JAX Mice Database - Mutant Strain

Search Criteria: Strain Type is "Mutant Strain"

Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
002052	B6.129P2-Apoe^tm1Unc/J	Level 1
	Mice homozygous for the Apoe^tm1Unc mutation show a marked increase in total plasma cholesterol levels that are unaffected by age or sex. Fatty streaks in the proximal aorta are found at 3 months of age. The lesions increase with age and progress to lesions with less lipid but more elongated cells, typical of a more advanced stage of pre-atherosclerotic lesion. Moderately increased triglyceride levels have been reported in mice with this mutation on a mixed C57BL/6 x 129 genetic background. Aged APOE deficient mice (>17 months) have been shown to develop xanthomatous lesions in the brain consisting mostly of crystalline cholesterol clefts, lipid globules, and foam cells. Smaller xanthomas were seen in the choroid plexus and ventral fornix. Recent studies indicate that APOE deficient mice have altered responses to stress, impaired spatial learning and memory, altered long term potentiation, and synaptic damage.
001303	NOD.CB17-Prkdc^scid/J	Level 1
	Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdc^scid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen ..... For more information please see the full phenotype on the strain data sheet
000465	B10.BR-H2^k H2-T18^a/SgSnJ	Level 2
	Some phenotypic parameters of the B10.BR-H2^k H2-T18^a/SgSnJ mice may have changed recently relative to the strain's previous performance. In order to confirm that a change had occurred and in order to better characterize any differences that may have arisen, animals were recovered from cryo-preserved embryos of the strain (Stock No. 004804) that had been frozen in 1991, and the two lines of B10.BR-H2^k H2-T18^a/SgSnJ were compared. Differences between the two strains have been identified in the CD4/CD8 ratios among several cell populations, and in some dendritic cell populations. As more information is gathered, this website will be updated. Both colonies of B10.BR-H2^k H2-T18^a/SgSnJ (Stock No's. 000465 and 004804) may exhibit white belly ..... For more information please see the full phenotype on the strain data sheet
000457	B10.RIII-H2^r H2-T18^b/(71NS)SnJ	Level 2
	This congenic strain develops chronic and relapsing experimental autoimmune encephalomyelitis (EAE) after immunization with myelin basic protein (MBP). Susceptibility is associated with the major histocompatibility complex (MHC) allele, H2^r, the T cell receptor V β8 chain, and other non MHC loci. This strain also is susceptible to induction of collagen-induced arthritis.
001162	B6(C)-H2-Ab1^bm12/KhEgJ	Level 2

000058	B6(Cg)-Tyr^c-2J/J	Level 2
	Mice homozygous for Tyr^c-2J are phenotypically identical to homozygotes for the classic albino allele. Pigment is completely absent from skin, hair and eyes. While Tyr mRNA levels of Tyr^c-2J homozygotes are similar to those of wild-type mice, there is virtually no tyrosinase protein present (Le Fur et al. 1996). Both homozygote and heterozygote mice are highly resistant to light damage and exhibit retinal degeneration (increased photoreceptor death) into young adulthood. Degeneration does not continue in adult mice (Bravo-Nuevo et al. 2004).
002684	B6.129P2-Nos3^tm1Unc/J	Level 2
	Mice homozygous for the Nos3^tm1Unc targeted mutation are viable and fertile. They have elevated blood pressure that is about 20 mmHg higher than that seen in normal wildtype siblings. They also show a decreased heart rate. Female homozygotes are smaller in body weight than normal wildtype siblings. Hyperglycemic-euglycemic clamp studies demonstrate that homozygotes exhibit insulin resistance at the level of the liver and peripheral tissues.
002287	B6.129S7-Ifng^tm1Ts/J	Level 2
	Mice homozygous for the Ifng^tm1Ts targeted mutation are viable and fertile. Homozygotes appear normal in a "clean" environment but display reduced macrophage function in response to pathogens. Specifically, macrophages show impaired production of antimicrobial products and reduced expression of MHC II antigens. There is also uncontrollable proliferation of splenocytes from homozygotes in response to mitogens and alloantigens and a reduced resting natural killer cell activity.
002207	B6.129S7-Ldlr^tm1Her/J	Level 2
	Mice homozygous for the Ldlr^tm1Her mutation have an elevated serum cholesterol level of 200-400 mg/dl and they have very high levels (>2,000 mg/dl) when fed a high fat diet. Normal serum cholesterol in the mouse is 80-100 mg/dl.
000406	B6.PL-Thy1^a/CyJ	Level 2
	This C57BL/6J congenic strain is useful because it carries the T lymphocyte specific Thy1^a (Thy1.1) allele. Donor T cells can be easily distinguished from recipient T cells by both flow cytometric and histological analysis using appropriate antibodies.
002014	B6.SJL-Ptprc^a Pepc^b/BoyJ	Level 2
	This is a congenic strain used in transplant studies because it carries the differential B cell antigen originally designated Ly5.1 and CD45.1 The current use of the Ptprc designation for Cd45 and Ly5 was based on work in humans following the report of Charbonneau and colleagues who first showed that a protein-tyrosine phosphatase (human placental protein-tyrosine phosphatase 1B) was homologous to the CD45 protein. Ptprc is one of a family of protein-tyrosine phosphatase genes involved in the regulation of cell growth. The b allele is normally present in the BALB and C57BL inbred strains.
000632	B6.V-Lep^ob/J	Level 2
	Mice homozygous for the obese spontaneous mutation, (Lep^ob; commonly referred to as ob or ob/ob), are first recognizable at about four weeks of age. Homozygous mutant mice gain weight rapidly and may reach three times the normal weight of wild-type controls. In addition to obesity, mutant mice exhibit hyperphagia, a diabetes-like syndrome of hyperglycemia, glucose intolerance, elevated plasma insulin, subfertility, impaired wound healing, and an increase in hormone production from both pituitary and adrenal glands. They are also hypometabolic and hypothermic. The obesity is characterized by an increase in both adipocyte number and size. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase in body weight, and probably results from it. Homozygotes have an ab ..... For more information please see the full phenotype on the strain data sheet
000642	BKS.Cg-m +/+ Lepr^db/J	Level 2
	Mice homozygous for the diabetes spontaneous mutation (Lepr^db) become identifiably obese around three to four weeks of age. Elevations of plasma insulin begin at 10 to 14 days of age and of blood sugar at four to eight weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. A number of features are observed on the C57BLKS background, including an uncontrolled rise in blood sugar, severe depletion of the insulin-producing beta-cells of the pancreatic islets, and death by 10 months of age. Exogenous insulin fails to control blood glucose levels and gluconeogenic enzyme activity increases. Peripheral neuropathy and myocardial disease are seen in C57BLKS-Lepr^db homozygotes. Wound healing is delayed, and metabolic efficiency is increased. Female homozygotes exhibit decreased uterine and ovarian weights, decreased ovarian hormone production and hypercytolipidemia in fol ..... For more information please see the full phenotype on the strain data sheet
001801	C57BL/10ScSn-Dmd^mdx/J	Level 2
	The X-linked dystrophin gene (Dmd) is highly expressed in muscle cells and encodes a cytoskeletal protein which localizes to the inner face of the sarcolemma. Dystrophin molecules bind to cytoskeletal F-actin and transmembrane beta-dystroglycan as part of a complex, multimolecular unit that mediates signaling between the intracellular cytoskeleton and the extracellular matrix. The structure and localization also suggest that dystrophin is important for stabilizing the plasma membrane, particularly during contraction. The mdx mutation of Dmd is recessive and heterozygous females are visually indistinguishable from wild-type mice. Females homozygous and males hemizygous for the Dmd^mdx allele retain a normal lifespan and can survive up to two years. Like human patients who suffer from one of the most common neuromuscular diseases, Duchenne muscular dystrophy (DMD), the Dmd^mdx mutants do not express dystrophin and therefore have been ..... For more information please see the full phenotype on the strain data sheet
001011	CBA/CaHN-Btk^xid/J	Level 2
	CBA/CaHN-Btk^xid/J mice have a mutation in the Bruton's tyrosine kinase gene (Btk), and are a model of human X-linked immunodeficiency. They have a B-lymphocyte-specific defect that results in an inability to launch an antibody response to thymus-independent type II antigens, although they do produce normal amounts of antibody in response to some protein antigens. They have low serum IgM and IgG3 and a reduced number of B-cells. Moreover, the B-cells that are present have a reduced surface IgM to IgD ratio, which suggests a disorder in B-cell maturation.
001803	CBySmn.CB17-Prkdc^scid/J	Level 2
	Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdc^scid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen ..... For more information please see the full phenotype on the strain data sheet
000469	B10.A-H2^a H2-T18^a/SgSnJ	Level 3

004804	B10.BR-H2^k H2-T18^a/SgSnJJrep	Level 3
	Some phenotypic parameters of the B10.BR-H2^k H2-T18^a/SgSnJ (Stock No. 000465) mice may have changed recently relative to the strain's previous performance. In order to confirm that a change has occurred and in order to better characterize any differences that may have arisen, animals were recovered from cryopreserved embryos of the strain (B10.BR-H2^k H2-T18^a/SgSnJJrep Stock No. 004804) that had been frozen in 1991, and the two lines of B10.BR-H2^k H2-T18^a/SgSnJ were compared. Differences between the two strains have been identified in the CD4/CD8 ratios among several cell populations, and in some dendritic cell populations. As more information is gathered, this website will be updated. Both colonies of B10.BR-H2^k H2-T18^a/SgSnJ (000465 and 004804) may exhibit whit ..... For more information please see the full phenotype on the strain data sheet
002024	B10.D1-H2^q/SgJ	Level 3

000461	B10.D2-Hc⁰ H2^d H2-T18^c/oSnJ	Level 3
	This congenic strain carries the H2^d haplotype from DBA/2J following six generations of backcrossing to C57BL/10Sn. This strain still carries the Hc⁰ allele from DBA/2J, making them serum C5 deficient. Mice have increased susceptibility to certain pathogens and impaired chemotactic responses of neutrophils. Allograft rejection is prolonged. The following inbred strains are also homozygous for the Hc⁰ allele: A/HeJ (Stock No. 000645), AKR/J (Stock No. 000648), DBA/2J (Stock No. 000671), NOD/LtJ (Stock No. 001976), NZB/BlNJ (Stock No. 000684), and SWR/J (Stock No. 000689).
000463	B10.D2-Hc¹ H2^d H2-T18^c/nSnJ	Level 3

000458	B10.PL-H2^u H2-T18^a/(73NS)SnJ	Level 3

002251	B6.129P2-Il10^tm1Cgn/J	Level 3
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
002609	B6.129P2-Nos2^tm1Lau/J	Level 3
	Mice homozygous for the Nos2^tm1Lau targeted mutation resemble wildtype mice in appearance and histology. Homozygotes are viable and fertile. Unlike Nos1 and Nos3, Nos2 is synthesized de novo in response to a variety of inflammatory stimuli. Induction of Nos2 results in the production of large amounts of nitric oxide (NO) over prolonged periods of time. Excessive NO production has been shown to be beneficial through its antitumor and antimicrobial activities. It is also thought to cause tissue damage and contribute to pathology in a variety of inflammatory conditions including rheumatoid arthritis, inflammatory bowel disease, cardiac allograft rejection, hepatoxicity, myocardial ischemia-reperfusion and septic shock. NO has been demonstrated to play a role in the regulation of blood pressure and hemodynamics. In an LPS-induced model of septic shock, Nos2^tm1Lau homozygotes had virtually no serum NO response, but were ..... For more information please see the full phenotype on the strain data sheet
002288	B6.129S2-Igh-6^tm1Cgn/J	Level 3
	Mice homozygous for the Igh-6^tm1Cgn targeted mutation are viable and fertile. Homozygous mutant mice lack mature B-cells. There is no expression of membrane-bound IgM, although some B-cells may be produced using a C gene other than mu. It may be useful as a model for B-cell immunodeficiency found in humans. Also known as muMT.
002650	B6.129S2-Il6^tm1Kopf/J	Level 3
	Mice homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of lipopolysaccharide (LPS) challenged macrophages. Bioassay and enzyme-linked immunosorbent assay (ELISA) analysis of serum from LPS-challenged homozygotes reveals no detectable protein activity. These interleukin 6 (IL6) mutant mice show defects in responses to various viruses and in inflammatory responses to tissue damage or infection. Of note, IL6-mutant mice may be available on different genetic backgrounds including mixed B6;129S2 (Stock No. 002254), C57BL/6J (Stock No. 002650), and BALB/cByJ.
002216	B6.129S7-Rag1^tm1Mom/J	Level 3
	Mice homozygous for the Rag1^tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdc^scid/Prkdc^scid) (Prkdc^scid mice produce some B cells and IgM). They have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8^-CD4^- and most are IL2 receptor-positive. Neither the spleen nor the bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings.
001913	B6.CB17-Prkdc^scid/SzJ	Level 3
	Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdc^scid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen ..... For more information please see the full phenotype on the strain data sheet
000697	B6.Cg-m +/+ Lepr^db/J	Level 3
	Mice homozygous for the diabetes spontaneous mutation (Lepr^db) become identifiably obese around 3 to 4 weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at 4 to 8 weeks. Affected mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. On the C57BL/6 background there is compensatory hyperplasia of the islet B-cells, and continued hyperinsulinemia throughout an 18- to 20-month life span. Wound healing is delayed and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Lepr^db/+) also have increased metabolic efficiency and can survive a prolonged fast longer than controls. Experiments involving destruction of the ventromedial nucleus of the hypothalamus suggest that Lepr^db may cause a defect in the hypothalamus. Steroid sulfotransferase enzymes, aberrantly expressed in diabet ..... For more information please see the full phenotype on the strain data sheet
000482	B6.MRL-Fas^lpr/J	Level 3
	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
002810	B6CBA-Tg(HDexon1)62Gpb/1J	Level 3
	This line is transgenic for the 5' end of the human HD gene carrying (CAG)115-(CAG)150 repeat expansions. The transgene is ubiquitously expressed. Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. They urinate frequently and exhibit loss of body weight and muscle bulk through the course of the disease. Neurologically they develop Neuronal Intranuclear Inclusions (NII) which contain both the huntingtin and ubiquitin proteins. Previously unknown, these NII have subsequently been identified in human HD patients. The age of onset of HD symptoms is reported to occur between nine and 11 weeks. Commonly known as the "R6/2" strain. Transgenic mice develop hyperglycemia by 12 weeks of age with a corresponding decrease in insulin levels. Pancreatic beta cells devel ..... For more information please see the full phenotype on the strain data sheet
002726	B6SJL-Tg(SOD1*G93A)1Gur/J	Level 3
	Mice hemizygous for this SOD1-G93A (also called G93A-SOD1) transgene are viable and fertile, with transgenic expression of a G93A mutant form of human SOD1. This founder line (often referred to as G1H) is reported to have high transgene copy number. Hemizygotes exhibit a phenotype similar to amyotrophic lateral sclerosis (ALS) in humans; becoming paralyzed in one or more limbs with paralysis due to loss of motor neurons from the spinal cord. Transgenic mice have a life span of approximately 19-23 weeks. These SOD1-G93A (also called G93A-SOD1) transgenic mice may be useful in studying neuromuscular disorders, including Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig's Disease).
003303	C.Cg-Tg(DO11.10)10Dlo/J	Level 3
	Mice carrying the MHC class II restricted rearranged T cell receptor transgene, Tg(DO11.10)10Dlo, react to ovalbumin (OVA) peptide antigen. Intraperitoneal administration of OVA to transgenic mice results in a rapid deletion of the immature CD4⁺ CD8⁺ TCR^lo thymocytes with progression to mature thymocytes. Apoptosis of cortical thymocytes within 20 hours of treatment indicates that apoptosis in important in the development of antigen-induced tolerance. Use of this rearranged T cell receptor transgene requires H2^d background.
000438	C3.SW-H2^b/SnJ	Level 3
	Male mice from the C3.SW-H2^b/SnJ congenic strain are predisposed to maturity-onset impairment of glucose tolerance and hyperinsulinemia with some mice exhibiting hyperglycemia. Symptoms occur much later, between 5 and 8 months of age, than most of the single gene obese and diabetic strains. In addition, male mice are susceptible to the diabetogenic effects of multiple low doses of streptozotocin (40 mg/kg BW.day X 5).
004326	C3Bir.129P2(B6)-Il10^tm1Cgn/Lt	Level 3
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
001927	C57BL/6-Tg(APOA1)1Rub/J	Level 3
	Mice carrying the human apolipoprotein A-I transgene show a two fold increase in total plasma cholesterol levels and greater than a four fold decrease in the levels of mouse apoAI. Homozygous transgenic mice exhibit reduced susceptibility to diet induced fatty streak lesions. Mice homozygous for the transgenic insert are viable, fertile and normal in size. This human apolipoprotein AI transgene is under the control of its natural promoter. The Jackson Laboratory imported mice derived from the founder line A2 as described in Rubin EM, et al., 1991.
002020	C57BL/6J-Apc^Min/J	Level 3
	The C57BL/6J-Apc^Min/J strain is highly susceptible to spontaneous intestinal adenoma formation. Homozygous mice are not viable. It was initially reported that one hundred percent of the C57BL/6J-Apc^Min heterozygous mice raised on a high fat diet develop in excess of 30 adenomas throughout the intestinal tract and most die by 120 days of age. Heterozygotes also develop anemia. (Moser et al., 1990, Su et al., 1992). A small number of C57BL/6J-Apc^Min heterozygous female mice develop mammary tumors. A subsequent publication indicates that this strain may carry a dominant modifier (Mom2) gene that reduces the number and incidence of polyp formation in C57BL/6J-Apc^Min heterozygous mice (Silverman et al., 2002).
002376	FVB/N-Tg(MMTVneu)202Mul/J	Level 3
	Mice homozygous for the MMTVneu (rat) transgene are viable and fertile. There is no phenotypic effect in males. The transgene is expressed at low levels in normal mammary epithelium, salivary gland, and lung. Higher expression is detected in tumor tissue. Focal mammary tumors first appear at 4 months, with a median incidence of 205 days. Both virgin and breeder mice develop tumors. Tumors arise as foci in hyperplastic, dysplastic mammary glands. Seventy-two percent of tumor-bearing mice that live to 8 months or longer develop metastatic disease to the lung. The phenotype of MMTV/unactivated neu transgenic mice differs from that of the MMTV/activated neu produced by Phil Leder, in which multifocal tumors involving the entire mammary epithelium arise.
005557	NOD.Cg-Prkdc^scid Il2rg^tm1Wjl/SzJ	Level 3
	The NOD.Cg-Prkdc^scid Il2rg^tm1Wjl/SzJ mice, commonly known as NOD scid gamma (NSG), do not express the Prkdc gene nor the X-linked Il2rg gene. NSG mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Histological examination of lymphoid tissues reveals absence of lymphoid cells and some cystic structures in the thymus, an absence of follicles in the spleen and markedly diminished celluarity of lymph nodes. NSG mice are deficient in mature lymphocytes, serum Ig is not detectable and natural killer (NK) cell cytotoxic activity is extremely low. These mice are resistant to lymphoma development even after sublethal irradiation treatment. These mutant mice have been shown to readily support engraftment of human CD34⁺ hematopoietic stem cells and represent a superior, long-lived model suitable for studies employing xenotransplantation strategies. Please note that the NSG carries the tr ..... For more information please see the full phenotype on the strain data sheet
000471	A.SW-H2^s H2-T18^b/SnJ	Level 4

004650	B6.129-Tlr2^tm1Kir/J	Level 4
	Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of isolated peritoneal macrophages. Bone marrow derived macrophages do not respond to spirochete (Borrelia burgdorferi) lipoprotein challenge, although non-lipoprotein sonicate stimulates activation. Arthritis due to B. burgdorferi infection, as assessed by rear ankle swelling, is more severe in mutant mice. Tissues of infected mutants can contain up to 100 times higher bacteria levels than those found in wildtype littermates. Elevated spirochete numbers persist 8 weeks post-infection. Homozygotes do not produce TNF-alpha or IL-6, and do not develop symptoms of illness when treated with leptospiral (Leptospira interrogans) lippolysaccharide (LPS). This mutant mouse strain may be useful in studies of host response to bacterial endotoxins such as septic shock.
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.
002087	B6.129P2-B2m^tm1Unc/J	Level 4
	Mice homozygous for the B2m^tm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8⁺ cytotoxic T-cells and under some circumstances a compensatory increase in CD4⁺ cytotoxic T-cells. Immune responses involving CD8⁺ T-cells are severely deficient providing a model to assess the role of CD8⁺ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). 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 ..... For more information please see the full phenotype on the strain data sheet
002118	B6.129P2-Tcrb^tm1Mom/J	Level 4
	Mice homozygous for the Tcrb^tm1Mom targeted mutation are viable and fertile. Mice are deficient in alpha beta T-cell receptor. The total number of cells in the thymus is ~8% that of wildtype; CD4⁺CD8⁺ cells ~6% of wildtype. The proportion of CD4^-CD8^- (IL2 receptor positive) cells increases to about 50% of the total cell number. Alpha beta thymocyte differentiation is blocked at an earlier stage than the Tcra^tm1Mom strain. There is normal differentiation of gamma delta thymocytes. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
002120	B6.129P2-Tcrd^tm1Mom/J	Level 4
	Mice homozygous for the Tcrd^tm1Mom targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4⁺CD8^- and CD4^-CD8⁺ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease.
002693	B6.129S1-Il12b^tm1Jm/J	Level 4
	Mice homozygous for the Il12b^tm1Jmtargeted mutation have a severely restricted ability to mount a TH1 response to in vivo endotoxin administration as evidenced by decreased interferon-gamma production although IL2 (IL-2) production is not compromised. The TH2 response is enhanced as evidenced by increased secretion of IL4 (IL-4). Delayed type hypersensitivity (DTH) responses are reduced. Also see the Il12a-deficient strains (Stock No. 002691 & 002692).
002663	B6.129S2-Cd4^tm1Mak/J	Level 4
	Mice homozygous for the Cd4^tm1Mak targeted mutation have a significant block in CD4⁺ T-cell development; 90% of their circulating T-cells are CD8⁺. Cell surface expression of CD4 protein is not detected on thymocytes and lymph node cells from homozygous mice. Homozygous mutant mice also show a Class II restricted deficit in helper T-cell activity and other T-cell responses. This mutant mouse strain may be useful in studies of T cell development, susceptibility to viral infection and inflammation.
002665	B6.129S2-Cd8a^tm1Mak/J	Level 4
	Mice homozygous for the Cd8a^tm1Mak targeted mutation are deficient in functional cytotoxic T-cells; however, helper T-cell development and function is comparable to normal.
002116	B6.129S2-Tcra^tm1Mom/J	Level 4
	Mice homozygous mice for the Tcra^tm1Mom targeted mutation are viable and fertile. They are deficient in the alpha beta T-cell receptor. The thymus is devoid of CD4⁺CD8^- and CD4^-CD8⁺ cells. Normal numbers of CD4⁺CD8⁺ cells are retained without the IL2 receptor. There are normal numbers of CD4^-CD8^- cells. ~1% of the thymocytes express the gamma delta TCR. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
004434	B6.129S4-Ccl2^tm1Rol/J	Level 4
	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 is detected in lipopolysaccharide (LPS) -stimulated peritoneal macrophages isolated from homozygous mice. The numbers of peritoneal macrophages, Kupffer cell and alveolar macrophages were similar to levels found in wildtype mice. Thioglycollate induced peritonitis results in impaired recruitment of monocytes and macrophages to peritoneal cavity. Cellular recruitment to delayed-type hypersensitivity challenges and secondary granulomata is reduced. This mutant mouse strain represents a model that may be useful in studies related to leukocyte trafficking.
003474	B6.129S4-Gt(ROSA)26Sor^tm1Sor/J	Level 4
	Homozygous mice are viable and fertile, with a loxP-flanked DNA STOP sequence preventing expression of the downstream lacZ gene. When crossed with a cre transgenic strain, the STOP sequence is removed and lacZ is expressed in cells/tissues where cre is expressed. These mutant mice may be used as a Cre-reporter strain; to test the tissue/cellular expression pattern of cre transgenic mice.
002365	B6.129S6-Cybb^tm1Din/J	Level 4
	Chronic granulomatous disease (CGD) is a recessive disorder characterized by a defective phagocyte respiratory burst oxidase, life-threatening pyogenic infections and inflammatory granulomas. Gene targeting was used to generate mice with a null allele of the gene involved in X-linked CGD, which encodes the 91 kD subunit of the oxidase cytochrome b. Affected hemizygous male mice lack phagocyte superoxide production, manifest an increased susceptibility to infection with Staphylococcus aureus and Aspergillus fumigatus and have an altered inflammatory response in thioglycollate peritonitis. This animal model should aid in developing new treatments for CGD and in evaluating the role of phagocyte-derived oxidants in inflammation.
003288	B6.129S7-Ifngr1^tm1Agt/J	Level 4
	Mice homozygous for the Ifngr1^tm1 targeted mutation are viable and fertile with no overt abnormalities. They have normal T cell responses but are defective in natural resistance, evidenced by an increased susceptibility to infection by Listeria monocytogenes and vaccinia virus.
003770	B6.129X1-Trpv1^tm1Jul/J	Level 4
	Mice that are homozygous 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 in dorsal root ganglia. Cultured dorsal root ganglia neurons and skin preparations display no, or markedly attenuated, response to vanilloid compounds, acidified environments or heat (43 degrees C). In intact wild type mice, a subcutaneous injection of vanilloid compounds into the hind paw elicits a pain response with subsequent swelling. No pain response is observed in homozygotes and swelling is noticeably reduced. Also absent is the profound reduction in body temperature following a subcutaneous injection of capsaicin. Homozygotes appear to display robust deficits in thermally evoked pain-related behavior and do not display an aversion to ingesting capsaicin-supplemented drinking water.
001060	B6.C-H2^bm1/ByJ	Level 4

000819	B6.Cg-Foxn1^nu/J	Level 4
	The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1^nu, formerly Hfh11^nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when ..... For more information please see the full phenotype on the strain data sheet
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
002282	BTBR T⁺ tf/J	Level 4
	BTBR mice exhibit a 100% absence of the corpus callosum and a severly reduced hippocampal commissure (Wahlsten D, 2003 Brain Res). This strain exhibits several symptoms of autism including: reduced social interactions, impaired play, low exploratory behavior, unusual vocalizations and high anxiety as compared to other inbred strains (McFarlane HG, 2008, Gen, Brain Behav; Moy SS, 2007, Behav Br Res, Scattoni ML, 2008, PLos).
002286	C.129S7(B6)-Ifng^tm1Ts/J	Level 4
	Mice homozygous for the Ifng^tm1Ts targeted mutation are viable and fertile. Homozygotes appear normal in a "clean" environment but display reduced macrophage function in response to pathogens. Specifically, macrophages show impaired production of antimicrobial products and reduced expression of MHC II antigens. There is also uncontrollable proliferation of splenocytes from homozygotes in response to mitogens and alloantigens and a reduced resting natural killer cell activity.
003145	C.129S7(B6)-Rag1^tm1Mom/J	Level 4
	Mice homozygous for the Rag1^tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdc^scid/Prkdc^scid) (Prkdc^scid mice produce some B cells and IgM). They have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8^-CD4^- and most are IL-2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or wildtype siblings.
002930	C.C3-Tlr4^Lps-d/J	Level 4
	In addition to the Tlr4^Lps-d congenic interval from C3H/HeJ, this strain is also congenic for the wild type tyrosinase allele from C3H/HeJ on chromosome 7. This strain provides a tool for analysis of markers in the region and for examining functional effects of Lps^d on BALB/c, a strain susceptible to infection, neoplastic disease including the induction of plasmacytomas and other tumors.
001131	C3SnSmn.CB17-Prkdc^scid/J	Level 4
	Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdc^scid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depe ..... 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.
003291	C57BL/6-Tg(CAG-EGFP)1Osb/J	Level 4
	This transgenic mouse line with an "enhanced" GFP (EGFP) cDNA under the control of a chicken beta-actin promoter and cytomegalovirus enhancer makes all of the tissues, with the exception of erythrocytes and hair, appear green under excitation light. Note that mice homozygous for this transgene die within the first two weeks following birth.
003475	C57BL/6-Tg(HLA-A2.1)1Enge/J	Level 4
	Homozygous mice carrying the Tg(HLA-A2.1)1Enge transgene express significant quantities of the human class I MHC Ag HLA-A2.1 on cells from the spleen, bone marrow and thymus. Expression of this human class I molecule did not result in expansion of the number of cytotoxic T lymphocyte (CTL) precursors specific for other human class I Ag, HLA-B27 or HLA-A2.2. These transgenic mice have been used to identify hepatitic C virus (HCV) peptides expressing a sequence for HLA-A2.1 binding that are actually recognized by human A2.1-restricted CTLs. Thus, this transgenic model is important for the study of HLA-restricted CTL determinants and in potential development of a vaccine against HCV. *Note: copy number may be variable. Hemizygotes are tested for expression prior to distribution.
003831	C57BL/6-Tg(TcraTcrb)1100Mjb/J	Level 4
	These mice contain transgenic inserts for mouse Tcra-V2 and Tcrb-V5 genes. The transgenic T cell receptor was designed to recognize ovalbumin residues 257-264 in the context of H2K^b and used to study the role of peptides in positive selection and the response of CD8⁺ T cells to antigen. Like most TCR transgenics, these mice are somewhat immunodeficient.
004194	C57BL/6-Tg(TcraTcrb)425Cbn/J	Level 4
	These transgenic mice express the mouse alpha-chain and beta-chain T-cell receptor that pairs with the CD4 coreceptor and is specific for chicken ovalbumin 323-339 in the context of I-A b. Homozygous mice are viable and fertile. In these mice there is a four-fold increase in the CD4 to CD8 peripheral T-cell ratio, and lymph node T-cells demonstrate a dose-dependent proliferative response to the specific ovalbumin ligand. These transgenic mice are useful for studying in vivo T-cell biology such as TCR-ligand interactions, T-cell activation, thymic selection, cross-presentation of antigens, process of thymic selection and central and peripheral T-cell tolerance and induction.
004353	C57BL/6-Tg(UBC-GFP)30Scha/J	Level 4
	These transgenic mice express Green Fluorescent Protein (GFP) under the direction of the human ubiqutin C promoter. Mice homozygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mice express GFP in all tissues examined. Certain hematapoetic cell types display distinct expression levels of GFP, allowing identification of different cells types by FACS analysis. GFP expression is uniform within a cell type lineage and remains constant throughout development. T cells have a 2-fold higher GFP expression than CD19⁺B220⁺ B cells or peripheral blood cells. Leukocytes and red blood cells from homozygous mice fluoresce at approximately twice the level of cells from hemizygous mice. This mutant mouse strain represents a useful tool in studies related to hematopoetic cell differentiation and in vivo tracking of leukocytes.
000051	C57BL/6J-A^w-J/J	Level 4
	Mice are agouti (hairs are black with a subapical yellow band) with a cream or white belly. Females may be used as foster mothers for ovary transplantation of mutations maintained in a/a strains because A^w-J is dominant to the nonagouti a. Since a to A^w is a common mutation, strains possessing this mutation in laboratory stock may not be of a common origin.
000049	C57BL/6J-Kit^W-v/J	Level 4
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone.
000629	C57BL/6J-Lyst^bg-J/J	Level 4
	Mice homozygous for the beige-J spontaneous mutation (Lyst^bg-J) are identical to the original beige mutation (Lyst^bg). The phenotype closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syn ..... For more information please see the full phenotype on the strain data sheet
000711	CByJ.Cg-Foxn1^nu/J	Level 4
	The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1^nu, formerly Hfh11^nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when d ..... For more information please see the full phenotype on the strain data sheet
004104	FVB.Cg-Mmp9^tm1Tvu/J	Level 4
	Mice that are homozygous null for the Mmp9 gene are viable and fertile. No Mmp9 activity is detected in spleen cell lysates. Long bones (tibia, femur) are 10% shorter in homozygous null mice. Histological examination of 3-week-old mice reveals a dramatically lengthened zone of hypertrophic cartilage (6 to 8 times larger vs. wildtype) due to delayed apoptosis, vascularization, and ossification. Subsequent remodeling resolves the condition, resulting in normal appearing bones by 8 weeks of age. Null mice show altered responses to repair of injury in skin, cornea, central nervous system and bone marrow reconstitution, and altered inflammatory responses.
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
002570	NOD.Cg-Prkdc^scid B2m^tm1Unc/J	Level 4
	Mice homozygous for both the B2m^tm1Unc and Prkdc^scid (commonly referred to as scid) mutations on the NOD/ShiLtSz background are class I deficient, B and T cell deficient, C-5 deficient (Hc⁰), and have low NK cells. This strain is an ideal model for xenograft transplantation studies and is an excellent source for insulitis-free, MHC class I-negative islets for transplantation studies.
000692	WB/ReJ Kit^W/J	Level 4
	Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. The lack of germ cells in homozygous mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone.
006616	129(B6)-Ccni^tm1Jro/J	Repository- Live
	Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. No protein product from 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.
004368	129(B6)-Il10^tm1Cgn/J	Repository- Live
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
004337	129(Cg)-Foxg1^tm1(cre)Skm/J	Repository- Live
	This strain expresses Cre recombinase from the endogenous Foxg1 locus. Forkhead box G1 is required for telencephalon development and is expressed specifically in the telencephalon and discrete head structures. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in the telencephalon, anterior optic vesicle (developing lens and retina), otic vesicle, facial and head ectoderm, olfactory epithelium, mid-hindbrain junction and pharyngeal pouches. Mice that are homozygous for the targeted mutation die perinatally. Heterozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain represents a model that may be useful in studies of telencephalic development.
006373	129-Braf^tm1Sva/J	Repository- Live
	Homozygous "floxed B-raf" (B-raf^f/f) mice are viable and fertile with normal B-raf protein expression. When bred to mice expressing Cre recombinase under the control of a promoter of interest, exon 12 of the targeted gene is deleted in the tissue of interest. These mutant mice may be useful in neurological studies such as Ras/Raf and MEK/ERK signaling, synaptic (neural) plasticity, learning and memory. For example, when crossed to a strain expressing Cre recombinase in nervous tissue (see Stock No. 003771), this mutant mouse strain may be useful in studies of neuron development. For example, when crossed to a strain expressing interferon inducible Cre recombinase (see Stock No. 003755), this mutant mouse strain may be useful in studies of extraembryonic mammmalian development.
006365	129-Cckar^tm1Kpn Cckbr^tm1Kpn/J	Repository- Live
	Mice that are homozygous for both of the targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The donating investigator reports that the double mutants have a combined phenotype. No CCKBR receptor function was detected in competition binding assay of brain (cerebral plasma) membranes. When compared to wildtype, gastric pH in homozygotes is higher, pH 5.2, after overnight fast. Histological analysis reveals diminished parietal cell, enterochromaffin-like cell and antral comatostatin-producing D cell densities. An increase in the number of gastrin-producing G cells is observed. There is an increased number of H+, K+ -ATPase immunoreactive negative cells and abnormal distribution of parietal cells in oxyntic glands. Circulating gastrin levels are 10-fold higher in homozygotes. No CCKAR receptor function was detected in competition binding assay of pancreatic membranes. Homozygotes do not exhibit decreased ..... For more information please see the full phenotype on the strain data sheet
006369	129-Cckbr^tm1Kpn/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No receptor function was detected in competition binding assay of brain (cerebral plasma) membranes. When compared to wildtype, gastric pH in homozygotes is higher, pH 5.2, after overnight fast. Histological analysis reveals diminished parietal cell, enterochromaffin-like cell (ECL) and antral comatostatin-producing D cell densities. An increase in the number of gastrin-producing G cells is observed. There is an increased number of H+, K+ -ATPase immunoreactive negative cells and abnormal distribution of parietal cells in oxyntic glands. Circulating gastrin levels are 10-fold higher in homozygotes. Gastric mucosal histamine levels are greatly reduced and histamine-immunoreactive ECL cells are absent. This mutant mouse strain may be useful in studies of hypochlorhydria, hypergastinemia, gastric antral endocrine regulation, and ..... For more information please see the full phenotype on the strain data sheet
002292	129-Gt(ROSA)26Sor/J	Repository- Live
	Mice heterozygous or homozygous for the ROSA26 retroviral insertion display no distinguishing phenotype. lacZ is expressed in all tissues of the developing embryo and in most tissues of the adult mouse. Formerly named TgR(ROSA26)26Sor.
006053	129-Gt(ROSA)26Sor^tm1Luo/J	Repository- Live
	MADM-GG mice are viable with no gross behavioral or observable abnormalities. Regardless of Cre-recombination, these mice express EGFP as their N- and C-terminal coding sequences are interrupted by the beta-actin intron in-frame. High EGFP expression in every cell can be visualized in vivo and in fixed samples. These mutant mice are a control EGFP-expressing strain for use with MADM (mosaic analysis with double markers) mice (see Stock No. 006041 [MADM-GR (EGFP/Dsred2)] and Stock No. 006067 [MADM-RG (Dsred2/EGFP)]). Using the MADM system, a researcher can generate genetic mosaics in which an individual organism contains somatic cells of different genotypes. This allows the researcher to ascertain lineal relationships and pleiotropic gene function in multicellular organisms. These mice may also be useful in studies of cell differentiation and mitosis. Mice harbor ..... For more information please see the full phenotype on the strain data sheet
002702	129-Ifngr1^tm1Agt/J	Repository- Live
	Mice homozygous for the Ifngr1^tm1Agt targeted mutation are viable and fertile with no overt abnormalities. They have normal T cell responses but are defective in natural resistance, evidenced by an increased susceptibility to infection by Listeria monocytogenes; and vaccinia virus.
008349	129-Ptger3^tm1Csml/J	Repository- Live

004293	129-Shh^tm2Amc/J	Repository- Live
	Mice that are homozygous for the Shh^tm2Amc targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This conditional mutant contains two loxP sites flanking exon 2 of the targeted allele. Cre-mediated recombination excises exon 2 and some surrounding intronic sequence, generating a null allele. When the conditional mutant is crossed with a ubiquitously-expressing Cre recombinase carrier to remove Shh activity in the early embryo, the resulting phenotype resembles the Shh null mutation. These conditional mutant mice may be mated to strains expressing Cre recombinase to study the effects of temporal and tissue-specific ablation of the targeted allele. This mutant mouse strain represents a model that may be useful in studies of developmental defects resulting from disruption of Shh-dependent pathways. When bred to a strain expressing Cre recombinase under the control of a tet ..... For more information please see the full phenotype on the strain data sheet
003328	129-Tg(Prm-cre)58Og/J	Repository- Live
	Mice homozygous for this PrmCre transgene are viable and fertile. Embryonic stem cells containing recombinase transgenes that are expressed in the male germ line, but not in other tissues or in the embryonic stem cells themselves, substantially simplify the production of subtle or conditional mutations in mice. This strain shows that transgenes comprised of the mouse protamine 1 promoter and the Cre recombinase coding sequence mediate the efficient recombination of a cre target transgene in the male germ line, but not in other tissues. This system can be used for reducing the time, effort, and resources required to produce homologously recombined alleles in mice that have been secondarily rearranged by site-specific recombinase.
006500	129.NOD-(D17Mit175-H2)/J	Repository- Live
	129S1.NOD-H2^g7 congenic mice are viable, fertile, normal in size, do not display any gross physical or behavioral abnormalities and are diabetes free. Because targeted mutations frequently are made using 129 ES cells, this strain may be useful for identifying Idds in 129 strains.
007175	129S-Cyp4a14^tm1Jhc/J	Repository- Live
	Mice homozygous for this "Cyp 4a14" mutant allele are viable and fertile. Homozygous deficiency of the targeted gene leads to spontaneous hypertension (more severe in males) that is androgen-sensitive. Homozygotes also exhibit other interrelated metabolic and regulatory effects; increased renal vascular resistance, impaired renal hemodynamics, elevated plasma androgens (5a-dihydrotestosterone (DHT) and testosterone), upregulated Cyp4a12 gene expression, and increased formation of prohypertensive 20-HETE. These "Cyp 4a14" mutant mice may be useful studying kidney function and metabolism, cardiovascular physiology, hypertension, and the relationships between blood pressure, sex hormones, and p450 ω-hydroxylases.
007664	129S-Efnb1^tm1Sor/J	Repository- Live
	These mice possess loxP sites flanking exons 2 through 5 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 2 through 5 deleted in the cre-expressing tissue(s). These Efnb1 conditional mutant mice may be useful in studying cellular signaling in embryonic development and adult mice; specifically receptor tyrosine kinases. For example, when crossed to a strain expressing Cre recombinase in epiblast-derived tissues (see Stock No. 003755), this mutant mouse strain may be useful in embryogenesis research.
007205	129S-Myo1e^{Gt(ROSA)74Sor}/J	Repository- Live
	Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mice are anemic (low hemoglobin concentration, red blood cell count, hematocrit). These mice also exhibit polychromasia (abnormally high number of immature blood cells). Homozygotes occur at lower than Mendelian ratio (15%). Although homozygotes are fertile, pregnancy is occasionally lethal for homozygous females. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Myo1e-mutant mice may be useful in studying vascular development, hematopoiesis and cellular signaling during development and in adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation.
004545	129S-Npy^tm1Rpa/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 brain or adrenal gland tissue. Beta-galactosidase activity assays and in situ hybridization demonstrate similar expression patterns for the lacZ gene and the endogenous wildtype gene. Spontaneous seizures are exhibited by some mice at age 6 to 8 weeks. Homozygous mice are susceptible to seizures induced by GABA antagonist treatment. Mutant mice have an increased sensitivity to leptin treatment which results in a greater initial reduction of food intake and weight loss when compared to wildtype mice. This mutant mouse strain may be useful in studies related to the role of neuropeptide Y in obesity.
007587	129S-Park2^tm1Rpa/J	Repository- Live
	Mice carrying this mutation are viable, fertile, and display no apparent defects or abnormalities. Mutations in the human homolog of this gene are associated with autosomal juvenile parkinsonism, a heritable form of Parkinson's disease.
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.
007846	129S-Pdgfrb^tm1Sor/J	Repository- Live
	One third of homozygous embryos, aged E16 to E18.5, exhibit purpura and edema with some embryos in this group dying at this stage. Homozygous embryos delivered by Caesarean section at E18.5 die within minutes. Homozygotes exhibit anemia, elevated numbers of nucleated erythrocytes, polychromasia, irregularly shaped mature erythrocytes (anisocytosis), and hemorrhaging. Glomerular capillary tufts are absent and the capsule space is filled with blood cells. No gene product (protein) is detected by Western blot analysis of total protein. A truncated transcript presumed to be due to exon skipping is detected by Northern blot analysis. This mutant mouse strain may be useful in studies of hematopoiesis, kidney development and and cellular signaling during development.
007005	129S-Scg5^tm1Led/J	Repository- Live
	The following text reflects the phenotype reported by the donating investigator on a "129Sv" genetic background (probably "Taconic Sv129" (129S6/SvEvJ)). While heterozygotes are viable and fertile, mice homozygous for this mutation (7B2-null) die in prepubertal or pubertal ages (5 weeks) with severe cardio-respiratory failure, convulsions, and hypothermia. No transcripts are detected in brain tissue from the targeted gene. 7B2 null mice are unable to make an active form of prohormone convertase 2 (PC2) and have high circulating corticosterone. Homozygotes on the 129S genetic background exhibit Cushing's-like disease pathologies of liver, pancreas, and pituitary; including pituitary-dependent hyperadrenocorticosteronism, severe hypoglycemia, hyperproinsulinemia, adrenal hypertrophy, pituitary hypotrophy, and altered islet cell morphology. 7B2-null mice develop the disease from intermediate lobe ACTH hypersecretion (rather than from pituitary adenomas). Other abnormalities include thinni ..... For more information please see the full phenotype on the strain data sheet
007209	129S-Schip1^{Gt(ROSA)77Sor}/J	Repository- Live
	Homozygotes occur at lower than Mendelian ratio (19%), and 20% die by age 1 week. Heterozygotes viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit abnormalities in neural crest-derived and thoracic skeleton development, and palate bone fusion. These Schip1-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation.
006661	129S.B6-Tg(KRT14-RAF1/ESR1)1Pkha/J	Repository- Live
	Mice hemizygous for this "K14-Raf:ER" transgene are viable and fertile. Inducible expression of the human Raf1(Raf-1 [DD]):estrogen receptor (ER) fusion protein is observed in the epidermis following topical application of 4-hydroxytamoxifen (4OHT). Prolonged (4 weeks) induction of human Raf-1[DD] activity promotes the undifferentiated, proliferative phenotypic characteristics observed in epidermal cancer; including hyperplasia, increased mitotic index, decreased expression of differentiation markers and increased expression of beta-1 and beta-4 integrin subunits. Raf-1[DD]-induced skin abnormalities are entirely reversed within one month after 4OHT cessation. These mice have a similar 4OHT-inducible skin phenotype as the transgenic mice expressing human H-Ras^G12V (Stock No. 006403) or human Mek1^R4F (Stock No. 006822), and may be useful in studies of the ..... For more information please see the full phenotype on the strain data sheet
006409	129S1.129(Cg)-Tg(APPSw)40Btla/J	Repository- Live
	These R1.40 transgenic mice express all mRNA and protein isoforms of the human amyloid beta (A4) precursor protein APP containing the Familial Alzheimer's Disease (FAD) Swedish mutation K670N/M671L. Transgene expression (mRNA and full-length protein) is 2 to 3 fold the wild-type mouse App expression level in the hemizygous state in brain tissue as revealed by RT-PCR and Western Blot analysis. Transgene expression pattern mimics wild-type mouse gene expression patterns. These R1.40 transgenic mice may be useful in studying the pathogenesis of Familial Alzheimer's Disease and possible therapeutic treatments. Of note, this is one of two 129S1/SvImJ congenic R1.40 transgenic strains (129S1-R1.40) segregating for transgene copy number; one with lower trangene copy number (Stock No. 006409) and one with higher transgene copy number (Stock No. 008609). At the ..... For more information please see the full phenotype on the strain data sheet
007859	129S1/Sv-Sufu^tm1Aeb/J	Repository- Live
	Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null mice have an embryonic lethal phenotype, failing to develop past embryonic days 9.5 to 10. No gene product (protein) is detected by Western blot analysis. Truncated gene product (mRNA) is detected by Northern blot analysis. Homozygous embryos at 9 to 9.5 embryonic day exhibit growth retardation, incomplete embryonic turning, abnormal somite development, abnormal heart looping (due to abnormal left-right axial patterning) and open neural tubes. This mutant mouse strain may be useful in studies of the Hedgehog signaling pathway and embryonic development.
000395	129S1/Sv-Vsx2^or-J/J	Repository- Live

003580	129S4/SvJae-Ppara^tm1Gonz/J	Repository- Live
	Mice homozygous for the Ppara^tm1Gonz targeted mutation are viable, fertile and appear normal in appearance and behavior. An altered response to a group of compounds (peroxisome proliferators) that induce peroxisome proliferation and hapatocarcinogenesis is observed. No peroxisome proliferation response is detected when these mice are challenged with classical peroxisome proliferators. Typically, such a response includes hepatomegaly, peroxisome proliferation and transcriptional activation of a set of target enzyme genes. Accumulation of lipid droplets observed in liver tissue suggests that Ppara is involved in maintaining the homeostasis of hepatic lipid metabolism.
003946	129S4/SvJaeSor-Gt(ROSA)26Sor^tm1(FLP1)Dym/J	Repository- Live
	This knock-in strain expresses a variant of the Saccharomyces cerevisiae FLP1 recombinase gene under the direction of the Gt(ROSA)26Sor promoter. The FLPe recombinase variant exhibits enhanced thermostability with recombination activity being four-fold and ten-fold that of wild type FLP at 37C and 40C, respectively. Homozygous mice for the knock-in allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Gt(ROSA)26Sor promoter drives expression in a constitutive fashion from preimplantation onward. Extensive target gene recombination can be achieved in most tissue types, including cells of the developing germ line. This mutant strain is suitable for use as a deleter strain and serves as a source of FLP1-expressing primary cell lines.
007689	129S4/SvJaeSor-Gt(ROSA)26Sor^{tm4(attB/attP)Sor}/J	Repository- Live
	These mutant mice contain a beta-galactosidase gene, lacZ, inserted into the Gt(ROSA)26Sor locus. Expression of the lacZ gene is blocked by a attB and attP site flanked STOP fragment placed between the lacZ sequence and the Gt(ROSA)26Sor promoter. This strain serves as a reporter strain, with successful PhiC31o recombination being indicated by beta-galactosidase expression in PhiC31o-expressing tissues. Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
002753	129S6/SvEvTac-Atm^tm1Awb/J	Repository- Live
	Mice homozygous for the Atm^tm1Awb targeted mutation display many of the characteristics of ataxia telangiectasia, including growth retardation, neurologic dysfunction, infertility, defects in T lymphocyte maturation, and extreme sensitivity to gamma-irradiation. Most homozygotes develop thymic lymphoma between 2 and 4 months of age. Heterozygous mice display no abnormalities through eight months of age.
002211	129S7/SvEvBrd-Mt1^tm1Bri Mt2^tm1Bri/J	Repository- Live
	Mice homozygous for the Mt1^tm1Bri Mt2^tm1Bri mutation are viable and fertile. They show an increased sensitivity to hepatic poisoning by cadmium. Most homozygous mice given daily injections of cadmium die within 4 days, with most of the males dying within 2 days.
006555	A.129(B6)-Tg(APPSw)40Btla/J	Repository- Live
	These R1.40 transgenic mice express all mRNA and protein isoforms of the human amyloid beta (A4) precursor protein APP containing the Familial Alzheimer's Disease (FAD) Swedish mutation K670N/M671L. Transgene expression (mRNA and full-length protein) is 2 to 3 fold the endogenous mouse App expression level in the hemizygous state in brain tissue as revealed by RT-PCR and Western Blot analysis. Transgene expression pattern mimics endogenous mouse gene expression patterns. The donating investigator reports increased mortality in young homozygous animals (higher incidence in females). These R1.40 transgenic mice may be useful in studying the pathogenesis of Familial Alzheimer's Disease and possible therapeutic treatments. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could va ..... For more information please see the full phenotype on the strain data sheet
002565	A.B6-Tyr⁺/J	Repository- Live

001649	A.BY H2^bc H2-T18^f/SnJ-Dstn^corn1/J	Repository- Live
	Mice homozygous for the recessive Dstn^corn1 mutation have abnormally proliferative basal corneal epithelial cells. Focal areas of corneal epithelial hyperplasia are found by one week of age, and neovascularization is found by 14 days of age when the eyes open. This neovascularization, which progresses during the first two months of age, is not found in mice homozygous for the Dstn^corn-2J allele (which is a point mutation leading to a change in a single amino acid residue). In both mutants the corneal epithelial cells show increased levels and altered organizational pattern of filamentous actin. The areas of thickened cortical epithelia yield a roughened, opaque corneal surface. At 4 weeks of age in Dstn^corn1 homozygotes, expression of keratin 14 and involucrin extend into the suprabasal layer in the areas of hyperplastic corneal epithelia. There is also an increase in the levels of expression of cofilin 1, lumican and kerat ..... For more information please see the full phenotype on the strain data sheet
000140	A.BY-H2^bc H2-T18^f/SnJ	Repository- Live
	Dr. George Snell, of The Jackson Laboratory, created this H2-congenic strain by crossing of mice of a non-inbred stock carrying the brachyury mutation (and therefore called BY) to mice of the A/Lilly inbred strain, then repeatedly backcrossing to the latter strain mice that proved resistant to A-derived tumors. A/Lilly was a subline of strain A that Snell obtained from the Lilly Company after the 1947 fire at The Jackson Laboratory; when it was learned that this strain was contaminated, Snell performed a single additional backcross to the A/WySn subline, taking it to generation N11 (Rodgers 2004; Klein 1989). The BY stock apparently was obtained from Dr. Dobrovolskaia-Zavadskaia, who described a short-tailed mouse sired by a gonadally-irradiated male; she believed the brachyury mutation not to have been caused by the radiation, but to have been a pre-existing spontaneous mutation (Dobrovoskaya-Zajadkaya 1927; Rodgers 2004). In a subsequent article, she described short tailed (b ..... For more information please see the full phenotype on the strain data sheet
006246	A/J-sunk/J	Repository- Live

005136	A/WySnJ-ctl/J	Repository- Live
	Mice homozygous for the ctl mutation are easily recognizable at birth by their curly or bent tails.
002250	B10.129P2(B6)-Il10^tm1Cgn/J	Repository- Live
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
002249	B10.129S2(B6)-Igh-6^tm1Cgn/J	Repository- Live
	Mice homozygous for the Igh-6^tm1Cgn targeted mutation are viable and fertile. Homozygous mutant mice lack mature B-cells. There is no expression of membrane-bound IgM, although some B-cells may be produced using a C gene other than mu. It may be useful as a model for B-cell immunodeficiency found in humans. Also know as muMT.
000468	B10.A-H2^h2/(2R)SgSnJ	Repository- Live

006102	B10.Cg-H2^k Tg(Il2/NFAT-luc)83Rinc/J	Repository- Live
	Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator reports that homozygous females in their colony are subfertile. These transgenic mice express luciferase under the regulation of the Il2 minimal promoter and 3 binding sites for the NFAT inducible nuclear factor involved in the regulation of interleukin-2 and other cytokine expression. Luciferase activity in these transgenic mice identifies NFAT-mediated transcription. These NFAT-luc transgenic mice may be useful be useful as reporters for NFAT-mediated expression during thymocyte development and selection and in studies related to signal transduction, apoptosis, and transcriptional regulation.
006100	B10.Cg-H2^k Tg(NFkB/Fos-luc)26Rinc/J	Repository- Live
	Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Mutant mice have the luciferase gene driven by two copies of the NF-kappaB (NF-kB or NFkB) regulatory element. The presence of nuclear NF-kB DNA binding activity (as detected by electrophoretic mobility shift assay [EMSA]) is consistent with luciferase reporter activity; these reporter mice identify NF-kB transcriptional activity in any tissue. These transgenic mice may be useful in studies of immunology, cellular signaling, signal transduction, apoptosis, and transcription factor function.
002761	B10.Cg-Tg(TcrAND)53Hed/J	Repository- Live
	Mice carrying the (TcrAND)53Hed transgene express a rearranged T-cell receptor (V alpha 11.1 / V beta 3) specific for the carboxy-terminal fragment of pigeon cytochrome c and the E^k molecule, resulting in a major subpopulation of T cells restricted to class II MHC proteins. There are an abnormally high percentage of mature CD4⁺CD8^- cells. The peripheral T-cell population is almost exclusively CD4⁺. The original C57BL/6 and SJL mixed background strain (Stock number 002408) was backcrossed to C57BL/10 to create this strain. Both strains are fixed for H2^b. Because C57BL/10 mice do not express I-E, this mouse must be crossed to a strain that expresses I-E^k to study the interaction of the transgenic T-cell receptor with the pigeon cytochrome c antigen. The lack of I-E^k expression in the transgenic line allows it to serve as a universal donor for crossing the transgene onto other strains expressing I-E^k< > ..... For more information please see the full phenotype on the strain data sheet
001953	B10.S-H2^s/SgMcdJ	Repository- Live

006963	B6(101)-Mdh1^am1H/LvtJ	Repository- Live
	Homozygotes die at approximately embryonic day 17.5 (E17.5), but heterozygotes are viable and fertile. Homozygous embryos are nearly colorless, are approximately half the size of heterozygous and wildtype littermates, and show altered or delayed brain/body development. There may be a vascular defect. Decreased expression of this gene has previously been implicated with cases of schizophrenia.
004684	B6(129P2) Nos2^tm1Lau-chtl/J	Repository- Live
	This mutant has an overall lighter coat, tail and ears than a black +/+ control. Both males and females breed and it is maintained as a homozygous stock.
005559	B6(129S4)-Hps6^ru-7J/J	Repository- Live

005379	B6(A)-Rpe65^rd12/J	Repository- Live

005071	B6(Cg)-Dct^Slt-lt3J/J	Repository- Live
	Dct^Slt-lt3J heterozygous mice are diluted to a dark brown and homozygous mice are diluted to a light brown.
008149	B6(Cg)-Snord116^tm1.1Uta/J	Repository- Live
	Mice homozygous for this Snord116del (1-loxP or knockout) allele are viable and fertile. As the Snord116 gene cluster is imprinted and expressed only from the paternal allele, mice with paternal inheritance of the deletion lack expression of the targeted Snord116 small nucleolar RNAs (snoRNAs) gene cluster in brain tissues. Similarly, paternal transmission of the mutant allele is required to obtain the mutant phenotype in offspring. Affected heterozygotes (paternal deleted/maternal wildtype) recapitulate a subset of Prader-Willi syndrome (PWS) characteristics, including early-onset postnatal growth retardation, delayed sexual maturation, increased anxiety, motor learning deficit and hyperphagia (but not obesity). Other reported abnormalities include altered metabolic fuel usage, prolonged meal time, and increased levels of circulating ghrelin. These Snord116del mice may be useful in studying growth and feeding regulation, mechanisms of obesity, and pa ..... For more information please see the full phenotype on the strain data sheet
008118	B6(Cg)-Snord116^tm1Uta/J	Repository- Live
	Mice homozygous for this 2-loxP (floxed) allele are viable and fertile, with loxP sites flanking the Snord116 small nucleolar RNAs (snoRNAs) gene cluster. When bred to mice that express Cre recombinase, the resulting offspring will have this gene cluster deleted in the cre-expressing tissue(s). Because the Snord116 gene cluster is imprinted and only expressed from the paternal allele, breeding 2-loxP males with cre-expressing females may be required to generate deleted offspring with the knockout phenotype. The donating investigator reports that the distance between the two loxP sites (~140 kb) may reduce the recombination efficiency in somatic cells. As deletions of the Snord116 cluster are associated with Prader-Willi syndrome (PWS), mice carrying the 2-loxP (floxed) allele may be useful in generating conditional mutations for studying the role of Snord116 in growth and feeding regulation, mechanisms of obesity, and patho ..... For more information please see the full phenotype on the strain data sheet
007212	B6(Cg)-Tnfrsf13c^tm1Mass/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 RT-PCR or FACS analysis of spleen tissue and cells, respectively. Homozygotes have reduced numbers of mature recirculating bone marrow and splenic B cells. B cell development is arrested between the transitional IgM+ (T1 + T2) and IgM^low (T3) stages. Homozygotes exhibit diminished antigen-specific antibody responses with decreased levels of IgM, IgG1, IgG2, IgG2b and IgG3. This mutant mouse strain may be useful in studies of B cell development and differentiation.
006111	B6(Cg)-Ush1g^js-2J/J	Repository- Live

004640	B6(MOR)-Tmhs^hscy/J	Repository- Live
	Mice homozygous for the Tmhs^hscy mutation circle rapidly, shake their heads from side to side, fail to swim, and are congenitally deaf. Although hair cells appear normal at birth, they degenerate. At 4 months of age, degeneration of the organ of Corti is also found, more pronounced in the basal region of the cochlea than the apex, with loss of inner and outer hair cells and decreased spiral ganglia (Longo-Guess et al., 2005).
005717	B6(NOD) H2^g7-Sostdc1^shk/J	Repository- Live

005999	B6(SJL)-Tg(SBE/Tk-luc)7Twc/J	Repository- Live
	Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express luciferase in response to activation of the Smad2/3-dependent signaling pathway. Cultured primary astrocytes isolated from transgenic mice exhibited luciferase activity when stimulated with TGF-beta. Higher treatment levels of activin and nodal elicited similar luciferase activity. Lipopolysaccharide (LPS) challenge results in strong bioluminescence emissions from the intestinal region and brain. Mechanical injury to the neocortex results in an increase of bioluminescence in 2 hours, which peaks at 4 hours and returns to baseline approximately 48 hours after the injury. Biochemical assays for luciferase activity correlated with noninvasive bioluminescence imaging analysis. The strain was backcrossed to the albino C57BL/6J-Tyr^c-2J/J strain for 2 generations to facilitate bioluminescence imaging. ..... For more information please see the full phenotype on the strain data sheet
005624	B6(V) Lep^ob-whe/J	Repository- Live

008129	B6(V)-Bhrd/J	Repository- Live

001809	B6-A^w-J.Cg-Eda^Ta-6J +/+ Ar^Tfm/J	Repository- Live
	Testicular feminization (Ar^Tfm) is a dominant spontaneous mutation on the X chromosome. Hemizygous male mice are outwardly female in appearance except that the vagina does not open until 3 months of age if at all. Male reproductive development is abnormal leading to very small testes, and the absense of vas deferens, the epididymis, and male accessory glands. Spermatogonia and Sertoli cells are present in the testes, but spermatogenesis does not proceed past meiotic prophase. Leydig cells, which normally produce androgen in males, fail to develop normally. This strain is also segregating for the tabby 6J mutation (Eda^Ta-6J) that affects both the coat color and hair pattern growth. The tabby mutation is maintained in repulsion with the testicular feminization mutation and is used as a coat color marker to assist in identifying resulting genotypes obtained from matings.
004178	B6.129(Cg)-Tg(CAG-Bgeo/GFP)21Lbe/J	Repository- Live
	These Z/EG transgenic mice constitutively express lacZ under the control of the CMV enhancer/chicken actin promoter. Expression is widespread with notable exceptions being liver and lung tissue. Expression is observed throughout all embryonic and adult stages. When crossed with a Cre recombinase-expressing strain, lacZ expression is replaced with enhanced GFP expression in tissues expressing Cre. This double reporter system makes it possible to distinguish a lack of reporter expression from a lack of Cre recombinase expression while providing a means to assess Cre excision activity in live animals and cells. As an example, when crossed to a strain expressing Cre recombinase in olfactory sensory neurons (see Stock No. 006668), this mutant mouse strain may be useful in lineage tracing. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved t ..... For more information please see the full phenotype on the strain data sheet
008104	B6.129(FVB)-Ptgs2^{tm2.1(Ptgs1)Fun}/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. Female homozygotes have a longer period between successive pregnancies and reduced litter sizes. Ptgs1 gene product (protein), COX1, is increased approximately 5 fold in LPS-stimulated macrophages from homozygotes. Prostacyclin metabolite level in urine is reduced by 55% when compared to wildtype controls. No increase in prostaglandin-glycerol in mutant macrophages after LPS challenge is observed. Homozygotes exhibit reduced bradykinin-induced vasculature permeability and at 6 months of age have enlarged glomeruli due to increased inflammatory infiltrate. By 5 months of age, mutant mice develop chronic peritonitis and progressive renal cortex deterioration. This mutant mouse strain may be useful in studies of prostaglandin synthesis and inflammation.
004218	B6.129(ICR)-Tg(CAG-ECFP)CK6Nagy/J	Repository- Live
	Mice that are hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. All tissues from hemizygous animals display fluorescence in all cell types under appropriate lighting conditions. Notable exceptions to this phenotype are erythrocytes and adipocytes in which fluorescence is negligible or absent. 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.
006257	B6.129-Aldh5a1^tm1Kmg/J	Repository- Live
	Homozygous mutation of this gene results in reduced body weight, ataxia, seizures, gliosis of the hippocampus, and eventual status epilepticus. From 19-26 days of age, repetitive tonic-clonic seizures results in more than 95% mortality. Biochemical assays shows complete ablation of the endogenous enzymatic activity in the brains, livers, hearts, and kidneys of homozygous mutant mice. Homozygotes have increased levels of GHB and GABA in liver and brain tissues, as well as in urine. Phenotype can be rescued to varying degrees utilizing a number of both pharmacotherapeutic and gene therapeutic approaches. Although heterozygous mice have approximately 50% of the endogenous enzyme activity compared to wildtype mice, they are viable and fertile. Mice with this targeted mutation may be useful in studying succinate semialdehyde dehydrogenase (SSADH) deficiency and to explore the effect of GABA and GHB accumulation on central nervous system development and function.
004714	B6.129-Bace1^tm1Pcw/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of brain tissue. Primary cultures of cortical neurons isolated from homozygotes aged embryonic day 16.5 do not secrete amyloid beta peptides (Aβ1-40/42 or Aβ11-40/42) or beta C-terminal fragments (βCTFs). When transfected with a recombinant adenovirus expressing the mutant humanized Beta amyloid precursor protein (APP), hAPPSwe, cultured embryonic cortical neurons do not secrete detectable levels of Aβ1-40/42 or Aβ11-40/42 peptides. This mutant mouse strain may be useful in studies of Alzheimer's disease.
004183	B6.129-Bak1^tm1Thsn/J	Repository- Live
	Mice that are homozygous null for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. There were no statistically significant differences in apoptotic cell survival assays between the mutant and wild-type. Used in conjunction with strain B6.129X1-Bax^tm1Sjk (see Stock No. 002994), to generate the double knock-out Bak/Bax, a model for demonstrating severe defects in the regulation of apoptosis during development and tissue homeostasis. When bred to a strain with loxP sites inserted into one Bax locus and a null allele at the other locus (Stock No. 006329) and a strain with a Cd19 null allele and expressing Cre recombinase during B lymphocyte development and differentiation (Stock No. 004126), this muta ..... For more information please see the full phenotype on the strain data sheet
006353	B6.129-B

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