. CD4^- CD8^- expressing T lymphocytes were also normal. NOD mice show a progressive infilitatraion of mononuclear cells into pancreatic islets beginning around 5 weeks of age. NOD wildtype and PRF1 deficient mice show similar development of insulititis. However, disease incidence was decreased from 77% in wildtype females to 16% in homozygotes. The onset of disease was also delayed from a median of 19 weeks to 39.5 weeks of age. These results show the importance of perforin-mediated cytotoxic T cells in development of autoimmune diabetes. (Kagi et al., 1994; Kagi et al., 1997.)
008223	NOD.C3(B6)-Fasl^gld /LwnJ	Cryopreserved - Ready for recovery
	NOD congenic mice homozygous for the Fasl^gld spontaneous mutation are viable and fertile. The donating investigator reports that homozygous males and females develop lymphadenopathy and systemic autoimmunity beginning at 8 weeks of age, but do not develop diabetes. The Lupus phenotype is accelerated in this strain when compared to the B6-Fasl^gldstrain. This mutant strain may be useful in the studies of apoptosis of lymphocytes, particularly T cells, and in studies of Lupus. 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.
002380	NOD.Cg-Tg(Ins2-TAg)1Lt Prkdc^scid/DvsJ	Cryopreserved - Ready for recovery
	Homozygous NOD/Lt-TgN(RipTag)1Lt-Prkdc^scid mice develop pancreatic beta cell adenomas. They are able to produce 2-3 litters before the insulin secreted from the adenoma makes them too hypoglycemic. Because Prkdc^scid mice lack T-cells the adenomas from this strain are free of the autoimmune T-cells found in the adenomas of NOD/Lt-TgN(RipTag)1Lt mice.
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 ..... For more information please see the full phenotype on the strain data sheet
004519	NOD.MRL(C3)-Fas^lpr/DoiJ	Cryopreserved - Ready for recovery
	NOD mice homozygous for the Tnfrsf6^lpr mutation are deficient in Fas antigen expressed on cell surfaces, and the disruption of the Fas-mediated apoptotic pathway results in severe lymphoma in NOD by 4 months of age. This lymphoma is characterized by an expansion of unusual CD4^-, CD8^-, CD3^low, B220⁺ lymphocytes. Forty week-old NOD mice homozygous for the Tnfrsf6^lpr mutation are completely protected from spontaneous diabetes and insulitis (as compared to 68% diabetes incidence in the control NOD), even after adoptive transfer of lymphocytes from diabetic NOD mice (0% diabetes incidence 12 weeks post transfer, as compared to NOD controls with 85% incidence 12 weeks post transfer). Recent evidence indicates that Fas-deficient NOD mice are resistant to the adoptive transfer because the abnormal subset of CD4^-, CD8^-, CD3^low, B220⁺ lymphocytes ..... For more information please see the full phenotype on the strain data sheet
004922	NOD.MRL-Fas^lpr/Dvs	Cryopreserved - Ready for recovery

002033	NOD/ShiLt-Tg(Ins2-TAg)1Lt/J	Cryopreserved - Ready for recovery
	Homozygous NOD/Lt-Tg(RipTag)1Lt mice develop pancreatic beta cell adenomas. They are able to produce 2-3 litters before the insulin secreted from the adenoma makes them too hypoglycemic.
002979	STOCK Apaf1^fog/J	Cryopreserved - Ready for recovery
	Mice homozygous for the forebrain overgrowth recessive spontaneous mutation (fog) display forebrain, lumbo-sacral, and facial defects most likely due to excessive growth or cellular proliferation ultimately causing abnormalities in neural tube closure. The phenotypes manifest as head bumps and sacral spina bifida and individual mice can have either or both. Three unique features of the mutant are (1) the growth of telencephalon cells into the surrounding mesenchyme, (2) presence of an encephalocele through the midline cleft in some mutants, and (3) dissociation of the tail defect from the caudal neural tube defect. The fog mutation maps to mouse Chromosome 10 near D10Mit262 and D10Mit230.
002267	STOCK Bdnf^tm1Jae/J	Cryopreserved - Ready for recovery
	Mice heterozygous for the Bdnf^tm1Jae mutation show about 1/2 normal levels of Bdnf mRNA, but appear normal. Mice homozygous for the Bdnf^tm1Jae mutation are smaller than normal siblings and most die within the second postnatal week. They have defective coordination of movements and balance. They also exhibit head bobbing and spinning during periods of hyperactivity. There are rare survivors to adulthood. There is excessive degeneration in all sensory ganglia examined, including the vestibular ganglion. Motor neurons are not affected. BDNF can prevent death of central motor neurons and other neurons in vitro, but does not affect these in vivo.
002276	STOCK Ntf3^tm1Jae/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Ntf3^tm1Jae targeted mutation are smaller than their normal littermates and most die shortly after birth. Survivors die prior to weaning. They display limb ataxia, an inability to position the limbs properly when attempting to move, and there is a tendency for all four limbs to intermittently stiffen in an extensor posture. Autopsy showed all peripheral ganglia markedly smaller in the mutant. Spinal proprioceptive afferents and their peripheral sense organs are completely absent. Heterozygous mice appear normal; however, the number of muscle spindles in heterozygotes is half that of normal wildtype siblings. There is approximately a 50% reduction in the sympathetic superior cervical ganglion (SCG) neurons caused by excessive apoptosis of sympathetic neuroblasts during neurogenesis.
006085	STOCK Rad9^tm1Lieb/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 Rom1^tm1Mci/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
017575	STOCK Jup^tm1.1Glr/J	Under Development - Now Accepting Orders
	These PG^flox mutant mice possess loxP sites flanking exon 1 of the junction plakoglobin (Jup) gene. PG is a member of the armadillo protein family found in submembranous plaques of desmosomes and adherens junctions where it directly interacts with cadherins. Mutations in PG have been found in cases of Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC). Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exon 1 deleted in the cre-expressing tissues. For example, when bred to mice carrying the Tg(Myh6-cre/Esr1*)1Jmk transgene (see Stock No. 005657), PG deletion in the adult myocardium after tamoxifen induction results in progressive loss of cardiac myocytes, extensive inflammatory infiltration, fi ..... For more information please see the full phenotype on the strain data sheet

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New Strains Awaiting Transfer

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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.

Stock Number	Strain Name Strain Description	Standard Supply
017729	B6.129-Aurka^tm1.1Tvd/J	Awaiting Transfer from the Donor
These AurA^f mice possess loxP sites flanking exon 2 of the aurora kinase A ( Aurka) gene and have applications in studies related to regulation of mitosis and carcinogenesis.
017601	B6.129-Eif2s1^tm1Rjk/J	Awaiting Transfer from the Donor
Mutation of the EIF2α phosphorylation site results in a lack of translational and transcriptional regulation in the endoplasmic reticulum.
013536	B6.129-Mapk8ip1^tm3.1Rjd/J	Awaiting Transfer from the Donor
In this strain, codon 103 in exon 3 of the endogenous mitogen-activated protein kinase 8 interacting protein 1 (Mapk8ip1 or Jip1) gene is mutated from a Threonine (ACT) to an Alanine (GCC). These mice may be useful for studying MAP kinase signaling pathways and activation of JNK in response to metabolic stress.
017838	B6.129X1(Cg)-Csf3r^tm1Link/J	Awaiting Transfer from the Donor
These Csf3r knockout mice are useful for studying granulopoiesis and hematopoietic stem cell regulation.
017615	C.129(B6)-Trp53bp2^tm1Cdlo/J	Awaiting Transfer from the Donor
Exons 10-17 of the Trp53bp2 gene are disrupted in this strain, abolishing gene function. These mice may be useful for studying tumor development and treatment.
017720	C57BL/6-Sh2d3c^tm1Ebp/J	Awaiting Transfer from the Donor
These Shep1^flox mutant mice possess loxP sites on either side of exon 7 of the Sh2d3c (SH2 domain containing 3C) gene and have applications in studies related to cell adhesion and migration.
017530	STOCK Tg(ACTB-tdTomato,-EGFP)11Luo Trp53^tm1Tyj Nf1^tm1Par/J	Awaiting Transfer from the Donor
The MADM-TG,p53KO,NF1-flox strain may be used as a genetic mosaicism model for different types of cancers when bred to the companion MADAM strain (Stock No. 013749), and to a Cre recombinase expressing strain.
002318	C.Cg-Tg(BCL2)22Wehi/J	On Hold
Expression of the human BCL2 transgene is restricted to B cell lineage (no T cell expression) in which it enhances cell survival. Hemizygotes show increased numbers of B lymphocytes, Ig-secreting cells and serum Ig, as well as a heightened and prolonged antibody response to immunization. This phenotype is somewhat greater on the BALB/c than on the C57BL/6 background. Hemizygotes on a mixed B6,SJL background (but not on the BALB/c background) develop autoimmune disease characterized by immune complex glomerulonephritis, anti-nuclear antibodies, lymphadenopathy and myocardial infarction. These mice serve as a robust source for the production of B cells and antibodies. Although mice bearing this allele exhibit a mild increase in spontaneous lymphoma and plasmacytoma occurrence (<10% to 18 months) on a (C57BL/6 x SJL)F2 background, on the BALB/c and C57BL/6 backgrounds tumor incidence is insignificant. When this transgene is crossed with an Emu-myc transgene bearing strain (Stock ..... For more information please see the full phenotype on the strain data sheet

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New Strains Awaiting Transfer
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The 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.
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.
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JAX® Mice Strains

New Strains Awaiting Transfer

JAX^® Mice Strains