Search Criteria: Strain Type is "Mutant Strain"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 001303 | NOD.CB17-Prkdcscid/J | Level 1 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, 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 | ||
| 000457 | B10.RIII-H2r H2-T18b/(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, H2r, the T cell receptor V β8 chain, and other non MHC loci. This strain also is susceptible to induction of collagen-induced arthritis. | ||
| 000058 | B6(Cg)-Tyrc-2J/J | Level 2 |
| Mice homozygous for Tyrc-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 Tyrc-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). | ||
| 002052 | B6.129P2-Apoetm1Unc/J | Level 2 |
| Mice homozygous for the Apoetm1Unc 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. Additional studies indicate that apoE-deficient mice have altered responses to stress, impaired spatial learning and memory, altered long term potentiation, and synaptic damage. | ||
| 002207 | B6.129S7-Ldlrtm1Her/J | Level 2 |
| Mice homozygous for the Ldlrtm1Her mutation have an elevated serum cholesterol level of 200-400 mg/dl and they have very high levels (>2,000 mg/dl) when fed a high fat diet. Normal serum cholesterol in the mouse is 80-100 mg/dl. | ||
| 002216 | B6.129S7-Rag1tm1Mom/J | Level 2 |
| Mice homozygous for the Rag1tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdcscid/Prkdcscid) (Prkdcscid mice produce some B cells and IgM). They have no CD3+ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8-CD4- and most are IL2 receptor-positive. Neither the spleen nor 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. | ||
| 000697 | B6.BKS(D)-Leprdb/J | Level 2 |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) 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 four to eight 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 (Leprdb/+) 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 Leprdb may cause a defect in the hypothalamus. Steroid sulfotransferase enzymes, aberrantly expressed in ..... For more information please see the full phenotype on the strain data sheet | ||
| 000406 | B6.PL-Thy1a/CyJ | Level 2 |
| This C57BL/6J congenic strain is useful because it carries the T lymphocyte specific Thy1a (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-Ptprca Pepcb/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-Lepob/J | Level 2 |
| Mice homozygous for the obese spontaneous mutation, (Lepob; 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. Adipose tissue transplants in Lepob homozygotes protect them from obesity, normalize insulin sensitivity, and restore fertility. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight mainte ..... For more information please see the full phenotype on the strain data sheet | ||
| 000642 | BKS.Cg-Dock7m +/+ Leprdb/J | Level 2 |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) 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-Leprdb 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 | ||
| 001011 | CBA/CaHN-Btkxid/J | Level 2 |
| CBA/CaHN-Btkxid/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-Prkdcscid/J | Level 2 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, 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 | ||
| 005557 | NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ | Level 2 |
| The NOD.Cg-Prkdcscid Il2rgtm1Wjl/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 | ||
| 000465 | B10.BR-H2k2 H2-T18a/SgSnJ | Level 3 |
| Some phenotypic parameters of the B10.BR-H2k2 H2-T18a/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 cryopreserved embryos of the strain (Stock No. 004804) that had been frozen in 1991, and the two lines of B10.BR-H2k2 H2-T18a/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-H2k2 H2-T18a/SgSnJ (Stock No's. 000465 and 004804) may exhibit white bell ..... For more information please see the full phenotype on the strain data sheet | ||
| 000461 | B10.D2-Hc0 H2d H2-T18c/oSnJ | Level 3 |
| This congenic strain carries the H2d 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). | ||
| 002251 | B6.129P2-Il10tm1Cgn/J | Level 3 |
| Mice homozygous for the Il10tm1Cgn 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 | ||
| 002288 | B6.129S2-Ighmtm1Cgn/J | Level 3 |
| Mice homozygous for the Ighmtm1Cgn 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-Il6tm1Kopf/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. | ||
| 001913 | B6.CB17-Prkdcscid/SzJ | Level 3 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, 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 | ||
| 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 an abbreviated life span: 50% survive at 128.9+/-9.1 days (in contrast to C57BL/6J background where 50% survival is observed at 157.1+/-9.3 days). 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+ TCRlo 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 H2d background. | ||
| 001801 | C57BL/10ScSn-Dmdmdx/J | Level 3 |
| 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 Dmdmdx 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 Dmdmdx mutants do not express dystrophin and therefore have been ..... For more information please see the full phenotype on the strain data sheet | ||
| 000469 | B10.A-H2a H2-T18a/SgSnJ | Level 4 |
| 004804 | B10.BR-H2k H2-T18a/SgSnJJrep | Level 4 |
| Some phenotypic parameters of the B10.BR-H2k2 H2-T18a/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-H2k H2-T18a/SgSnJJrep Stock No. 004804) that had been frozen in 1991, and the two lines of B10.BR-H2k2 H2-T18a/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-H2k2 H2-T18a/SgSnJ (000465 and 004804) may exhibit w ..... For more information please see the full phenotype on the strain data sheet | ||
| 002024 | B10.D1-H2q/SgJ | Level 4 |
| 000463 | B10.D2-Hc1 H2d H2-T18c/nSnJ | Level 4 |
| 000458 | B10.PL-H2u H2-T18a/(73NS)SnJ | Level 4 |
| 001162 | B6(C)-H2-Ab1bm12/KhEgJ | Level 4 |
| 004650 | B6.129-Tlr2tm1Kir/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-Tnfrsf1atm1Mak/J | Level 4 |
| Mice homozygous for the Tnfrsf1atm1Mak targeted mutation (formerly Tnfr1tm1Mak) 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-B2mtm1Unc/J | Level 4 |
| Mice homozygous for the B2mtm1Unc 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 | ||
| 002609 | B6.129P2-Nos2tm1Lau/J | Level 4 |
| Mice homozygous for the Nos2tm1Lau targeted mutation resemble wildtype mice in appearance and histology. Homozygotes are viable and fertile. Unlike Nos1 and Nos3, Nos2 is synthesized de novo in response to a variety of inflammatory stimuli. Induction of Nos2 results in the production of large amounts of nitric oxide (NO) over prolonged periods of time. Excessive NO production has been shown to be beneficial through its antitumor and antimicrobial activities. It is also thought to cause tissue damage and contribute to pathology in a variety of inflammatory conditions including rheumatoid arthritis, inflammatory bowel disease, cardiac allograft rejection, hepatoxicity, myocardial ischemia-reperfusion and septic shock. NO has been demonstrated to play a role in the regulation of blood pressure and hemodynamics. In an LPS-induced model of septic shock, Nos2tm1Lau homozygotes had virtually no serum NO response, but were ..... For more information please see the full phenotype on the strain data sheet | ||
| 002684 | B6.129P2-Nos3tm1Unc/J | Level 4 |
| Mice homozygous for the Nos3tm1Unc 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. | ||
| 002118 | B6.129P2-Tcrbtm1Mom/J | Level 4 |
| Mice homozygous for the Tcrbtm1Mom 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 Tcratm1Mom strain. There is normal differentiation of gamma delta thymocytes. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age. | ||
| 002365 | B6.129S-Cybbtm1Din/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. | ||
| 002693 | B6.129S1-Il12btm1Jm/J | Level 4 |
| Mice homozygous for the Il12btm1Jmtargeted 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-Cd4tm1Mak/J | Level 4 |
| Mice homozygous for the Cd4tm1Mak 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-Cd8atm1Mak/J | Level 4 |
| Mice homozygous for the Cd8atm1Mak targeted mutation are deficient in functional cytotoxic T-cells; however, helper T-cell development and function is comparable to normal. | ||
| 002116 | B6.129S2-Tcratm1Mom/J | Level 4 |
| Mice homozygous mice for the Tcratm1Mom 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-Ccl2tm1Rol/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)26Sortm1Sor/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. | ||
| 002287 | B6.129S7-Ifngtm1Ts/J | Level 4 |
| Mice homozygous for the Ifngtm1Ts 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. | ||
| 003288 | B6.129S7-Ifngr1tm1Agt/J | Level 4 |
| Mice homozygous for the Ifngr1tm1 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-Trpv1tm1Jul/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. | ||
| 000819 | B6.Cg-Foxn1nu/J | Level 4 |
| The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) 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 | ||
| 004194 | B6.Cg-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. | ||
| 000482 | B6.MRL-Faslpr/J | Level 4 |
| Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) 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 Faslpr allele is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Faslpr/Faslpr at a 24 fold increase over control lymph node weight, MRL/Mp-Faslpr/Faslpr at 75 fold and congenic strain C3H/HeJ-Faslpr/Faslpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Faslpr/Faslpr at 4 to 7 months to negligible at 14 to 16 months in mice with C57BL/6J and C3H/HeJ backgrounds and homozygous for Faslpr> ..... For more information please see the full phenotype on the strain data sheet | ||
| 002810 | B6CBA-Tg(HDexon1)62Gpb/1J | Level 4 |
| This line is transgenic for the 5' end of the human HD gene carrying approximately 160 +/- 10 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 cell ..... | ||
| 001021 | B6Smn.C3-Faslgld/J | Level 4 |
| Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasllpr 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 ..... | ||
| 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)-Ifngtm1Ts/J | Level 4 |
| Mice homozygous for the Ifngtm1Ts 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)-Rag1tm1Mom/J | Level 4 |
| Mice homozygous for the Rag1tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdcscid/Prkdcscid) (Prkdcscid mice produce some B cells and IgM). They have no CD3+ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8-CD4- and most are 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-Tlr4Lps-d/J | Level 4 |
| In addition to the Tlr4Lps-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 Lpsd on BALB/c, a strain susceptible to infection, neoplastic disease including the induction of plasmacytomas and other tumors. | ||
| 000438 | C3.SW-H2b/SnJ | Level 4 |
| Male mice from the C3.SW-H2b/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)-Il10tm1Cgn/Lt | Level 4 |
| Mice homozygous for the Il10tm1Cgn 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 | ||
| 001131 | C3SnSmn.CB17-Prkdcscid/J | Level 4 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, 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-Prf1tm1Sdz/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. | ||
| 001927 | C57BL/6-Tg(APOA1)1Rub/J | Level 4 |
| 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. | ||
| 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 the donating investigator reports that mice homozygous for this transgene die within the first two weeks following birth.
Of note, it has been the experience at The Jackson Laboratory that Stock No. 006567 (C57BL/6-Tg(CAG-EGFP)131Osb/LeySopJ) demonstrates the highest proportion of GFP expressing cell populations in bone marrow, thymus, spleen and peripheral blood when compared to Stock No. 003291 (C57BL/6-Tg(CAG-EGFP)1Osb/J) and Stock No. 007075 (CByJ.B6-Tg(CAG-EGFP)1Osb/J).
View the pdf document on For more information please see the full phenotype on the strain data sheet | ||
| 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 H2Kb 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. | ||
| 004353 | C57BL/6-Tg(UBC-GFP)30Scha/J | Level 4 |
| These transgenic mice express enhanced 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-Aw-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 Aw-J is dominant to the nonagouti a. Since a to Aw is a common mutation, strains possessing this mutation in laboratory stock may not be of a common origin. | ||
| 002020 | C57BL/6J-ApcMin/J | Level 4 |
| The C57BL/6J-ApcMin/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-ApcMin 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-ApcMin 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-ApcMin heterozygous mice (Silverman et al., 2002). | ||
| 000049 | C57BL/6J-KitW-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. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 004104 | FVB.Cg-Mmp9tm1Tvu/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. | ||
| 002376 | FVB/N-Tg(MMTVneu)202Mul/J | Level 4 |
| 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. | ||
| 000485 | MRL/MpJ-Faslpr/J | Level 4 |
| Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) 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 Faslpr gene is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Faslpr/Faslpr at a 24 fold increase over control lymph node weight, MRL/Mp-Faslpr/Faslpr at 75 fold and congenic strain C3H/HeJ-Faslpr/Faslpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Faslpr> ..... For more information please see the full phenotype on the strain data sheet | ||
| 000692 | WB/ReJ KitW/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. | ||
| 004368 | 129(B6)-Il10tm1Cgn/J | Repository- Live |
| Mice homozygous for the Il10tm1Cgn 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 | ||
| 014634 | 129(B6)-Nr1h2tm1Djm/J | Repository- Live |
| In this strain a neomycin (neo) resistance cassette replaces exons 5-6 of the nuclear receptor subfamily 1, group H, member 2 (Nr1h2) gene, abolishing gene function. Homozygous are viable, fertile, and normal in size. Also known as liver X receptor beta (Lxrβ), Nr1h2 binds to retinoid X receptors (RXRα, RXRβ, RXRγ; NR2B1, NR2B2, and NR2B3) and is activated by oxysterols to regulate the expression of genes involved in cholesterol metabolism. . Homozygous Lxrβ-/- mice lose their ability to appropriately regulate cholesterol, lipid, and carbohydrate metabolism, and have defects in immune function. These defects are more severe when combined with the knockout of Lxrα (available as Stock No. 013762). These mice may be useful for studying lipid and cholesterol metabolism, and regulation of the immune response. | ||
| 004337 | 129(Cg)-Foxg1tm1(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. | ||
| 006830 | 129-Dysftm1Kcam/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable, fertile and show a normal growth rate. Mice develop a slowly progressive muscular dystrophy. By the age of 2 months, a few individual necrotic and centrally nucleated fibers can be detected throughout the muscle; the number increases with age. By 8 months, the muscle develops all of the pathological characteristics of muscular dystrophy (e.g. regenerating fibers, split fibers, muscle necrosis with macrophage infiltration and fat replacement). The severity of the pathology varies in different muscles. Muscle fibers are defective in Ca2+-dependent sarcolemma resealing/repair. No protein product from the targeted gene is detected in skeletal muscle microsomes. This mutant mouse strain represents a model that may be useful in studies of muscle disease and repair. | ||
| 002702 | 129-Ifngr1tm1Agt/J | Repository- Live |
| Mice homozygous for the Ifngr1tm1Agt 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. | ||
| 013762 | 129-Nr1h3tm1Djm/J | Repository- Live |
| Homozygous Nr1h3 (nuclear receptor subfamily 1, group H, member 3) targeted mutation mice lose their ability to respond normally to dietary cholesterol. Mice maintained on cholesterol diets fail to induce transcription of the Cyp7a1 (cytochrome P450, family 7, subfamily a, polypeptide 1) gene, a rate-limiting enzyme in bile acid synthesis, and fail to induce expression of ABCG5 (ATP-binding cassette, sub-family G (WHITE), member 5) and ABCG8 (ATP-binding cassette, sub-family G (WHITE), member 8), ATP-binding cassette transporters that are required for cholesterol secretion into bile. Large amounts of cholesterol rapidly accumulate in the liver leading to impaired hepatic function. Impaired reverse cholesterol transport from peripheral tissues is also observed. The ability to regulate lipids and carbohydrates is also lost. Defects in innate immune responses by activated macrophages have also been described. Males are not infertile, but show a significantly higher number ..... For more information please see the full phenotype on the strain data sheet | ||
| 016240 | 129-Plk1s1tm1Cpl/J | Repository- Live |
| These mice possess loxP sites on either side of exons 5 and 6 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 5 and 6 deleted in the cre-expressing tissue(s). When bred to a strain with Cre recombinase expression in primordial germ cells (see Stock No. 008569 for example), this mutant mouse strain may be useful in studies of mammalian germ cell differentiation. | ||
| 012771 | 129-Sirt7tm1Fwa/J | Repository- Live |
| This mutant mouse line has not been characterized. | ||
| 014133 | 129/Sv-Maobtm1Shih/J | Repository- Live |
| In this strain, a neomycin resistance (neo) cassette replaces exon 6 of the endogenous X-linked monoamine oxidase B (Maob) gene, abolishing gene function. Maob deficient mice are viable, fertile, and normal in size. Maob is a mitochondrial enzyme which oxidizes neurotransmitters and dietary amines. These mutants lack MAOB activity in the brain and liver resulting in increased levels of phenylethylamine. These mice exhibit increased reactivity to stress and increased aggression. These mice also show decreased susceptibility to the neurodegenerative effects of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), which induces Parkinson's disease-like symptoms when administered to mice. These mice may be useful for studying neurodegeneration and MAOB-related behaviors. | ||
| 013596 | 129S-Batf3tm1Kmm/J | Repository- Live |
| These Batf3-/- knockout mice have a loxP-flanking neomycin (neo) resistance cassette replacing exons 1-2 of the basic leucine zipper transcription factor, ATF-like 3 (Batf3) gene, abolishing gene function. Mice that are homozygous for this allele are viable and fertile. Batf3 is highly expressed in CD11c+ CD8α+ conventional dendritic cells (cDCs), with low to absent expression in other immune cells.The deletion of Batf3 prevents development of splenic CD8α+ cDCs, which are important for cross-presentation during infections. Lymph nodes and thymi of Batf3-/- mice lack CD8α+ DCs, and DCs generated from Batf3-/- bone marrow (BM) and spleens are deficient in Toll-like receptor (TLR) 3-induced interleukin (IL)-12 production. These mice also lack CD103+CD11b- DCs in the lung, intestine, mesenteric lymph nodes (MLNs), dermis, and skin-draini ..... For more information please see the full phenotype on the strain data sheet | ||
| 013757 | 129S-Batftm1.1Kmm/J | Repository- Live |
| These knockout mice lack exons 1-2 of the basic leucine zipper transcription factor(Batf), ATF-like gene, abolishing gene function. Mice that are homozygous for this allele are viable and fertile. Batf is highly expressed in T helper (TH) 1, TH2 and TH17 cells. Batf is required for the differentiation of interleukin (IL)-17-producing TH17 cells which are CD4+ T cells that coordinate inflammatory responses in host defense. These mice exhibit normal TH1 and TH2 differentiation, but show a defect in TH17 differentiation with a reduction in IL-17 production, but maintain normal levels of IL-2, interferon (IFN)-γ, and IL-10 under TH17 conditions. Since TH17 cells are the major pathogenic population in experimental autoimmune encephalomyelitis (EAE), these Batf-/- mice are completely resistant EAE even when immunized with myelin oligodendrocyt ..... For more information please see the full phenotype on the strain data sheet | ||
| 004545 | 129S-Npytm1Rpa/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. | ||
| 002779 | 129S-Parp1tm1Zqw/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. | ||
| 013039 | 129S-Spictm1Kmm/J | Repository- Live |
| In these mutant mice a loxP-flanked neomycin resistance (neo) cassette replaces exons 2-5 of the Spi-C transcription factor (Spi-1/PU.1 related) gene (Spic), abolishing gene function. Heterozygous mice are viable and fertile, while homozygotes are born at a frequency lower than the expected Mendelian ratio and they have small litters. Spi-C is highly expressed in red pulp macrophages which are a distinct splenic subset required for red blood cell recycling and iron homeostasis. These Spi-C-/- mice exhibit a defect in the development of red pulp macrophages, which fail to efficiently phagocytose red blood cells trapped in the spleen. They also develop an iron overload localized selectively to splenic red pulp. These mice may be useful for studying the development and function of red pulp macrophages. | ||
| 011120 | 129S-Wwtr1tm1Benj/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, small in size and less active than wildtype controls. Only 10-25% of the expected homozygotes are born. The Donating Investigator reports that breeding homozygous females successfully is uncommon and homozygotes usually succumb before breeding age. No gene product (protein) is detected by Western blot analysis. Homozygotes develop severe polycystic renal disease, with an onset as early as a few weeks of age, and emphysema, with swollen alveoli and breakdown of alveolar walls. Kidney size increases with age. Intestinal and pulmonary inflammation is observed in some homozygotes. Levels of protein polycystin 2 (PC2) is increased in kidney epithelial cells of homozygotes. Histological analysis reveals adipocytes are smaller than wildtype control. | ||
| 014606 | 129S.129(B6)-Arl6tm1Vcs/J | Repository- Live |
| A targeted mutation in this strain alters the sequence of the splice acceptor and splice donor sites (AG -> AC and GT -> CT respectively) of exon 8 of the ADP-ribosylation factor-like 6 (Arl6 or Bbs3) gene. A neomycin resistance cassette was also inserted downstream of the modified exon 8. Homozygous mice are viable and fertile. Bbs3 is associated with human Bardet-Biedl syndrome, a pleiotropic disorder characterized by retinal and photoreceptor degeneration. The Bbs3 "long" isoform, Bbs3L, is evolutionally conserved across human and mouse and is expressed specifically in the ganglion cell layer, nerve fiber layer, and photoreceptor cells of mouse retinal tissue. Exon 8 is only present in Bbs3L and alteration of the spice sites results in loss of Bbs3L expression while still expressing Bbs3. These Bbs3L-/- mice exhibit disruption of normal photoreceptor architecture, specifically the inner segments of t ..... For more information please see the full phenotype on the strain data sheet | ||
| 016251 | 129S.Cg-Tg(Hoxb7-EGFP)33Cos/J | Repository- Live |
| Hoxb7-EGFP transgenic mice have the homeobox B7 promoter/enhancer sequences driving expression of an enhanced green fluorescent protein, EGFP. Hemizygotes are viable, fertile, and normal in size. Under control of Hoxb7, EGFP labels the Wolffian duct and branching ureteric bud (UB) of the kidney during embryonic development. Fluorescence is evident in tissues specific to the UB lineage in adult and newborn kidneys, including the ureter, pelvis, and collecting ducts. This strain allows for the visualization of tissues specific to the UB lineage. In contrast, mice containing the Tg(Hoxb7-Venus*)17Cos allele (Stock No. 016252) are useful for viewing individual cells. These mice may be useful for visualizing UB growth and branching in vivo or in vitro. | ||
| 016567 | 129S.Cg-Tg(Hoxb7-rtTA*M2)2Cos/J | Repository- Live |
| RS-HTA2 transgenic mice have the homeobox B7 promoter/enhancer sequences driving expression of an optimized form of the reverse tetracycline-controlled transactivator (rtTA*M2) protein. Hemizygotes are viable, fertile, and normal in size. When mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (tetO), expression of the gene of interest may be regulated by the tetracycline analog, doxycycline (dox). In the presence of dox, transcription of the target gene is induced in cells where rtTA is expressed. When bred to B6;SJL-Tg(tetop-lacZ)2Mam/J mice (Stock No. 002621), adult mice carrying both transgenes, which were maintained on Dox during pre and postnatal life, show strong expression of βgal in the renal collecting duct system, and embryos display strong expression throughout the Wolffian duct, ureteric bud, vas deferens, epididymis ..... For more information please see the full phenotype on the strain data sheet | ||
| 007179 | 129S.Cg-Tg(UBC-cre/ERT2)1Ejb/J | Repository- Live |
| Mice hemizygous for this Cre-ERT2 transgene are viable and fertile. Mice from this founder line have strong tamoxifen-inducible cre activity in all reported tissue types. The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OHT) and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to OHT. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone may be coadministered. When these Cre-ERT2 mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the flanked sequences in widespread cel ..... For more information please see the full phenotype on the strain data sheet | ||
| 003328 | 129S/Sv-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. | ||
| 007853 | 129S/SvEv-Tg(Alb1-Ren)2Unc/CofJ | Repository- Live |
| Mice heterozygous for the RenTgMK transgene are viable and fertile. The RenTgMK transgene contains a liver-specific albumin promoter/enhancer controlling the expression of a synthetic renin gene (engineered to allow efficient cleavage and secretion of the prorenin transgene product by the liver). This, and because the transgene was targeted to the apolipoprotein locus on Chromosome 9, results in active renin secretion from the liver independently of renal or other homeostatic cardiovascular control mechanisms (i.e. genetically clamped). RenTgMK heterozygotes have high ectopic levels of active mouse renin in the liver and elevated plasma levels of prorenin and active renin. Heterozygous mice display significantly elevated blood pressure, enhanced thirst, high urine output, proteinuria, and kidney damage. Because active renin overexpression results in increased circulating levels of angiotensin II (Ang II), heterozygotes also exhibit cardiac hypertrophy and 50% male mortality between 6-8 ..... For more information please see the full phenotype on the strain data sheet | ||
| 016158 | 129S1.B6-Zic2m1Nisw/J | Repository- Live |
| 007844 | 129S4/SvJae-Gt(ROSA)26Sortm2(FLP*)Sor/J | Repository- Live |
| Homozygous ROSA26Flpo mice are viable and fertile, with widespread expression of the mouse codon-optimized FLP recombinase (FLPo) variant of the Saccharomyces cerevisiae FLP1 recombinase gene driven by the GT(ROSA)26Sor promoter. The GT(ROSA)26Sor promoter drives expression in a constitutive fashion from preimplantation onward. When bred with mice containing a FRT site flanked sequence of interest with the FRT sites in the same orientation, FLP-mediated recombination will result in deletion of the FRT-flanked sequence(s) in the offspring. Flpo exhibits enhanced recombinase activity compared to Flpe in vivo. | ||
| 010977 | 129S4/SvJae-Pdgfrbtm11Sor/J | Repository- Live |
| These mice possess loxP sites on either side of the exons encoding the first and second immunoglobulin domain of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have the exons encoding the first and second immunoglobulin domain deleted in the cre-expressing tissue(s). When bred to a strain with Cre recombinase expression in adrenal tissue (see Stock No. 006364 for example), this mutant mouse strain may be useful in studies of steroidogenesis. | ||
| 003580 | 129S4/SvJae-Pparatm1Gonz/J | Repository- Live |
| Mice homozygous for the Pparatm1Gonz 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)26Sortm1(FLP1)Dym/J | Repository- Live |
| Homozygous FLPeR mice are viable and fertile, with widespread expression of the FLPe variant of the Saccharomyces cerevisiae FLP1 recombinase gene driven by 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. The Gt(ROSA)26Sor promoter drives expression from preimplantation onward and extensive target gene recombination can be achieved in most tissue types, including cells of the developing germ line. When bred with mice containing a frt-flanked sequence of interest, FLP-mediated recombination will result in deletion of the frt-flanked sequence(s) in the offspring. This FLP deleter strain may be useful for generating frt-FLP conditional mutations and serves as a source of FLP1-expressing primary cell lines. | ||
| 013184 | 129S4/SvJaeSor-Mycl1tm1.1Rne/J | Repository- Live |
| These L-Mycflox mutant mice possess loxP sites flanking all three exons v-myc myelocytomatosis viral oncogene homolog 1 (Mycl1) 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 all three Mycl1 exons deleted in the cre-expressing tissue. The donating investigator states that this strain may be useful, in combination with other Myc knock-out models, for studying early embryonic growth and organogenesis of the brain, olfactory bulb, and lungs. | ||
| 008286 | 129S6.129P2(B6)-Nos3tm1Unc/J | Repository- Live |
| Homozygous mutant mice 129S6/SvEvTac background are viable, fertile, normal in size and do not exhibit any gross physical or behavioral abnormalities. On the C57BL/6 congenic background homozygous mutants mice exhibit 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. This mutant mouse strain may be useful in studies of wound healing, hypertension and other cardiovascular defects, insulin resistance, hyperlipidemia and lung development. 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 ..... | ||
| 002753 | 129S6/SvEvTac-Atmtm1Awb/J | Repository- Live |
| Mice homozygous for the Atmtm1Awb 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 and are more sensitive to ionizing radiation than wildtype mice. | ||
| 002211 | 129S7/SvEvBrd-Mt1tm1Bri Mt2tm1Bri/J | Repository- Live |
| Mice homozygous for the Mt1tm1Bri Mt2tm1Bri 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. | ||
| 016830 | 129X1.Cg-Gabrg2tm2Lusc/J | Repository- Live |
| These mice possess loxP sites on either side of exon 8 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 8 deleted in the cre-expressing tissue(s).
When bred to a strain with Cre recombinase expression in glutamatergic neurons, this mutant mouse strain may be useful in studies of postsynaptic clustering of GABA-A receptors during synaptogenesis. | ||
| 006859 | 129X1/SvJ-Lamc2jeb/DcrJ | Repository- Live |
| Mice that are heterozygous for this mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Northern blot analysis of skin from homozygotes detects the wildtype and a dominant larger sized mutant gene product (mRNA). Homozygotes express a reduced level of gene product (protein), as detected by Western blot analysis of keratinocytes. Mean onset of progressive skin blistering disease in homozygotes on the 129X1 background is age 154 days. Homozygotes exhibit ulcerated lesions and tissue granulation in ear skin, which develops into deformed pinna; ulcerated lesions in the footpads and tail. Thickened epidermis (hyperplasia) and subepidermal separation, with little to no inflammation, occurs in the skin of the footpads and tail. Ultrastructural analysis of skin with electron microscopy reveals that the dermal-epidermal separation occurs at the lamina lucida. | ||
| 006246 | A/J-sunk/GrsrJ | Repository- Live |
| Mice homozygous for the sunken mutation are small and have severe kyphosis with the abdomen appearing sunken in. | ||
| 002250 | B10.129P2(B6)-Il10tm1Cgn/J | Repository- Live |
| Mice homozygous for the Il10tm1Cgn 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)-Ighmtm1Cgn/J | Repository- Live |
| Mice homozygous for the Ighmtm1Cgn 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. | ||
| 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 Ek 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 H2b. Because C57BL/10 mice do not express I-E, this mouse must be crossed to a strain that expresses I-Ek to study the interaction of the transgenic T-cell receptor with the pigeon cytochrome c antigen. The lack of I-Ek expression in the transgenic line allows it to serve as a universal donor for crossing the transgene onto other strains expressing I-Ek<> ..... For more information please see the full phenotype on the strain data sheet | ||
| 001953 | B10.S-H2s/SgMcdJ | Repository- Live |
| 011128 | B10.SJL-Dysfim/AwaJ | Repository- Live |
| Mice that are homozygous for this mutation exhibit a progressive muscular dystrophy characterized by myofiber degeneration and increased fibrosis. Disease onset on the C57BL/10 background is apparent by 4 weeks of age and is severe by 8 months of age, although, mice can survive until 19 months. During the late stage of the disease muscles exhibit fatty and fibrotic tissue as well as inflammatory cells. Affected muscles include the proximal limbs, (quadriceps femoris and triceps brachii) and abdominals. The distal limbs, (gastocnemius, soleus, and tibialis anterior), diaphram, and biceps brachii appear to be only mildly affected even in the late stages of the disease. Both pyruvate and creatinine kinase levels are increased. Regeneration following notexin-induced muscle damage is impaired by delayed removal of necrotic fibers and an extended inflammatory period. This mutant mouse strain may be useful as a model of limb-girdle muscular dystrophy type 2B (LGMD2B) and Miyoshi myopath ..... For more information please see the full phenotype on the strain data sheet | ||
| 009575 | B6(129S4)-Et(cre/ERT2)119Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OH ..... | ||
| 012688 | B6(129S4)-Et(cre/ERT2)13866Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap lentiviral transgene are viable and fertile, with expression of a a CreERT2 fusion gene (Cre recombinase fused to Cre-ERT2 [a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain]) under control of the promoter/enhancer regions surrounding the site where the enhancer trap lentiviral transgene randomly inserted. While Cre-ERT2 fusion gene activity is designed to be inducible (observed following tamoxifen administration), the donating investigator reports CreERT2 activity for this line is the same with or without tamoxifen exposure. Specifically, the donating investigator reports Cre recombinase activity in brain tissues as:
nice staining in amygdala, with some cells in ventral striatum, hypothalamus, pallidum, and midbrain. No staining in other tested tissues is reported. When these enhancer trap lentiviral transgenic mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducibl ..... For more information please see the full phenotype on the strain data sheet | ||
| 009581 | B6(129S4)-Et(cre/ERT2)1642Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)1642Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre re ..... | ||
| 009582 | B6(129S4)-Et(cre/ERT2)1645Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OH ..... | ||
| 009585 | B6(129S4)-Et(cre/ERT2)2047Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OH ..... | ||
| 009577 | B6(129S4)-Et(cre/ERT2)296Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)296Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre re ..... | ||
| 010689 | B6(129S4)-Et(cre/ERT2)6959Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration (although some cre activity is reported prior to tamoxifen administration). The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)6959Rdav images). The Cre- ..... | ||
| 010690 | B6(129S4)-Et(cre/ERT2)7089Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)7089Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre re ..... | ||
| 010696 | B6(129S4)-Et(icre/ERT2)10596Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration (although some cre activity is reported prior to tamoxifen administration). The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind th ..... | ||
| 012689 | B6(129S4)-Et(icre/ERT2)14163Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap lentiviral transgene are viable and fertile, with expression of an iCreERT2 fusion gene (an optimized variant of Cre recombinase [iCre; improved with mammalian codon usage, removed putative cryptic splice sites, altered stop codon, and reduced CpG content to limit the chances of epigenetic silencing in mammals] fused to Cre-ERT2 [a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain]) under control of the promoter/enhancer regions surrounding the site where the enhancer trap lentiviral transgene randomly inserted. Cre-ERT2 fusion gene activity is designed to be inducible (observed following tamoxifen administration).
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as:
only in hypothalamus (perhaps arcuate nucleus only), no Cre recombinase activity is observed prior to tamoxifen exposure, no Cre recombinase activity in other tested tissues.
When these ..... For more information please see the full phenotype on the strain data sheet | ||
| 012690 | B6(129S4)-Et(icre/ERT2)14208Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap lentiviral transgene are viable and fertile, with expression of an iCreERT2 fusion gene (an optimized variant of Cre recombinase [iCre; improved with mammalian codon usage, removed putative cryptic splice sites, altered stop codon, and reduced CpG content to limit the chances of epigenetic silencing in mammals] fused to Cre-ERT2 [a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain]) under control of the promoter/enhancer regions surrounding the site where the enhancer trap lentiviral transgene randomly inserted. Cre-ERT2 fusion gene activity is designed to be inducible (observed following tamoxifen administration).
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as:
scattered cells in the neocortex, hippocampus, amygdala, striatum, thalamus, hypothalamus, midbrain, pons, medulla, and many cerebellar granule cells. No Cre recombinase activity is observ ..... For more information please see the full phenotype on the strain data sheet | ||
| 012694 | B6(129S4)-Et(icre/ERT2)14915Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap lentiviral transgene are viable and fertile, with expression of an iCreERT2 fusion gene (an optimized variant of Cre recombinase [iCre; improved with mammalian codon usage, removed putative cryptic splice sites, altered stop codon, and reduced CpG content to limit the chances of epigenetic silencing in mammals] fused to Cre-ERT2 [a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain]) under control of the promoter/enhancer regions surrounding the site where the enhancer trap lentiviral transgene randomly inserted. Cre-ERT2 fusion gene activity is designed to be inducible (observed following tamoxifen administration).
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as:
scattered cells in all areas of the brain; with high density of staining in granule cell layer. Dentate Gyrus projections are very obvious. No Cre recombinase activity is observed prior t ..... For more information please see the full phenotype on the strain data sheet | ||
| 012687 | B6(129S4)-Tg(SYN1-icre/mRFP1)9934Rdav/J | Repository- Live |
| Mice hemizygous for this lentiviral transgene are viable and fertile, with expression of a codon-improved Cre recombinase/monomeric red fluorescent protein fusion protein (iCre/mRFP1) under control of the human synapsin I promoter. The donating investigator reports Cre recombinase activity in brain tissues as widespread, with no staining in other tested tissues. The donating investigator did not characterize fluorescent expression of the mRFP1 portion of the fusion protein. When these transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring. | ||
| 011065 | B6(C3)-Tg(Pgk1-FLPo)10Sykr/J | Repository- Live |
| These transgenic mice express the mouse codon-optimized FLP recombinase under the direction of the mouse Pgk1, phosphoglycerate kinase 1, promoter. Transgene expression is detected in testis, ovary, brain, heart, liver and muscle by RT-PCR. When crossed with a strain containing a FRT site-flanked sequence of interest, FLPo recombinase activity is detected in all cells with complete recombinase mediated excision of the target. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make the strain homozygous. | ||
| 010774 | B6(Cg)-Calb2tm1(cre)Zjh/J | Repository- Live |
| The Cr-IRES-Cre (Calb2-IRES-Cre) allele harbors an internal ribosome entry site and Cre recombinase in the 3' UTR of the Calb2 (calbindin 2; also called calretinin or CR) locus. As such, cre expression is directed to calretinin interneurons in the brain and cortex by the endogenous Calb2 promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When Cr-IRES-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Calb2-expressing cells of the offspring.
The donating investigator reports Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Calb2 expression pattern with highly efficient recombination). The donating investigator did not examine cre expression in tissues other than brai ..... | ||
| 013730 | B6(Cg)-Calb2tm2.1(cre/ERT2)Zjh/J | Repository- Live |
| The CR-CreER (or CR-CreERT2) knock-in allele was designed to both abolish Calb2 (calbindin 2; also called calretinin or CR) gene function and expresses CreERT2 fusion protein from the Calb2 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when CR-CreERT2 mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the CR-expressing cells of the offspring.
Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The donating investigator reports that the phenotype of CR-CreER homozygous mice has not been assessed. However, CR-CreER homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene on a similar genetic background (impaired motor coordination, abn ..... | ||
| 012710 | B6(Cg)-Ccktm2.1(cre/ERT2)Zjh/J | Repository- Live |
| The Cck-CreER (or Cck-CreERT2) knock-in allele both abolishes cholecystokinin (Cck) gene function and expresses the CreERT2 fusion protein from the Cck promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygotes may be expected to have a phenotype similar to other null mutations of this gene and may exhibit metabolic abnormalities of the endocrine/exocrine glands (increased pancreatic amylase).
Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Cck-CreERT2 mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Cck-expressing cells of the offspring. These Cck-CreERT2 mice may be useful in studying brain anatomy, physiology and behavior. The donat ..... | ||
| 010705 | B6(Cg)-Dlx5tm1(cre/ERT2)Zjh/J | Repository- Live |
| The Dlx5-CreERT2 knock-in allele both abolishes Dlx5 gene function and expresses a CreERT2 fusion protein (creERT2 fusion protein) from the Dlx5 promoter/enhancer elements. Heterozygous mice are viable and fertile. Homozygous mice are expected to have a knockout phenotype similar to other null mutations of this gene and may exhibit prenatal/perinatal death with craniofacial and nervous system abnormalities. Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Dlx5-CreERT2 mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Dlx5-expressing cells of the offspring.
The donating investigator reports tamoxifen-inducible Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Dlx5 expression pattern with highly efficient inducibility). They report tamox ..... | ||
| 013048 | B6(Cg)-Etv1tm1.1(cre/ERT2)Zjh/J | Repository- Live |
| The ER81-CreER (or ER81-CreERT2, Etv1-CreER, Etv1-CreERT2) knock-in allele was designed to both abolish ets variant gene 1 (Etv1) gene function and expresses CreERT2 fusion protein from the Etv1 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when ER81-CreERT2 mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Etv1-expressing cells of the offspring.
Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Although mice homozygous for other null mutations of this gene on a similar genetic background exhibit neuromuscular abnormalities, ataxia and premature lethality, the donating investigator reports that ER81-CreER homozygous mice show no gross abnormalities. ER81 mRNA or protein expression fr ..... | ||
| 013175 | B6(Cg)-Grntm1.1Aidi/J | Repository- Live |
| In these Grn-/- mice exons 1-4 are deleted from the targeted granulin (Grn) allele. Homozygotes are viable, fertile, and normal in size. These mice show progressive development of frontotemporal dementia-like behavior and neuropathology. This includes enhanced activation of microglia and astrocytes, and ubiquitination and cytoplasmic accumulation of phosphorylated transactivation response element DNA binding protein-43 (TDP-43) in hippocampal and thalamic neurons. By eighteen months they demonstrate impaired spatial learning and memory. Macrophages from these mice release less interleukin-10 and more inflammatory cytokines in response to microbial agents. Contrary to increased inflammation, these mice exhibit a delay in clearing infections due to a dysregulated inflammatory response, allowing bacteria to proliferate in vivo. Activated PGRN-deficient macrophages and microglia are cytotoxic to hippocampal cells, and PGRN-deficient hippocampal slices are hypers ..... For more information please see the full phenotype on the strain data sheet | ||
| 010633 | B6(Cg)-Gt(ROSA)26Sortm1(CAG-taulacZ)Bene/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. A loxP-flanked neo cassette prevents transcription of the downstream tau- beta galactosidase (tauLacZ) gene. When bred to mice that express Cre recombinase, the resulting offspring will have the neo cassette deleted in the cre-expressing tissue(s); resulting in expression of taulacZ. Upon histochemical staining with X-gal, the tau beta galactosidase activity is revealed as an intense blue precipitate found in the entire cell, regardless of cell type. When tested with an olfactory sensory neuron specific cre-expressing strain, expression of lacZ labels axon projections. This mutant mouse strain may be useful as a cre reporter. | ||
| 008242 | B6(Cg)-Gt(ROSA)26Sortm1(Ikbkb)Rsky/J | Repository- Live |
| Mice homozygous for the R26StopFLikk2ca conditional allele are viable and fertile, with a loxP-flanked STOP cassette preventing transcription of the downstream bicistronic sequences (a FLAG-tagged, constitutively active form of IKbkb (IKK2ca) and EGFP). When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissue(s); resulting in expression of the IKK2ca as well as EGFP fluorescence. Expression of IKK2ca leads to constitutively active NF-kappaB transcription factor activity. These R26StopFLikk2ca mice allow inducible expression of an activated form of Ikbkb (IKK2 or IKK-beta) and subsequent activation of the NF-kappaB transcription factor pathways.
For example, when bred to a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 006785), this ..... | ||
| 014530 | B6(Cg)-Il10tm1.1Karp/J | Repository- Live |
| A targeting vector was designed to place an internal ribosome entry site (IRES)-enhanced green fluorescent protein (eGFP) fusion protein, downstream of exon 5 of the interleukin 10 (Il10) gene. Homozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Il10 is expressed in leukocytes and other cells and is integral to immune homeostasis. These Vert-X mice exhibit intracellular GFP expression in Il10 containing cells. Specifically, GFP expression was seen in B cells, T cells, myeloid cells, dendritic cells, and Natural Killer (NK) cells. B cells were the predominant expressers of GFP with plasma cells, plasmablasts, and CD19+B220+ cells being the highest expressing. These mice may be useful as a tool for studying the localization and initiation of Il10 gene regulation. | ||
| 014175 | B6(Cg)-Irf8tm1.1Hm/J | Repository- Live |
| These mice possess loxP sites on either side of exon 2, which encodes the DNA binding domain. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 deleted in the cre-expressing tissue(s). When bred to a strain with Cre recombinase expression in B lymphocytes (see Stock No. 006785 for example), this mutant mouse strain may be useful in studies of B cell differentiation | ||
| 010776 | B6(Cg)-Lhx6tm1(cre/ERT2)Zjh/J | Repository- Live |
| The Lhx6-CreERT2 knock-in allele both abolishes Lhx6 (LIM homeobox protein 6) gene function and expresses the CreERT2 fusion protein (creERT2 fusion protein) from the Lhx6 promoter/enhancer elements. Heterozygous mice are viable and fertile. Homozygous mice are expected to have a knockout phenotype similar to other null mutations of this gene and may exhibit neurological abnormalities and death within a few weeks of birth. Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Lhx6-CreERT2 mice are bred with mice containing loxP-flanked sequence(s), tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequence(s) in the Lhx6-expressing cells of the offspring.
The donating investigator reports tamoxifen-inducible Cre recombinase activity recapitulates the endogenous Lhx6 expression pattern, but with low efficiency of induction. They report tamoxifen-induc ..... | ||
| 016235 | B6(Cg)-Narfltm1.1Fsl/J | Repository- Live |
| These Iop1flox mutant mice possess loxP sites flanking exon 1 of the nuclear prelamin A recognition factor-like (Narfl or Iop1) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. IOP1 is required for cytosolic iron-sulfur protein assembly pathways. Iron-sulfur proteins are involved in the Krebs Cycle, oxidative phosphorylation, translation, iron regulatory pathways, and purine metabolism. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exon 1 deleted in the cre-expressing tissues. This strain may be useful for conditional deletion of IOP1 to study the cytoplasmic iron-sulfur complex assembly pathway. | ||
| 004742 | B6(Cg)-Ncf1m1J/J | Repository- Live |
| Peritoneal neutrophils and macrophages, bone marrow cells and neutrophils isolated from bone marrow of mice homozygous for Ncf1m1J fail to produce superoxide upon stimulation in vitro with N-formyl-methionyl-leucyl-phenylalanine (fMLP) or phorbol 12-myristate 13-acetate (PMA), as determined by kinetic spectrophotometric analysis of cytochrome c reduction. Western blot analysis detected no full-length NCF1/p47phox protein in cells from these mice; a faint band of slightly smaller molecular size than the wild type NCF1 protein was observed on probing with antibodies to NCF1. To exclude the possibility that the NCF1 protein is produced in cells of mutant mice but is degraded rapidly by endogenous proteases, bone marrow cells were isolated and samples prepared for western blot analysis in the presence of diisopropyl fluorophosphate (DFP); no difference was observed upon analysis of freshly prepared cell lysates made with and without DFP, indicatin ..... For more information please see the full phenotype on the strain data sheet | ||
| 014142 | B6(Cg)-Prkaa2tm1.1Sjm/J | Repository- Live |
| These Prkaa2 mutant mice possess loxP sites flanking exon 2 of the protein kinase, AMP-activated, alpha 2 catalytic subunit (Prkaa2) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Prkaa2 belongs to the serine/threonine protein kinase family and is the catalytic subunit of the 5'-prime-AMP-activated protein kinase (AMPK). AMPK is a sensor of the energy status of cells and ensures survival during stress. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exon 2 deleted in the cre-expressing tissues. When bred to transgenic mice expressing Cre recombinase driven by myxovirus (influenza virus) resistance 1 (Mx1) promoter/enhanced elements, PRKAA2 expression is abolished in hematopoietic cells. This strain may be useful for studying cell growth and energy expenditure. | ||
| 010777 | B6(Cg)-Pvalbtm1(cre/ERT2)Zjh/J | Repository- Live |
| The Pv-CreERT2 (Pvalb-CreERT2) knock-in allele both abolishes Pvalb (parvalbumin; also called PV or Pva) gene function and expresses a CreERT2 fusion protein (creERT2 fusion protein) from the Pvalb promoter/enhancer elements. Homozygous mice are viable and fertile. Homozygotes are expected to have a knockout phenotype similar to other null mutations of this gene and may exhibit muscle contractile, mitochondrial, and/or Purkinje cell abnormalities. Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Pv-CreERT2 mice are bred with mice containing loxP-flanked sequence(s), tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequence(s) in the Pvalb-expressing cells of the offspring.
The donating investigator reports tamoxifen-inducible Cre recombinase activity recapitulates the endogenous Pvalb expression pattern, but with low efficiency of induction. The ..... | ||
| 008449 | B6(Cg)-Rag2tm1.1Cgn/J | Repository- Live |
| These RAG-2del mutant mice harbor a pan deletion of exon 3 of the targeted locus. Homozygotes (RAG-2del/del) are viable and fertile, with pan deletion of the entire RAG-2 protein coding region. Homozygous mice may be expected to have the same knockout phenotype as other RAG-2 null mutants or similarly created RAG-2 exon 3 pan-deleted mutants; with hematopoietic and immune system defects including arrested B cell and T cell development at the pro-B and the pro-T cell stages, respectively. These RAG-2del mice may be useful in studying the role of RAG-2 in B cell and T cell development (including cancer and toxicology research as a xenograft/transplant host), T and B cell receptor (V(D)J) recombination, hematopoiesis, hematology, immunology, and inflammation research.
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 ..... | ||
| 010708 | B6(Cg)-Ssttm1(cre/ERT2)Zjh/J | Repository- Live |
| The Sst-CreERT2 (or SOM-CreERT2) knock-in allele both abolishes Sst gene function and expresses a CreERT2 fusion protein (creERT2 fusion protein) from the Sst promoter/enhancer elements. Heterozygous mice are viable and fertile. Homozygous mice are expected to have a knockout phenotype similar to other null mutations of this gene and may exhibit nervous system and metabolic abnormalities. Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Sst-CreERT2 mice are bred with mice containing loxP-flanked sequence(s), tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequence(s) in the Sst-expressing cells of the offspring.
The donating investigator reports tamoxifen-inducible Cre recombinase activity recapitulates the endogenous Sst expression pattern, but with low efficiency of induction. They report tamoxifen-inducible Cre recombinase activity is observed ..... | ||
| 007212 | B6(Cg)-Tnfrsf13ctm1Mass/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 IgMlow (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. | ||
| 001934 | B6(D2)-LmnaDhe/TyGrsrJ | Repository- Live |
| Heterozygotes are slightly smaller than normal and develop a sparse, graying, scruffy coat. They have short ear pinnae, an underdeveloped lower jaw, malocclusion, protruding eyes, and low bone mineral density. The skulls are small and disproportionate, and the cranial sutures fail to close. Females can have decreased fertility, but males do not. Males have diminished total body fat. Homozygotes die by approximately 10 days of age, have dysplastic, ulcerated skin and oral mucosae, and a more severe deficiency in skull growth and mineralization. | ||
| 016239 | B6(FVB)-Mir146tm1.1Bal/J | Repository- Live |
| Mice that are homozygous for this targeted mutation develop splenomegaly (due to both myeloproliferation and expanded hematopoiesis), lymphadenopathy, multi-organ inflammation with lymphocytic and monocytic infiltrates, tissue damage, and reduced lifespan. At 6-8 weeks of age, homozygotes do not display a visible autoimmune or inflammatory phenotype. By 6-8 months of age, homozygotes start to develop lymphoproliferative and myeloproliferative disease, and a 60-fold higher titer for auto-antibodies against double-stranded DNA compared to wildtype controls. As mice age, they develop anemia, thrombocytopenia, lymphopenia, extramedullary erythropoiesis, as well as tumors in secondary lymphoid organs (mostly in the spleen). By 1 year of age, the mice exhibit a severe phenotype. Homozygotes on the 129.B6 background have a survival rate of less than 20%, while approximately 40% of knock out mice on the C57BL/6 background survive past 500 days, as compared to the more than 80% survival rat ..... For more information please see the full phenotype on the strain data sheet | ||
| 005717 | B6(NOD) H2g7-Sostdc1shk/J | Repository- Live |
| Mice homozygous for the sharkey mutation on this predominantly C57BL/6J background have both upper and lower supernumerary incisors with separate roots for the extra teeth. When outcrossed to CAST/EiJ the F2 only have upper supernumerary incisors. | ||
| 001809 | B6-Aw-J.Cg-EdaTa-6J +/+ ArTfm/J | Repository- Live |
| Testicular feminization (ArTfm) 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 (EdaTa-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. | ||
| 008849 | B6.129(C)-Smn1tm1.1Jme/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. Homozygotes have an embryonic lethal phenotype and die at embryonic day 9. Exon 7 of Smn1 was excised via Cre recombination. The Donating Investigator reports that the phenotype of this strain is similar to the phenotype exhibited by mice carrying the Smn1tm1Hung allele. | ||
| 005085 | B6.129(Cg)-Cd44tm1Hbg/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. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. 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 f ..... | ||
| 013702 | B6.129(Cg)-Cep290tm1.1Jgg/J | Repository- Live |
| Homozygous Cep290 (centrosomal protein 290) targeted mutation neonates are runted and display retinal degeneration. Normal body weight is attained 1-2 months after birth. Both male and female homozygotes are sterile. This strain may be useful in studies of retinal degeneration, cilia/flagella development and fertility. | ||
| 007676 | B6.129(Cg)-Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo/J | Repository- Live |
| Mice homozygous for this mT/mG mutation are viable and fertile. These mice possess loxP sites on either side of a membrane-targeted tdTomato (mT) cassette and express strong red fluorescence in all tissues and cell types examined. Tail or whole body epifluorescence is sufficient to identify mT/mG homozygotes. When bred to Cre recombinase expressing mice, the resulting offspring have the mT cassette deleted in the cre expressing tissue(s), allowing expression of the membrane-targeted EGFP (mG) cassette located just downstream. The donating investigator reports that the ACTB promoter allows stronger and persistent expression of the fluorescent proteins (especially in adult cells) compared to the endogenous Gt(ROSA) locus alone. This double-fluorescent system allows direct live visualization of both recombined and non-recombined cells at single cell resolution, offering an internal control for phenotypic analysis of Cre-induced mosaic mutants and providing a second marker fo ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 ..... | ||
| 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. | ||
| 012941 | B6.129(SJL)-Foxn1tm1.1Dmsu/J | Repository- Live |
| These mice possess loxP sites on either side of exons 5 and 6 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. RT-PCR analysis of thymic cells isolated from homozygotes reveals the gene product (mRNA) levels are the same as wildtype control. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 5 and 6 deleted in the cre-expressing tissue(s).
When bred to a strain with inducible widespread Cre recombinase expression (see Stock No. 004682 for example), this mutant mouse strain may be useful in studies of thymic epithelial differentiation and T cell development. | ||
| 008471 | B6.129(SJL)-Oxtrtm1.1Wsy/J | Repository- Live |
| Mice homozygous for the Oxtrflox allele are viable and fertile, with loxP sites flanking exons 2-3 of the targeted gene. Expression and receptor binding distributions from the Oxtrflox targeted allele are reported to be normal when compared to wild-type. When Oxtrflox mice are bred to mice that express Cre recombinase, the resulting offspring will have the floxed region deleted in the cre-expressing tissue(s). These Oxtrflox mice may be used for spatial and temporal inactivation of the oxytocin receptor in studying (for example) parturition and lactation, as well as social, behavioral, and learning disorders such as autism and anxiety.
These Oxtrflox mice may also be useful along with the Oxt/EGFP AI03 transgenic mice (Stock No. 006043) or oxytocin targeted mutant mice (Stock No. 002713) from the same ..... | ||
| 012465 | B6.129-Abca2tm1Kdt/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. Although homozygotes are viable and fertile, few pups born to homozygous females survive. The Donating Investigator maintains the C57BL/6 congenic strain using heterozygous crosses. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis of cerebrum, cerebellum, spinal cord, heart, lung, kidney, liver, spleen, thymus, uterus, prostate, and ovary. Homozygotes exhibit a quivering or shaking phenotype and are more easily startled by sound, hence the "skittish" nickname designation. The tremor is without ataxia. Homozygotes exhibit hyperactivity. Although growth rate and food consumption are similar to wildtype controls, homozygotes have a reduced body weight. The observed hyperactivity and reduced body weight is more significant in female homozygotes. Ultrastructural analysis of myelin sheath in cerebrum ..... For more information please see the full phenotype on the strain data sheet | ||
| 013733 | B6.129-Accn2tm1Wsh/J | Repository- Live |
| Homozygous Accn2 (amiloride-sensitive cation channel 2, neuronal; also called ASIC1a) targeted mutant mice display alterations in conditioned and unconditioned fear behaviors, eye blink conditioning, long term potentiation, learned helplessness, seizure termination, retinal function, pain perception, and neuronal death in several neurodegnerative disorders. Transcripts and protein are lacking in central and peripheral nervous system tissue. This strain may be useful in studies of synaptic transmission, synaptic plasticity, depression, fear, anxiety, learning and memory. | ||
| 013127 | B6.129-Accn3tm1Wsh/J | Repository- Live |
| Homozygous Accn3 (amiloride-sensitive cation channel 3) targeted mutation mice display alterations in normal and pain-associated cutaneous mechanosensitivity and inflammatory pain sensation, visual loss associated with night blindness, and age-induced hearing loss. Mice show increased sensitivity of mechanoreceptors detecting light touch. Sensitivity of mechanoreceptors responding to noxious pinch is decreased as is the response of acid- and noxious heat-sensitive nociceptors. No mRNA is detectable by RT-PCR in the dorsal root ganglion. Protein is not found in trigeminal and dorsal root ganglion. This strain may be useful in further elucidating the role of this gene in mechanosensation. | ||
| 012430 | B6.129-Adrbk1tm1Mca/J | Repository- Live |
| Adrbk1 (adrenergic receptor kinase, beta 1; also known as Grk2) is the main G-protein-coupled receptor kinase in developing embryos, and lack of GRK2 expression results in embryonic lethality before gestational day 15.5. Homozygotes with this targeted mutation show defects which include failure of the heart to develop properly (thin myocardium syndrome). This strain will be useful for delineating the role of GRK2 activity in developmental processes. Heterozygotes exhibit altered adrenergic receptor-regulated heart function when tested as adults, and these mice can be useful for exploring the role of GRK2 function in the regulation of any G-protein coupled receptor subtype. Homozygous embryos lack GRK2 immunoreactivity. Heterozygote mouse brain and heart have 50% of normal GRK2 immunoreactivity. | ||
| 012431 | B6.129-Adrbk2tm1Rjl/J | Repository- Live |
| Adrbk2 (adrenergic receptor kinase, beta 2; also called GRK3) is the major G protein-coupled receptor kinase family member in olfactory neurons, and mice lacking GRK3 exhibit a deficit in desensitization to olfactants. In homozygous mice, airway smooth muscle cells exhibit supersensitivity to muscarinic agents, and brain neurons exhibit altered kappa opioid receptor-dependent tolerance. Expression is eliminated in olfactory neuroepithelium, brain, and airway smooth muscle cells. | ||
| 006952 | B6.129-Akt2tm1.1Mbb Ldlrtm1Her/J | Repository- Live |
| Independently, homozygous Akt2 mutant mice develop insulin resistance and diabetes, while LDLR homozygotes are predisposed to atherosclerosis. Double mutant mice that are heterozygous for the Akt2 allele and homozygous for the LDLR mutation are viable and fertile. These double mutant mice may be useful in studies of diabetes, metabolism, hyperglycemia, and atherosclerosis. | ||
| 007741 | B6.129-Arg1tm1Rki/J | Repository- Live |
| Homozygous AI-mutant mice completely lack hepatic arginase (AI) activity, exhibit hyperagrininemia, severe symptoms of hyperammonemia (ncluding decerebrate posture, lethargy, and high-frequency tremor of the extremities, particularly the tail) and die between 10-14 days after birth. Neural stem cells (NCSs) isolated from homozygous mice exhibit abnormal proliferation and differentiation. In addition, haploid germ cells carrying the disrupted AI allele may be less fit/less effective in forming zygotes compared to wild-type spermatozoa. Heterozygotes are viable and fertile. These AI-mutant mice may be useful in studying metabolic defects of arginase I deficiency, urea cycle (excretion of excess nitrogen), and neuronal development and function. | ||
| 004714 | B6.129-Bace1tm1Pcw/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. | ||
| 006353 | B6.129-Btlatm1Kmm/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis of splenocytes isolated from homozygous animals. Mutant mice exhibit increased sensitivity to antigen-induced experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis). T-cell proliferation is enhanced in response to antigen challenge. Although acute experimental allergic airway inflammation intensity is only slightly increased, the response duration is significantly prolonged. This mutant mouse strain may be useful in studies of immune response and autoimmunity, and in transplantation studies.
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 var ..... | ||
| 013770 | B6.129-Cacna1htm1Kcam/J | Repository- Live |
| Homozygous Cacna1h (calcium channel, voltage-dependent, T type, alpha 1H subunit; also called α1 3.2) targeted mutant mice have constitutively constricted coronary arterioles and focal myocardial fibrosis. Isolated arteries show normal contractile responses but reduced relaxation in response to acetylcholine and nitroprusside. Diffuse areas of cardiac fribrosis are observed in ventricular walls from 10-week old mice, but not those of wildtype mice. At 1 year of age, their hearts have a more severe cardiac pathology, including larger areas of fibrosis, necrosis and lymphocyte infiltration. Homozygotes are smaller than littermate controls. Heterozygotes do not show any abnormalities. Northern and/or Western blot analysis of brain, testis and dorsal root ganglion tissues confirms the loss of RNA and protein in mice. This strain may be useful in studies of coronary artery function and disease. | ||
| 010533 | B6.129-Cdc25atm1Dvb/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. S123A Cdc25a protein is altered at a key phosphorylation site. When measured in dermal fibroblasts (DF), the mutant protein has a prolonged half-life as compared to wild-type (60 vs. 90 minutes) suggesting that the mutation stabilizes the protein. DF treated with nocodazole contain cells with an increase in centrosome number. When nocodazole is combined with radiation, aneuploid cells with nearly 4N DNA content are observed. In addition, eighteen months after treatment with ionizing radiation, mice develop tumors at much higher percentage than wild-type (80% vs. 30%).
This mutant mouse strain may be useful in studies of cell cycle regulation, centrosome amplification in dermal fibroblasts and radiation-induced tumorigenesis.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles a ..... | ||
| 005319 | B6.129-Cdh1tm2Kem/J | Repository- Live |
| These mice possess loxP sites flanking exons 6 to 10 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. | ||
| 006910 | B6.129-Crkltm1Hkp/J | Repository- Live |
| While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die in utero. Immunoblots from homozygous tissues show no protein expression from the targeted gene. The prenatal lethality exhibited by homozygotes on this C57BL/6J congenic background (and also on a 129Sv genetic background) likely results from heart, liver, and placental defects. Please note that homozygous mutants on a mixed/outbred genetic background (129/Sv X Black Swiss) are viable and fertile. These mutant mice may be useful in studying the role of Crkl tyrosine-phosphorylation in Bcr/Abl (Philadelphia chromosome) chronic myelogenous leukemia (CML), acute lymphoblastic leukemia (ALL), Digeorge Syndrome (DGS) and Velocardiofacial Syndrome. | ||
| 004152 | B6.129-Ctnnb1tm2Kem/KnwJ | Repository- Live |
| These mice possess loxP sites located in introns 1 and 6 of the targeted gene. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to a strain expressing Cre recombinase in chrondocytes (see Stock No. 003554 for example), this mutant mouse strain may be useful in studies of chrondocyte differentiation. When bred to a strain expressing Cre recombinase in heart(see Stock No. 005650 or 005657 for example), this mutant mouse strain may be useful in studies of cardiovascular disease. When bred to a strain expressing Cre recombinase in midbrain/dorsal spinal cord (see Stock No. 007807 or > ..... | ||
| 009106 | B6.129-Cyp27a1tm1Elt/J | Repository- Live |
| These mice harbor a targeted mutation of the Cyp27a1 (cytochrome P450, family 27, subfamily a, polypeptide 1) locus that abolishes endogenous gene expression. Homozygous mice (also called Cyp27a1-/-, cyp27-/-, or sterol 27-hydroxylase-deficient mice) are viable and fertile, with no RNA or protein expression from the targeted gene detected in liver tissue. Both formation of bile acids and excretion of fecal bile acids are decreased in homozygous mice. Compensatory up-regulation of hepatic enzymes that convert cholesterol to bile acids (bile acid synthesis) is also observed. Cyp27a1-/- mice exhibit a dramatic increase in cytochrome P450 3A (Cyp3a11) which catalyzes side-chain hydroxylations of bile acid intermediates subsequently facilitating their excretion in the bile and urine. Homozygous mice also have increased expression of other nuclear xenobiotic receptor PXR (pregnane X receptor) target genes. | ||
| 013099 | B6.129-Dlg4tm1Rlh/J | Repository- Live |
| Homozygous Dlg4 (discs, large homolog 4 (Drosophila); PSD95) targeted mutation mice completely lack protein expression in the brain. No gross anatomical or obvious behavioral abnormalities are apparent in these mice. By approximately the second week of life, a reduction in the synaptic expression of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptors (AMPARs), but not N-methyl-D-aspartate receptors (NMDARs) is apparent. AMPAR function is impaired due to an increase in the proportion of synapses that lack functional AMPARs (silent synapses) rather than a general decline in activity. Frequency, but not amplitude, of AMPAR-mediated miniature excitatory postsynaptic currents (EPSCs) is reduced. Decay kinetics of NMDAR-mediated synaptic currents are slower and the magnitude of long-term potentiation (LTP) is greater in homozygotes. This strain may be useful for further characterizing the role of this gene in glutamatergic neurotransmission. | ||
| 013149 | B6.129-Dysftm1Kcam/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable, fertile and show a normal growth rate. Mice develop a slowly progressive muscular dystrophy. By the age of 2 months, a few individual necrotic and centrally nucleated fibers can be detected throughout the muscle; the number increases with age. By 8 months, the muscle develops all of the pathological characteristics of muscular dystrophy (e.g. regenerating fibers, split fibers, muscle necrosis with macrophage infiltration and fat replacement). The severity of the pathology varies in different muscles. Muscle fibers are defective in Ca2+-dependent sarcolemma resealing/repair. No protein product from the targeted gene is detected in skeletal muscle microsomes. This mutant mouse strain represents a model that may be useful in studies of muscle disease and repair. | ||
| 012885 | B6.129-Fbn1tm1Hcd/J | Repository- Live |
| Mice homozygous for this Fbn1 (fibrillin 1) Cys1037Gly missense mutation are small and die before two weeks of age. A similar mutation in man (Cys1039Tyr) is known to cause classic manifestations of Marfan syndrome in humans. Heterozygous mice develop proximal aortic aneurysms, mitral valve thickenings, pulmonary alveolar septation defects, mild thoracic kyphosis, and skeletal myopathy, but 90% reportedly live to one year of age. | ||
| 011112 | B6.129-Flt3tm1Dgg/J | Repository- Live |
| These mice carry the human W51 mutation, ITD, internal tandem duplication of amino acids 596 to 602, in the endogenous mouse Flt3 locus, which confers constitutive FLT3 signaling.
Mice that are homozygous for the targeted mutation are viable and fertile. The Donating Investigator reports that BALB/c mice carrying this allele are not as viable as mutants on the C57BL/6 background. Although FLT protein levels are comparable to wildtype, increased phospho-Flt3 (p-FLT3) and phospho-Stat5 (pSTAT5) levels are detected by flow cytometric analysis of homozygous bone marrow and splenic cells. Homozygotes exhibit leukocytosis, monocytosis and progressive splenomegaly. Mature myeloid and monocytic populations in homozygotes are increased, with reduced B and T cell populations. B cell development is arrested at the pre-B stage.
Heterozygotes have decreased liver size, hemoglobin levels, platelet counts and exhibit a milder maturing myeloid hyperplasia phenotype when compared to hom ..... For more information please see the full phenotype on the strain data sheet | ||
| 008470 | B6.129-Fxntm1Pand/J | Repository- Live |
| These mice express a (GAA)230 expansion repeat from the endogenous Fxn locus. Homozygotes produce an average of 75% of wild-type levels of frataxin protein, as assayed by Western blot densitometry analysis. The GAA repeat size was found to be stable over the 6 generations studied. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of Friedreich's ataxia. Importation of this model was supported by the Friedreichs Ataxia Research Alliance (FARA). | ||
| 012942 | B6.129-Gabra2tm1.1Geh/J | Repository- Live |
| These mutant mice carry substitutions of serine to histidine at amino acid position 270 and leucine to alanine at amino acid position 277 of exon 9. The point mutations confer alcohol and anesthesia insensitivity, while retaining near-normal GABA sensitivity. Approximately half of the homozygous mutant mice (from heterozygous crosses) die between birth and weaning. Homozygotes that survive to adulthood are fertile, normal in size and do not display any gross physical abnormalities. Mutant gene product (mRNA) is detected by RT-PCR analysis of whole brain total RNA. The alpha2 subunit protein levels did not differ between mice homozygous for the mutation and wildtype mice in the cortex and hippocampus. Homozygotes exhibit enhanced fear conditioning, reduced sensitivity to anesthesia (isoflurane), increased alcohol consumption without typical conditioned taste aversion, reduced ethanol induced stimulation of motor activity, and recover more slowly from ethanol?induced hypnosis. Den ..... For more information please see the full phenotype on the strain data sheet | ||
| 016162 | B6.129-Gfi1tm2Tmo/J | Repository- Live |
| These mutant mice express EGFP (Enhanced Green Fluorescent Protein) from the endogenous Gfi1 locus. No endogenous gene product (protein) is detected in thymocytes from homozygotes, as detected by FACS analysis. Homozygotes exhibit neutropenia, decreased thymocyte number, and defective B cell and T cell differentiation. The Donating Investigator reports that homozygous mice must be maintained under spf conditions and have a lifespan of 1 year. GFP fluorescence expression mimics the expression pattern of the endogenous gene. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Almost all thymocytes from heterozygotes fluoresce. Fluorescence of thymocytes from homozygotes is more intense than fluorescence observed in heterozygotes. At embryonic day 17.5, homozygous embryos exhibit disorganized inner ear sensory epithelia, with abnormal outer hair cells morphology. Neonate ..... For more information please see the full phenotype on the strain data sheet | ||
| 016163 | B6.129-Gfi1tm3(Gfib1)Tmo/J | Repository- Live |
| These mutant mice express mouse Gfi1b (growth factor independent 1B) from the endogenous Gfi1 locus. Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. Higher expression levels of Gfi1b transcript is detected in inner ears as measured by RT-PCR analysis. The Gfi1b knock-in did not completely rescue the Gfi1 knock out phenotype (see STOCK No. 016161). Homozygotes have slightly fewer granulocytes in bone marrow, a small accumulation in bone marrow of immature myeloid cells and monocytes, and fewer mature circulating granulocytes when compared to wildtype controls. At 3 to 3.5 months in age, homozygotes are deaf, do not display a Preyer reflex, abnormal auditory brainstem response (over 100 dB at 8 kHz and over 90 dB at 16 and 32 kHz), and exhibit head bobbing and abnormal reaching response. In neonatal mutants, the cochlear inner hair cells are morphol ..... For more information please see the full phenotype on the strain data sheet | ||
| 016161 | B6.129-Gfi1btm1Tmo/J | Repository- Live |
| These mutant mice express EGFP (Enhanced Green Fluorescent Protein) from the endogenous Gfi1b locus. Homozygous mice have an embryonic lethal phenotype, failing to develop past embryonic days 15. Homozygous embryos, embryonic day 13.5, are pale, have internal hemorrhaging and exhibit very few maturing erythrocytes. No endogenous gene product (protein) is detected in fetal liver cells from homozygous embryos by Western blot analysis. GFP fluorescence expression mimics the expression pattern of the endogenous gene. Fluorescence is detected in fetal livers of heterozygous embryos, at age embryonic day 13.5. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. In adult heterozygotes, fluorescence is detected in maturing erythroblasts in the bone marrow, with the greatest expression in Ter119high, CD71high late erythroblasts. Fluorescence is also detecte ..... For more information please see the full phenotype on the strain data sheet | ||
| 007561 | B6.129-Hif1atm3Rsjo/J | Repository- Live |
| These mice possess loxP sites on either side of exon 2 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 deleted in the cre-expressing tissue(s).
For example, when crossed to a strain expressing Cre recombinase in skeletal and cardiac muscle (see Stock No. 006475), this mutant mouse strain may be useful in studies of the metabolic control of muscle function. When bred to a strain with the targeted null allele in von Hippel-Lindau syndrome homolog, Vhlh (Stock No. 004081) and a strain expressing Cre recombinase in liver (Stock No. 003574), this mutant mouse strain may be use ..... | ||
| 005867 | B6.129-Ido1tm1Alm/J | Repository- Live |
| Homozygous mice are viable and fertile with normal immune system development and function. They exhibit no spontaneous autoimmune disorders. No gene product (mRNA or protein) from the targeted gene is detected in the epididymis. At embryonic day 10.5, endogenous protein is absent from all cells at the maternal-fetal interface when both parents are homozygous for the targeted gene. Allogeneic and syngeneic pregnancy outcomes are unaffected by this mutation. In contrast to wild-type, anti-proliferative treatments (CTLA4-Ig, IFNalpha, or CpG-ODN) do not suppress T cell expansion both in vivo and in vitro. In addition, homozygous dendritic cells isolated from lymph nodes draining (induced) tumor sites have no suppressor activity. These mice may be useful in studies of pregnancy and reproductive immunology (tryptophan degradation, T cell activation, clonal expansion) as well as autoimmune disease, tissue transplantation, fostering, acquired tolerance/T cell anergy, and immunos ..... For more information please see the full phenotype on the strain data sheet | ||
| 010818 | B6.129-Ifnb1tm1Lky/J | Repository- Live |
| The Ifnb1 gene was targeted to introduce an internal ribosomal entry site (IRES) and enhanced yellow fluorescent protein (EYFP) immediately behind the stop codon of the gene. All regulatory elements, including the polyadenylation signal, are left intact and are derived from the endogenous gene. When activated, the targeted gene co-translates EYFP both in vitro and in vivo, leaving cells that have made type 1 interferon-beta readily detectable by flow cytometry or immunohistochemistry. Expression of EYFP faithfully mimics the expression of the targeted gene. | ||
| 006412 | B6.129-Il12btm1Lky/J | Repository- Live |
| Mice homozygous for this bicistronic "yet40" allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The IRES-EYFP is inserted downstream of the endogenous stop codon, allowing for normal expression of the endogenous gene and simultaneous EYFP reporter expression. ELISA assays confirm that p40 protein is expressed at similar levels in homozygous mutant and wildtype mice. The EYFP reporter marks dendritic cell (DC) and macrophage lineage cells that produce p40 following stimulation with toll-like receptor (TLR) ligands both in vivo and in vitro. These mice may be useful for labeling activated IL12/23 p40 expressing cells in studies of immunology and immunity, TLR signal cascades, cancer immunity, and vaccine development. | ||
| 007251 | B6.129-Mapttm1Hnd/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 analysis of total brain RNA, Western blot analysis of total brain homogenates or immunostraining of coronal brain sections. Hippocampal neurons from homozygous embryos, in primary culture, have delayed axonal extension and shorter total dendritic length when compared to wildtype controls. Mitochondria in the primary culture cells cluster at the distal end of axons. The frequency and velocity of mitochondrial anterograde movements is increased. This mutant mouse strain may be useful in studies of neuronal development, axonogenesis, and organelle movement. | ||
| 013577 | B6.129-Mesdc2tm1Bch/J | Repository- Live |
| Mutant homozygotes display an embryonic lethal phenotype, failing to develop past embryonic day 9.5. At embryonic day 7.5, homozygous embryos lack a primitive streak and mesodermal derivatives with a smaller epiblast surrounded by an expanded parietal endoderm. Mice homozygous for this targeted mutation exhibit a phenotype similar to homozygotes carrying the mesd deletion (Holdener et al., Development. 1994;120(5):1335-46. Hsieh, J-C et al Cell 2003; 112(3): 355-367). Wnt signaling is blocked in homozygous embryos (aged embryonic day 7.5) as assessed by crossing with B6.Cg-Tg(BAT-lacZ)3Picc/J (STOCK No. 5317) mice that express beta-galactosidase in the presence of activated beta-catenin. Expression of the pluripotency molecular markers, Oct4, Nanog, and Sox2, continues in the epiblast of homozygous embryos (day 8.5). LRP2, low density lipoprotein receptor-related protein 2, or Megalin, protein is not localized to the apical membrane of the visceral endoderm ..... For more information please see the full phenotype on the strain data sheet | ||
| 014607 | B6.129-Mkkstm1Vcs/J | Repository- Live |
| In this strain a neomycin (neo) resistance cassette replaces exon 3 of the McKusick-Kaufman syndrome protein (Mkks or Bbs6) gene, abolishing gene function. Homozygous females are viable and fertile, while homozygous males are infertile due to lack of flagellated sperm. These mice are also smaller at birth than littermates. Mutations in Mkks have been known to cause McKusick-Kaufman syndrome (MKS) and Bardet-Biedl syndrome (BBS). MKS is a disorder characterized by post-axial polydactyly, congenital heart defects and hydrometrocolpos, while BBS is a pleiotropic disorder characterized by retinal and photoreceptor degeneration, obesity, polydactyly, renal abnormalities, hypogenitalism and cognitive impairment. Mkks-/- mice lack MKKS expression in brain, lung, heart, kidney, eye, liver, spleen, testes, and muscle. They develop age-related blindness due to retinal degeneration, are obese, and have elevated blood pressure. These mice may be useful for ..... For more information please see the full phenotype on the strain data sheet | ||
| 005111 | B6.129-Mmp7tm1Lmm/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis of the small intestine. Immunohistochemical analysis of intestinal tissue from homozygotes does not detect the gene product (protein) in Paneth cells. Mutant mice have impaired innate host defense response due to the lack of mature crypt defensin proteins in intestinal epithelium. These mice are more susceptible to bacterial infection of the small intestine mucosal epithelium. Wound repair (reepithelialization) and neutrophil infiltration following respiratory airway injury is defective. Apoptosis is reduced in prostate tissue following castration, and in pancreatic acinar cells following pancreatic duct ligation. This mutant mouse strain may be useful in studies related to intestinal and pancreatic tumorigenesis, epithelial wound repair, inflammation and mucosal immune resp ..... For more information please see the full phenotype on the strain data sheet | ||
| 010491 | B6.129-Per1tm1Drw/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 superchiasmatic nuclei. Homozygotes housed in constant darkness exhibit gradual circadian arrhythmicity (rhythmicity is not lost initially). Homozygotes exhibit phase shift responses to light. This mutant mouse strain may be useful in studies of circadian rhythm and sleep pattern.
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. | ||
| 004584 | B6.129-Ppargtm2Rev/J | Repository- Live |
| These mice possess loxP sites on either side of exons 1 and 2 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to a strain expressing Cre recombinase in adipose tissue (see Stock No. 005069 for example), this mutant mouse strain may be useful in studies of insulin resistance. | ||
| 008597 | B6.129-Ppargc1atm1Brsp/J | Repository- Live |
| Mice that are homozygous for this targeted mutation are fertile, normal in size and do not display any gross physical or behavioral abnormalities. Approximately half of homozygotes exhibit postnatal lethality. The Donating Investigator reports maintaining homozygous pups at a higher temperature (77°F) increases their survival. No gene product (mRNA or protein) is detected by RNA hybridization, real-time PCR analysis of skeletal muscle or liver, or Western blot analysis of brown fat. Histological examination of the brown fat from homozygotes reveals abnormal accumulation of large lipid droplets. Examination of brain tissue shows spongiform lesions and gliosis. When fed a high fat diet homozygotes have increased insulin sensitivity, glucose tolerance and reduced body weight. After 24 hours of fasting, homozygotes develop mild hypoglycemia. Mutants have impaired mitochondrial function and gluconeogenesis and are hypermetabolic as well as hyperactive. Homozygotes are unable to survive ..... For more information please see the full phenotype on the strain data sheet | ||
| 008100 | B6.129-Prdm1tm1Clme/J | Repository- Live |
| These mice possess loxP sites in introns flanking exons 6 to 8 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 6 to 8 deleted in the cre-expressing tissue(s). When bred to a strain expressing Cre recombinase during B-lymphocyte development and differentiation (see Stock No. 004126 for example), this mutant mouse strain may be useful in studies of humoral immune response. | ||
| 011029 | B6.129-Rpl22tm1.1Psam/J | Repository- Live |
| Mice homozygous for this RiboTag allele are viable and fertile, with a targeted mutation of the ribosomal protein L22 (Rpl22) locus harboring a loxP-flanked wildtype C-terminal exon 4 followed by an identical C-terminal exon 4 that is tagged with three copies of the hemagglutinin (HA) epitope before the stop codon. Prior to exposure to Cre recombinase, RiboTag mice express the wildtype RPL22 protein (15 kDa). When the RiboTag mice are bred to cre-expressing mice, offspring will have the floxed wildtype exon 4 deleted in the cre-expressing tissue and subsequent use of the downstream HA epitope-tagged exon 4 as the terminal exon. The 23 kDa HA epitope-tagged ribosomal protein (RPL22HA) is incorporated into actively translating polyribosomes. These RiboTag mice allow Cre-mediated HA epitope tagging of ribosomes from user-defined cell types and/or immunoprecipitation of ribosomes bound to mRNA from those specific cell types. | ||
| 012772 | B6.129-Sirt2tm1.1Fwa/J | Repository- Live |
| 014604 | B6.129-Slc17a9tm1.1Rpa/J | Repository- Live |
| Mice homozygous for this Slc17a9flox allele are viable and fertile, with loxP sites flanking exons 2-3 of the solute carrier family 17, member 9 (Slc17a9) gene. Slc17a9 is is a vesicular nucleotide transporter expressed in the adrenal gland, brain, and thyroid gland. When bred to mice that express Cre recombinase, the resulting offspring will have the sequences encoding the endogenous signal peptide deleted in the cre-expressing tissue(s); this is expected to produce a null allele. These mutant mice may be useful in generating conditional mutations for studying the role of Slc17a9 in vesicular storage and ATP exocytosis. | ||
| 010773 | B6.129-Trpv3tm1Apat/J | Repository- Live |
| Homozygous (TRPV3-/-) mice are viable and fertile, with deletion of Trpv3 (transient receptor potential cation channel, subfamily V, member 3) exons resulting in low levels of truncated TRPV3 transcript that does not encode the putative pore region or adjacent transmembrane domains five and six (essential domains of the ion channel). Homozygous mice lack functional TRPV3 with no abnormal affects on TRPV1/TRPV4 expression or overall dorsal root ganglia or skin anatomy. TRPV3-/- mice have strong deficits in responses to innocuous and noxious heat stimuli, but not in other sensory modalities, and retain a residual sensitivity to warm temperatures. Compared to wildtype mice, TRPV3-deficient mice are resistant to the anxiolytic-like and antidepressive-like behavioral effects (and concomitant changes in c-Fos activation in the brain) following treatment of the TRPV3 agonist, incensole acetate. Unlike wildtype keratinocytes, TRPV3-deficient keratinocytes are not a ..... For more information please see the full phenotype on the strain data sheet | ||
| 004146 | B6.129-Tg(Pcp2-cre)2Mpin/J | Repository- Live |
| These transgenic mice express a cre gene inserted into exon 4 of a Pcp2 gene. Mice homozygous for the insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Recombinase activity is observed in most Purkinje cells and some retinal bipolar neurons. Small amounts of activity are observed in an unidentified population of cells of the central nervous system tissue. Recombination is first observed around postnatal day 6 and is fully established 2 to 3 weeks after birth.
View cre expression characterization. | ||
| 008451 | B6.129P(Cg)-Ptprca Cx3cr1tm1Litt/LittJ | Repository- Live |
| Mice that are homozygous for the CX3CR1-GFP targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. RT-PCR analysis of lymphoid tissue from homozygotes detects mutant gene product (mRNA) and no wild type gene product (mRNA). Flow cytometric analysis of peripheral blood cells identified a subset of green fluorescent cells not observed in wild type mice. Enhanced Green Fluorescent Protein (EGFP), but not the endogenous gene, is expressed in monocytes, dendritic cells, NK cells, and brain microglia, mimicking endogenous gene expression. The same subset of peripheral blood cells isolated from heterozygote mice express detectable levels of EGFP. Immunohistochemical analysis of spleen and peripheral nerve tissue from homozygotes does not detect EGFP. These mice also express the CD45.1 (Ly5.1 or Ptprca) allele, which is atypical for the C57BL/6 congenic background, and this marker may be used to track donor cell popul ..... For more information please see the full phenotype on the strain data sheet | ||
| 005582 | B6.129P-Cx3cr1tm1Litt/J | Repository- Live |
| Mice that are homozygous for the CX3CR1-GFP targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. RT-PCR analysis of lymphoid tissue from homozygotes detects mutant gene product (mRNA) and no wild type gene product (mRNA). Flow cytometric analysis of peripheral blood cells identified a subset of green fluorescent cells not observed in wild type mice. Enhanced Green Fluorescent Protein (EGFP), but not the endogenous gene, is expressed in monocytes, dendritic cells, NK cells, and brain microglia, mimicking endogenous gene expression. The same subset of peripheral blood cells isolated from heterozygote mice express detectable levels of EGFP. Immunohistochemical analysis of spleen and peripheral nerve tissue from homozygotes does not detect EGFP. These CX3CR1-GFP mutant mice may be useful in studies of leukocyte migration and trafficking, as well as for transplantation studies.
Of note, CX3CR1-GFP mice are also avail ..... | ||
| 016520 | B6.129P2(129S4)-Eif2c2tm1.1Tara/J | Repository- Live |
| These mice possess loxP sites on either side of exons 9-11 in the Eif2c2 (eukaryotic translation initiation factor 2C, 2) gene, also known as Ago2. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, the Mid domain is deleted and Ago2 expression is lost, causing functional inactivation of the gene.
For example, when crossed to a strain expressing interferon-inducible Cre recombinase (see Stock No. 003556), this mutant mouse strain may be useful in studies of microRNA homeostasis. | ||
| 006621 | B6.129P2(C)-Ccr7tm1Rfor/J | Repository- Live |
| Homozygous mice are viable and fertile and show delayed primary B or T cell immune responses. Lymph nodes from homozygous mice are devoid of naive T cells and dendritic cells (DCs), but the T cell populations in the blood, the red pulp of the spleen, and in the bone marrow are greatly expanded. Secondary lymph organs exhibit morphological abnormalities, and adoptive transfer experiments demonstrate impaired B- and T-cell migration. In a model of acute allogeneic tumor rejection, homozygous mice fail to reject subcutaneously injected MHC class I mismatched tumor cells, and cytotoxic activity of allospecific T cells is severely compromised. These mutant mice (along with CXCR5-deficient mice - Stock No. 006659) - may be useful in immunological studies of chemokine receptors, including T- and B-cell function in primary and adaptive immune responses, entry of lymphocytes and dendritic cells into secondary lymphoid organs (and their hom ..... For more information please see the full phenotype on the strain data sheet | ||
| 006785 | B6.129P2(C)-Cd19tm1(cre)Cgn/J | Repository- Live |
| Homozygous mutant mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Homozygotes have a deficiency in the B-1 subset of B-lymphocytes along with a concomitant reduction in serum IgM. Their ability to respond to T-cell-dependent antigens is severely impaired, and they fail to form splenic germinal centers. In addition to disrupting the targeted gene, the targeting construct also introduced a cre cassette into exon 2 of the targeted gene, effectively placing cre expression under the control of the endogenous promoter. The Cd19 promoter specifically directs cre expression at the earliest stages and throughout B-lymphocyte development and differentiation. Although homozygous mutant mice are Cd19-deficient, heterozygous mice are phenotypically normal, and can be used for specific deletion of loxP-flanked (floxed) targets in B-lymphocytes.
In an attempt to offer alleles on well-characte ..... | ||
| 003890 | B6.129P2(C)-Mecp2tm1.1Bird/J | Repository- Live |
| Homozygous null mice are viable and appear normal at birth. No Mecp2 gene product (mRNA or protein) is detected in tissues. Mobility problems are apparent at 3-8 weeks of age. Mice exhibit hindlimb clasping and uneven breathing. An uneven wearing of teeth associated with misalignment of the jaws is observed in 50% of the animals. Adult males do not mate and their testes remain internal although sperm are present in the cauda epididymis. Symptom progression is variable, but mice can be expected to undergo weight loss, shivering, continued mobility problems before succumbing. Expected lifespan is about 50-60 days. Heterozygous female mice display mobility problems and hindlimb clasping starting at about 6 months, but the symptoms appear not to be progressive. This mutant mouse strain represents a model that may be useful in studies related to Rett Syndrome. Importation of this model was supported in part by the Rett Syndrome Research Foundation. | ||
| 008289 | B6.129P2(C)-Ptprjtm1.2Weis/J | Repository- Live |
| Gene targeting was used to remove a transmembrane domain from the targeted protein. Homozygotes exhibit a partial peripheral B cell development block at the first transitional stage (T1), although total T or B cell numbers in the spleen and lymph node are unchanged. Truncated product (mRNA) is detected by Northern blot analysis of splenocytes isolated from homozygous animals. A secreted protein without known physiologic consequences is detected in serum from homozygous animals, but no surface protein is detected on cells of hematopoietic lineage, including T cells, B cells, and myeloid cells. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities; homozygotes are not fertile. This strain may be useful in studies of immune responses. | ||
| 006084 | B6.129P2(Cg)-Foxg1tm1(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. On the C57BL/6 background, forebrain volume in heterozygotes is substantially reduced especially in the cerebral cortex (40.7%), striatum (29.7%), and hippocampus (18.6%). In the adult, the thalamus is reduced in volume by 21.6%. This mutant mouse strain represents a model that ma ..... For more information please see the full phenotype on the strain data sheet | ||
| 011008 | B6.129P2(Cg)-Gt(ROSA)26Sortm1(tTA)Roos/J | Repository- Live |
| Mice heterozygous for the ROSA:LNL:tTA conditional mutation of the Gt(ROSA)26Sor locus are viable and fertile, with a loxP-flanked STOP cassette preventing transcription of a downstream optimized/modified tetracycline-controlled transactivator protein ("mtTA"). Applying both Cre-lox and Tet-Off technologies, these ROSA:LNL:tTA mutant mice may be useful to generate compound mutant mice in which expression of a tetracycline-responsive promoter element (TRE; also called tet-operator or tetO)-driven gene of interest can be both directed to the cell types defined by the chosen Cre recombinase expression, as well as turned off by the addition of tetracycline (or its analog doxycycline (dox)). | ||
| 010611 | B6.129P2(Cg)-Ighg1tm1(IRES-cre)Cgn/J | Repository- Live |
| Homozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre recombinase expression is induced by transcription of the immunoglobulin gamma1 heavy chain constant region gene (Cg1) segment and is detected as early as 4 days in 25-50% of germinal center B cells following immunization with T cell dependent antigens. By 12-14 days, 75-85% of germinal center B cells exhibit Cre-mediated recombination. Cre is detected mostly in IgG1, but also in IgG2 and IgA-expressing germinal center B cells as well as a small number of IgM+ germinal center B cells precursors.
Homozygotes exhibit a reduction in IgG1+ memory B cells and in IgG1 serum antibody titers. When bred with a mouse carrying a loxP site-flanked DNA sequence, Cre-mediated recombination results in deletion of the flanked genome segment in tissues that express the Cre transgene. This mutant mouse strain may be useful to study gene function in germinal cent ..... For more information please see the full phenotype on the strain data sheet | ||
| 007572 | B6.129P2(Cg)-Rorctm2Litt/J | Repository- Live |
| Mice homozygous for this Rorc(γtGFP (or RORγt)GFP) mutant allele are viable and fertile. While Rorcγ mRNA is detected in liver in Rorc(γ)tGFP homozygotes, mRNA and protein for the thymus-specific isoform (Rorcγt) encoded by the targeted allele are not detected in the thymus. EGFP expression reports Rorc(γt) transcription in the thymi of adult Rorc(γt)GFP mice. Homozygous mice exhibit abnormal lymph node, Peyer's patch, and lymphoid tissue inducer (LTi) cell development. Mice with Rorcγt-deficient T cells lack tissue-infiltrating proinflammatory T-helper cells (Th17 cells), and are protected from induced autoimmune disease (EAE) on this genetic background. The donating investigator also reports increased thymoma incidence with age in homozygotes. These RorcγtGFP mutant mice may be useful in studying immune system homeostasis, T cell repertoire selection, CD4/CD8 double positive (CD4+/CD8 For more information please see the full phenotype on the strain data sheet | ||
| 009088 | B6.129P2(SJL)-Myd88tm1.1Defr/J | Repository- Live |
| Homozygous mice are viable and fertile. The Myd88-deficient allele encodes a deletion of exon 3 of the myeloid differentiation primary response gene 88 locus. Myd88-deficiency is associated with a number of immune system abnormalities, as well as hematopoietic system, molecular signaling, and apoptotic abnormalities. | ||
| 013224 | B6.129P2-Abl1tm2.1Goff/J | Repository- Live |
| These Abl1flox/flox mutant mice posses loxP sites flanking exons 5-6 of the c-abl concogene 1, non-receptor tyrosine kinase gene, Abl1. Mice that are homozygous for this allele are viable, fertile, and normal in size. When these Abl1flox/flox mutant mice are bred to mice that express Cre recombinase, the resulting offspring will have exons 5-6 deleted in the cre-expressing tissue. This strain may be useful for studying the growth, development, and physiology of cardiac tissue. | ||
| 005775 | B6.129P2-Adipor2tm1Dgen/J | Repository- Live |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 002682 | B6.129P2-Agtr1atm1Unc/J | Repository- Live |
| Mice homozygous mice for the targeted mutation are viable and fertile. Pressor responses to angiotensin II infusions are absent and blood pressure levels are ~24 mmHg lower than normal wildtype siblings. Heterozygous mice have blood pressure levels ~12 mmHg lower than normal wildtype siblings and show qualitatively altered responses to angiotensin II infusions. | ||
| 004912 | B6.129P2-Akt1tm1Mbb/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and do not display any gross behavioral abnormalities. Homozygotes exhibit lower fertility. Female homozygotes do not nurse well; up to 50% perinatal mortality can occur. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of mouse embryonic fibroblasts. Homozygotes are only 80% of wildtype body weight at birth, and remain small. This mutant mouse strain may be useful in related to organismal growth. | ||
| 002055 | B6.129P2-Apoa1tm1Unc/J | Repository- Live |
| Mice homozygous for the Apoa1tm1Unc targeted mutation have no APOA1 protein in their plasma. They have severely reduced levels of plasma cholesterol and HDL-cholesterol after overnight fasting. They also show a deficiency in alpha-migrating HDL particles. The Apoa1tm1Unc mutant mice appear to develop normally. | ||
| 002053 | B6.129P2-Apobtm1Unc/J | Repository- Live |
| The Apobtm1Unc targeted mutation produces a truncated form of the apolipoprotein B protein (APOB70)and no apoB100 that is similar to human familial hypobetalipoproteinemia condition. Expression of apoB48 is not altered. Homozygous mice show greatly reduced levels of plasma APOB, beta-lipoproteins, and total cholesterol. They also have reduced plasma triglyceride concentrations, fasting chylomicronemia, and reduced high density lipoprotein (HDL) cholesterol. Homozygotes also have a high incidence of exencephaly and hydrocephaly. Heterozygous mice show a slight increase over wildtype in the incidence of hydrocephaly. | ||
| 009120 | B6.129P2-Axin2tm1Wbm/J | Repository- Live |
| Homozygous mice are viable and fertile, with the Axin2lacZ (or conductinlacZ) mutation that both abolishes endogenous Axin2 gene function and expresses NLS-lacZ under the control of the endogenous Axin2 promoter/enhancer regions. Homozygous mice exhibit cranial skull defects and malformations of skull structures; a phenotype resembling craniosynostosis in humans. Specifically, homozygous mice show an obvious reduction in head growth within the first 3 weeks after birth, resulting from developmental defects of the cranial skull (premature fusion of cranial sutures) at early postnatal stages. Axin2-deficient mice have abnormal calvarial morphogenesis/osteoblast development. Because Axin2 is a negative regulator of the canonical Wnt pathway that suppress signal transduction by promoting β-catenin degradation, the NLS-lacZ expression in these Axin2lacZ (or conductinlacZ) mutant mice may be useful in monitoring end ..... For more information please see the full phenotype on the strain data sheet | ||
| 002687 | B6.129P2-Ccl3tm1Unc/J | Repository- Live |
| Mice homozygous for the Scya3tm1Unc targeted mutation are viable and fertile. Homozygous mutant mice are resistant to Coxsakievirus-induced myocarditis. Mutant mice infected with influenza virus show reduced pneumonitis and delayed clearance of virus. There are no overt hematopoietic abnormalities. Also known as macrophage inflammatory protein 1a, Mip1a. | ||
| 005090 | B6.129P2-Ccl5tm1Hso/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis of lipopolysaccharide (LPS) stimulated peritoneal exudates cells. Homozygous mice have a reduced number of CD44 high CD4+ splenic T-cells. Delayed-type hypersensitivity (DTH) response (swelling) is impaired in homozygous mice sensitized with subcutaneous injection of keyhole limpet hemocyanin or bovine purified protein derivative. Immunohistochemical analysis of the DTH treated footpads reveals that the numbers of infiltrating macrophages is decreased, while infiltrating CD4+ and CD8+ T cells numbers remain unchanged. In vitro T cell proliferation, IFN-gamma and IL2 production is diminished. This mutant mouse strain may be useful in studies of delayed-type hypersensitivity and inflammatory responses. | ||
| 005427 | B6.129P2-Ccr5tm1Kuz/J | Repository- Live |
| At birth, mice homozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No transcript is detected in splenocytes or peritoneal macrophages. Thioglycollate-elicited peritoneal macrophages from homozygotes exhibit a delayed period before reaching peak mobilization (72 hours vs. 36 for wild type mice). 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 5427. 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. | ||
| 005793 | B6.129P2-Ccr6tm1Dgen/J | Repository- Live |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005794 | B6.129P2-Ccr7tm1Dgen/J | Repository- Live |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 002928 | B6.129P2-Cd40tm1Kik/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice exhibit impaired immunoglobulin class switching and germinal center formation. | ||
| 005786 | B6.129P2-Cnr2tm1Dgen/J | Repository- Live |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 016186 | B6.129P2-Cry1tm1Asn/J | Repository- Live |
| Cry1 (cryptochrome 1 (photolyase-like)) is required for normal expression of circadian behavioral rhythms. Homozygous targeted mutant ("knockout") mice have a circadian period 1 hour shorter than wild type mice and acute light induction of Per1 (period homolog 1 (Drosophila)) mRNA in the suprachiasmatic nucleus (SCN) is blunted. | ||
| 016185 | B6.129P2-Cry2tm1Asn/J | Repository- Live |
| These targeted mutant Cry2 (cryptochrome 2 (photolyase-like); blue-light photoreceptor) mice have a lower sensitivity to acute light induction of Per1 (period homolog 1 (Drosophila)) in the suprachiasmic nucleus (SCN), but exhibit normal circadian oscillations of Per1 and Cry1 (cryptochrome 1 (photolyase-like)) mRNA in the SCN. The mutant has an intrinsic circadian period about 1 hour longer than normal and exhibits high-amplitude phase shifts in response to light pulses administered at circadian time 17. Homozygotes are viable and born at predicted Mendelian ratios. Analysis of homozygotes by Northern and in situ hybridization revealed a complete lack of mRNA. | ||
| 005796 | B6.129P2-Cxcr3tm1Dgen/J | Repository- Live |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005693 | B6.129P2-Cxcr6tm1Litt/J | Repository- Live |
| Mice homozygous for this EGFP "knock-in" are viable, fertile, normal in size, and do not display any behavioral abnormalities when maintained under barrier conditions. Lymph nodes and spleen show no endogenous gene expression. Lymphocytes from heterozygotes, but not homozygotes, show endogenous ligand binding. EGFP expression is restricted to spleen and lymph nodes, specifically activated/memory T cells, with a slightly higher intensity in homozygotes. Homozygous null mice show decreased EGFP+ CD1d-reactive NKT patrolling efficiency and decreased severity of induced acute hepatitis, while heterozygotes and wildtype mice show no differences. This mutant may be useful in studies of hepatitis, HIV, SIV, fluorescent T cell tracking, and various immune responses. | ||
| 004744 | B6.129P2-Esr1tm1Ksk/J | Repository- Live |
| At birth, mice homozygous for the targeted allele are viable and normal in size and appearence. Female mice exhibit ovaries that lack corpora lutea and hypoplastic uteri that are unresponsive to estrogen. In males, below normal testis weight is associated with a diminished sperm count (10% of normal). Homozygous females are infertile. The fertility of homozygous males is greatly reduced, but not abolished. | ||
| 004745 | B6.129P2-Esr2tm1Unc/J | Repository- Live |
| Mice that are homozygous for this targeted allele are viable, normal in size and do not display any gross physical abnormalities. Stop codons inserted into exon 3 result in the production of truncated transcripts that are unlikely to be translated into a functional protein. Immunostaining of ovary tissue derived from homozygous females fails to detect protein product. Homozygous females are subfertile, producing fewer and smaller litters than wildtype controls. Decreased numbers of oocytes are also produced in response to superovulation (6 compared to 33.7 in wildtype controls). Male homozygotes are fertile and present no marked abnormalities other than epithelial hyperplasia in the bladder wall and prostatic collecting ducts. This mutant mouse strain may be useful in studies related to discerning the physiological roles of the estrogen signaling system. | ||
| 003171 | B6.129P2-Fcgr3tm1Sjv/J | Repository- Live |
| Mice homozygous for the Fcgr3tm1Sjv targeted mutation, which eliminates the ligand-binding alpha chain of FcgammaRIII, are viable and fertile. Homozygous mutant mice lack NK cell-mediated antibody-dependent cytotoxicity, phagocytosis of IgG1-coated particles by macrophages, and IgG-mediated mast cell degranulation. They are resistant to IgG-dependent passive cutaneous anaphylaxis, and exhibit an impaired Arthus reaction. | ||
| 016094 | B6.129P2-Git2Gt(XG510)Byg/WeisJ | Repository- Live |
| A targeting vector containing β-galactosidase was randomly inserted downstream of exon 2 of the endogenous G protein-coupled receptor kinase-interactor 2 (Git2) gene. Homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This β-geo secretory trap mutation abolishes endogenous gene function and expresses a Git2-exon1-2/lacZ fusion protein. Git2 belongs to the family of ADP-ribosylation factor GTPase-activating proteins (ARF-GAP) and has been implicated in the regulation of G protein-coupled receptor sequestration, cell migration, T-cell activation, neuronal spine formation, and aggregate formation in Huntington's disease. GIT2 expression is seen throughout the liver, lungs, spleen, muscle, and the central nervous system. Expression of GIT2 is also seen during absent spermatid differentiation but is absent in mature spermatids. These mice may be useful as a lacZ reporter for Git2 e ..... For more information please see the full phenotype on the strain data sheet | ||
| 013586 | B6.129P2-Gt(ROSA)26Sortm1Nik/J | Repository- Live |
| These 3373 3-state Cre-sensitive (3373 3SCS) mice contain a construct designed to insert (from 5' to 3') a floxed-STOP cassette, tdTomato open reading frame (ORF), and a floxed-internal ribosome entry site (IRES) fused to an enhanced green fluorescent protein (GFP) ORF. The IRES-eGFP element was flanked by 3373 mutant loxP sites (which recombine at 10% the efficiency of wildtype loxP sites). This vector was inserted into the Gt(ROSA)26Sor locus allowing for widespread expression. The floxed-STOP cassette causes termination of transcription and results in no expression of either fluorophore. When bred to mice that express Cre recombinase, offspring will have the floxed-STOP cassette deleted in the cre-expressing tissue(s). This deletion results in tdTomato and/or GFP expression depending on how much Cre-recombinase the cells express. When crossed with a strain expressing low amounts of Cre recombinase, partial recombination results in tdTomato+ GFP For more information please see the full phenotype on the strain data sheet | ||
| 013587 | B6.129P2-Gt(ROSA)26Sortm3Nik/J | Repository- Live |
| These 5172 3-state Cre-sensitive (5172 3SCS) mice contain a construct designed to insert (from 5' to 3') a floxed-STOP cassette, tdTomato open reading frame (ORF), and a floxed-internal ribosome entry site (IRES) fused to an enhanced green fluorescent protein (GFP) ORF. The IRES-eGFP element was flanked by 5172 mutant loxP sites (which recombine at 30% the efficiency of wildtype loxP sites). This vector was inserted into the Gt(ROSA)26Sor locus allowing for widespread expression. The floxed-STOP cassette causes termination of transcription and results in no expression of either fluorophore. When bred to mice that express Cre recombinase, offspring will have the floxed-STOP cassette deleted in the cre-expressing tissue(s). This deletion results in tdTomato and/or GFP expression depending on how much Cre-recombinase the cells express. When crossed with a strain expressing low amounts of Cre recombinase, partial recombination results in tdTomato+ GFP For more information please see the full phenotype on the strain data sheet | ||
| 013584 | B6.129P2-Hspa2tm1Dix/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. Homozygous male mice are infertile, homozygous female mice are fertile. No gene product (mRNA) is detected by Northern blot analysis of testis tissue from homozygous male animals. Immunohistochemical examination of seminiferous tubules does not detect protein gene product. Homozygous males have testes that weigh significantly less than testes from controls. Spermatogenesis in homozygotes is arrested in prophase of meiosis I with a reduced number of postmeitotic spermatids in seminiferous tubules, many with abnormal morphology, and no spermatozoa in the epididymis. Apoptosis of germ cells (late pachytene spermatocytes) in the testes is greatly increased in mutants. During backcrossing, the Y chromosome may not have been fixed to the C57BL/6J genetic background. | ||
| 016522 | B6.129P2-Htttm2Detl/100J | Repository- Live |
| 016523 | B6.129P2-Htttm2Detl/200J | Repository- Live |
| As early as 9 weeks of age heterozygous mice exhibit cytoplasmic aggregation foci of HTT (huntingtin) protein, and by 20 weeks of age exhibit striatal neuronal intranuclear inclusions (NIIs). By 40 weeks of age, the striatal aggregation foci are perinuclear and exhibit increased immunoreactivity for ubiquitin and autophagosome marker LC3. Heterozygotes exhibit impaired balance and diminished motor coordination by 50 weeks of age, and abnormal gait by 60 weeks. By 80 weeks of age, heterozygotes display loss of grip strength, striatal and cortical astrogliosis, and a loss of approximately 50% of striatal dopamine receptor binding with increased glial fibrillary acidic protein immunoreactivity. Increased glial fibrillary acidic protein immunoreactivity is present in the striatum and ubiquititin- and huntingtin-positive neuronal intranuclear inclusions (NIIs) are detected throughout the dorsal striatum, nucleus accumbens and to a lesser extent other regions of the brain. Mutant CAG/poly ..... For more information please see the full phenotype on the strain data sheet | ||
| 016524 | B6.129P2-Htttm2Detl/250J | Repository- Live |
| HdhQ250 mutant mice exhibit a visibly abnormal phenotype at an earlier age as compared to the HdhQ150 strain (STOCK no. 004595 ), but have yet to be fully characterized. Mutant CAG/polyQ repeat expression is slightly lower than wildtype levels as detected by Western blot analysis and qRTPCR of brain tissue. Mutant mice may be noticeably smaller than wild-type littermates. Mice homozygous for the targeted allele are viable and fertile. Onset of symptoms occurs earlier for homozygotes than for heterozygotes. After 20 weeks of age mutant mice may become infertile. The Donating Investigator reports that homozygotes do not breed well.
This strain is one of a set of different CAG/polyQ repeat length mutants derived from HdhQ150 (STOCK no. 004595 ). The set includes, STOCK numbers: 016521, For more information please see the full phenotype on the strain data sheet | ||
| 016521 | B6.129P2-Htttm2Detl/50J | Repository- Live |
| Although the 50 CAG repeat length is similar to the repeat size range observed in patients with Huntington's disease, these mutant mice exhibit no discernable disease phenotype. These mutant mice may have subtle defects not yet reported and may serve as a control for repeat length dependent phenotype for longer repeat Hdh mutant strains. Mice homozygous for the targeted allele are viable and fertile. After 30 weeks of age mutant mice may become infertile. This strain is one of a set of different CAG/polyQ repeat length mutants derived from HdhQ150 (STOCK no. 004595 ). The set includes, STOCK numbers: 016521, 016522, 016523, 016524, 016525. | ||
| 004859 | B6.129P2-Icostm1Mak/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. In wildtype mice, ICOS protein is expressed on activated but not resting T cells, and shows T-cell co-stimulatory function. It delivers a co-stimulatory signal that is essential both for efficient interaction between T and B cells and for normal antibody responses to T-cell-dependent antigens. In homozygous targeted mutation mice, gene product (protein) is undetected on activated T cells by flow cytometry analysis. Homozygotes exhibit severely impaired T cell dependent B cell immunological responses and defective isotype switching. Histological analysis reveals a reduction in the number and size of splenic germinal centers from antigen challenged mutant mice. The basal IgG1 serum level of 8 week-old homozygous mutant mice is 30% of the level found in the wildtype. This mutant mouse strain may be useful in studies of T cell dependent B ..... For more information please see the full phenotype on the strain data sheet | ||
| 004657 | B6.129P2-Icosltm1Mak/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by flow cytometry analysis of spleen cells. Homozygotes exhibit severely impaired T cell dependent B cell immunological responses, with defective B-cell isotype switching to IgG1 and IgE, and impaired T cell production of IL-4 and IL-10. Basal IgG1 serum levels are decreased in mutant mice. Following induction of allergic airway disease (AAD), an experimental model for asthma, IgE levels remain lower than wildtype levels. Antigenic challenges elicit reduced splenic germinal center size and number formation. This mutant mouse strain may be useful in studies of T cell dependent B cell immunological responses and T cell activation. | ||
| 004130 | B6.129P2-Il18tm1Aki/J | Repository- Live |
| Mice that are homozygous null for the Il18 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Il18 gene product (mRNA or protein) is detected. Homozygous null mice exhibit reduced levels of interferon gamma in response to heat killed bacteria and lipopolysaccharide. IL-12 levels in the serum are similar to wild type after LPS challenge, indicating that the decreased interferon gamma response in Il18 deficient mice is not due to low induction of IL-12. Il18 deficient mice also exhibit diminished natural killer cell activity and impaired T helper lymphocyte response. | ||
| 004131 | B6.129P2-Il18r1tm1Aki/J | Repository- Live |
| Mice that are homozygous null for the Il18r1 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Il18r1 mRNA is detected. Homozygous Il18r1 null mice are similar in phenotype to IL-18-deficient mice. They show reduced binding of IL-18 on the surface of Th1 cells, and exhibit decreased levels of interferon gamma production in response to IL-18. Natural killer cell activity is also diminished and the T helper lymphocyte response in impaired. | ||
| 002252 | B6.129P2-Il2tm1Hor/J | Repository- Live |
| Homozygous mutant mice show no apparent deficit in thymocyte differentiation or selection, types and numbers of T cells from spleens and lymph nodes are comparable to those of wild-type. They do have an impaired response to polyclonal T cell activators in the absence of additional IL2, deficits in their helper function and a reduction in natural killer cell activity. There is significant pre-weaning and post-weaning loss of homozygotes on the C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between six and 15 weeks of age and reportedly die within 10-25 weeks under conventional housing conditions. Homozygotes on the C57BL/6J genetic background show an atrophied pancreas with apparently intact islets. Homozygotes on the BALB/c genetic background do not develop inflammatory bowel disease symptoms but rather die three to five weeks postnatally of a form of hemolytic anemia. For a more detailed description please refer to the ..... For more information please see the full phenotype on the strain data sheet | ||
| 002253 | B6.129P2-Il4tm1Cgn/J | Repository- Live |
| Mice homozygous for the Il4tm1Cgn targeted mutation are viable and fertile. T and B cell development is normal but IgGl and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced. | ||
| 012909 | B6.129P2-Klf9tm1Yfk/J | Repository- Live |
| Coding sequence of the Klf9 (Kruppel-like factor 9; also known as BTEB) gene is replaced by lacZ in these targeted mutation mice. Homozygotes show reduced activity levels in rotorod and contextual fear-conditioning tests. They also show a subtle increase in anxiety-like behavior. During development, dentate granule neurons lacking expression of this gene show delayed maturation. Homozygous females exhibit sub-fertility and slightly delayed labor. Homozygous pups are generally smaller at birth but catch up in weight by the time of weaning. This strain may be useful in studies of reproduction, development and behavior. | ||
| 005108 | B6.129P2-Ltb/Tnf/Ltatm1Dvk/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) from any of the three targeted genes is detected by RT-PCR analysis of concanavalin-A activated splenocytes. Leukocyte numbers in the spleen, blood and peritoneal cavity are increased 2 to 3 fold. Homozygous mice have abnormal lymphoid development and do not develop Peyer's patches or lymph nodes. Spleen microarchitecture is abnormal. No germinal center forms in the spleen following antigenic challenge. Mutant mice display defective antibody responses. This strain displays a phenotype more severe than the phenotypes exhibited by any of the single targeted mutation strains of the genes and may be useful in studies of peripheral lymphoid organ development, and antibody response to T cell dependent antigens. | ||
| 004781 | B6.129P2-Lyz2tm1(cre)Ifo/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Lyzs locus. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in deletion of the targeted gene in the myeloid cell lineage, including monocytes, mature macrophages, and granulocytes. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This strain represents an effective tool for generating myeloid cell-specific targeted mutants. | ||
| 007177 | B6.129P2-Mecp2tm1Bird/J | Repository- Live |
| These mice possess two functional loxP sites flanking exons 3-4 of the targeted gene on the X chromosome (the donating investigator reports that the middle loxP site is non-functional). Homozygous females and hemizygous males are viable and fertile. Northern blot analysis showed the expected mature transcript from the Mecp2lox locus as well as a transcript in which the beta-globin intron was unspliced. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 3-4 deleted in the cre-expressing tissue(s). Mice with this X-linked floxed mutation may be useful in neurological and developmental studies of Rett syndrome. For example, when crossed to a strain expressing Cre recombinase in nervous tissue (see Stock No. 003771), this mutant mouse strain develops a neurological phenotype that mimics Rett syndrome. When crossed to a strain expressing Cre ..... | ||
| 006849 | B6.129P2-Mecp2tm2Bird/J | Repository- Live |
| These mice possess a loxP-flanked STOP cassette in intron 2 of the targeted gene on the X chromosome. Western blot and hybridization analysis confirm the absence of wildtype protein from the targeted allele (although the donating investigator reports that the targeted allele produces a "read-through" transcript which does not give rise to detectable levels of protein but makes it difficult to discriminate between the "flox-stopped" and reactivated alleles by RT-PCR). Hemizygous (Mecp2lox-Stop/y) males do not breed and develop Rett syndrome symptoms (reduced mobility, hindlimb clasping) at approximately 6 weeks of age, with death occurring at approximately 11 weeks of age. Heterozygous females are fertile until developing Rett syndrome characteristics at 4-12 months of age. This Rett syndrome-like phenotype is similar to that observed for the traditional knock-out allele (see Stock No. 003890). Cre recombin ..... For more information please see the full phenotype on the strain data sheet | ||
| 005576 | B6.129P2-P2rx7tm1Gab/J | Repository- Live |
| Mice that are homozygous for the targeted allele 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 cultured bone marrow mast cells or peritoneal macrophages. Samples of whole blood, as well as peritoneal macrophages, derived from mutant mice fail to produce extracellular interleukin 1 beta in response to lipopolysaccharide (LPS) and ATP treatment. Similarly, peritoneal lavage fluids from mutant animals that have been primed with LPS and subsequently challenged with ATP, are deficient in mature interleukin 1 beta, and at later time points, exhibit attenuated interleukin 6 levels when compared to fluids from similarly treated wildtype mice. Peripheral blood monocytes and leukocytes fail to change shape/volume and shed L-selectin in response to ATP. Mutant mice exhibit reduced induction and severity of monoclonal anti-collagen-induced arthritis. Mutant mice also display significant reduct ..... For more information please see the full phenotype on the strain data sheet | ||
| 009654 | B6.129P2-Sod3tm1Mrkl/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size, but reproductive performance is inconsistent for homozygous X homozygous crosses. No gene product (EC-SOD protein) activity is detected by gel-exclusion chromatography analysis of plasma and no protein is detected by Western blot analysis of blood vessels. EC-SOD activity is not detected in brain. When exposed to >99% oxygen conditions, homozygotes have a shorter survival time than wild-type controls and exhibit a more severe lung edema at death. Homozygotes are more sensitive to induced transient focal cerebral ischemia, which results in greater total infarct volume and more severe hemiparesis. Alloxan-induced diabetes causes increased initial hyperglycemia with delayed recovery of glycemic control. Extracellular superoxide radical concentration is doubled and normal age-related loss of endothelial cells is increased in the cornea. Mutant mice are more susceptible to LPS-induced inflammation of ..... For more information please see the full phenotype on the strain data sheet | ||
| 012723 | B6.129P2-Spnb3Gt(XK442)Byg/LlpJ | Repository- Live |
| Homozygous Spnb3-/- mice are viable and fertile, and are prone to a mild nonprogressive ataxia and stimulus-induced seizures. This gene trap mutation abolishes endogenous spectrin beta 3 (Spnb3) gene function and expresses a β-galactosidase (β-geo) reporter fusion protein. In these mice synapse morphology is altered, and there is a reduction in synapse-associated proteins, EAAT4, EAAT1, GluRδ, IP3R, and NCAM 140, leading to a failure to assemble transporters, receptors, and adhesion molecules. These Spnb3-/- mice may be useful as a lacZ reporter for Spnb3 expression or as a knockout model for studying glutamate transport dynamics, synaptogenesis, seizures, and neuronal damage. | ||
| 012915 | B6.129P2-Stmn1tm1Wed/J | Repository- Live |
| In this strain, the allele replaces exons 2-3 of the endogenous Stathimin 1 (Stmn1, or metablastin) gene with a neomycin resistance (neo) cassette, abolishing gene function. Mice homozygous for the metablastin allele are viable, fertile, and normal in size. Homozygous mice do not breed very well and pups have decreased weight and survival compared to wildtype. Metablastin-/- mice are deficient in innate and learned fear, and show improper threat assessment and a lack of motivation to care for or protect their young. They also exhibit a decrease in long-term memory associated with fear conditioning. These mice may be useful for studying microtubules, neural circuitry, innate and learned fear, behavior, cell cycle regulation, parental behaviors and adult social interactions | ||
| 002122 | B6.129P2-Tcrbtm1Mom Tcrdtm1Mom/J | Repository- Live |
| Mice homozygous for both the Tcrbtm1Mom and the Tcrdtm1Mom targeted mutations express no alpha beta T-cell receptor nor any gamma delta T-cell receptor. Under certain housing conditions homozygous mutant mice develop mild inflammatory bowel disease. | ||
| 002120 | B6.129P2-Tcrdtm1Mom/J | Repository- Live |
| Mice homozygous for the Tcrdtm1Mom 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. | ||
| 013755 | B6.129S(C)-Batf3tm1Kmm/J | Repository- Live |
| These Batf3-/- mutant mice are lacking exons 1-2 of the basic leucine zipper transcription factor, ATF-like 3 (Batf3) gene, abolishing gene function. Mice that are homozygous for this allele are viable and fertile. Batf3 is highly expressed in CD11c+ CD8α+ conventional dendritic cells (cDCs), with low to absent expression in other immune cells.The deletion of Batf3 prevents development of splenic CD8α+ cDCs, which are important for cross-presentation during infections. Lymph nodes and thymi of Batf3-/- mice lack CD8α+ DCs, and DCs generated from Batf3-/- bone marrow (BM) and spleens are deficient in Toll-like receptor (TLR) 3-induced interleukin (IL)-12 production. These mice also lack CD103+CD11b- DCs in the lung, intestine, mesenteric lymph nodes (MLNs), dermis, and skin-draining lymph nodes. Exhibiting defects in CD8+T cell r ..... For more information please see the full phenotype on the strain data sheet | ||
| 016222 | B6.129S(Cg)-Id2tm1.1(cre/ERT2)Blh/ZhuJ | Repository- Live |
| The Id2-CreERT2 knockin allele was designed to both abolish inhibitor of DNA binding 2 (Id2) gene function and express CreERT2 fusion protein from the Id2 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible and can be observed following tamoxifen administration. As such, when Id2-CreERT2 knockin mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Id2-expressing cells of the offspring.
No mRNA or protein expression from the Id2-CreERT2 allele is observed. The donating investigator reports that homozygous mice are runted with defective lung alveolarization. Other organ systems have not been evaluated. However, Id2-CreERT2 homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (including postnatal lethality and defects of the immune system, digestive tract, ..... | ||
| 013593 | B6.129S-Atoh1tm4.1Hzo/J | Repository- Live |
| These Math1M1GFP/M1GFP mice contain an enhanced green fluorescent protein (eGFP) fused to the 3' end of the atonal homolog 1 (Atoh1) gene. Homozygous mice are viable and fertile. GFP is expressed all Math1-expressing neurons including hindbrain neurons such as the suparafacial respiratory group/retrotrapezoid nucleus (pFRG/ RTN). These neurons are involved in respiratory rhythm generation and defects in these are associated with congenital central hypoventilation syndrome (CCHS). These mice may be useful for tracing the development, migration, and differentiation of Math1-expressing pFRG/RTN and paratrigeminal neurons. | ||
| 013594 | B6.129S-Atoh1tm5.1(Cre/PGR)Hzo/J | Repository- Live |
| A targeting vector was designed to replace the coding sequence of the atonal homolog 1 (Atoh1) gene with a modified Cre-recombinase-progesterone receptor fusion protein (Cre-PR), abolishing gene function. Homozygous Math1Cre*PR mice die before birth due to central respiratory failure. Heterozygous mice are viable,fertile, and normal in size. The Math1Cre*PR/+ allele has expression of the Cre*PR fusion protein under control of the Math1 promoter/enhancer elements. Cre*PR fusion gene activity is inducible; observed only 6-12 hours after administration of RU486, a competitive progesterone receptor antagonist. As such, when Math1Cre*PR/+ mice are bred with mice containing loxP-flanked sequence, RU486-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Math1-expressing cells of the offspring. As such Math1 is expressed in the hindbrain, specifically in the conscious pro ..... For more information please see the full phenotype on the strain data sheet | ||
| 013595 | B6.129S-Atoh1tm6.1Hzo/J | Repository- Live |
| These Atoh1FLAG mice contain three c-terminal FLAG tags fused to the 3' end of the atonal homolog 1 (Atoh1) gene. Homozygous mice are viable and fertile. Atoh1FLAG expression is evident evident in all Atoh1 expressing cells including cerebellar granule neuron precursors (GNPs) where it binds the active transcriptional enhancer region of the GLI-Kruppel family member GLI2 (Gli2) gene. These mice may be useful for studying postnatal cerebellar development and regulation of Sonic Hedgehog-induced medulloblastoma. | ||
| 013758 | B6.129S-Batftm1.1Kmm/J | Repository- Live |
| These Batf-/- mutant mice lack exons 1-2 of the basic leucine zipper transcription factor(Batf), ATF-like gene, abolishing gene function. Mice that are homozygous for this allele are viable and fertile. Batf is highly expressed in T helper (TH) 1, TH2 and TH17 cells. Batf is required for the differentiation of interleukin (IL)-17-producing TH17 cells which are CD4+ T cells that coordinate inflammatory responses in host defense. These mice exhibit normal TH1 and TH2 differentiation, but show a defect in TH17 differentiation with a reduction in IL-17 production, but maintain normal levels of IL-2, interferon (IFN)-γ, and IL-10 under TH17 conditions. Since TH17 cells are the major pathogenic population in experimental autoimmune encephalomyelitis (EAE), these Batf-/- mice are completely resistant EAE even when immunized wi ..... For more information please see the full phenotype on the strain data sheet | ||
| 003726 | B6.129S-Cd14tm1Frm/J | Repository- Live |
| Mice that are homozygous null for Cd14 are viable and fertile. No Cd14 protein product is detected in thioglycollate elicited peritoneal (T-EP) macrophages by Western blot analysis. Unlike wildtype T-EP macrophages, T-EP macrophages derived from these animals fail to secrete TNF-alpha and IL-6 in response to lipopolysaccharide (LPS). Such a response is observed when Cd14 -null T-EP macrophages are exposed to whole bacteria (in the form of E. coli bioparticles), apparently by a Cd14-independent mechanism. | ||
| 012377 | B6.129S-Cyp19a1tm1.1Shah/J | Repository- Live |
| Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mutant mice possess a reporter cassette, IRES-PLAP-IRES-nlacZ, downstream of the stop codon in the 3' UTR of the targeted locus. Nuclear β-galactosidase (β-gal) labels the nuclei of cells expressing aromatase, whereas human placental alkaline phosphatase (ALPP or PLAP) labels the cell membrane of such cells. These mice may be useful for visualizing aromatase-positive cells to define where testosterone may be converted into estrogen in the mouse brain. | ||
| 005530 | B6.129S-Ddit3tm1Dron/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (MRNA or protein) is detected by Northern or Western blot analysis of toxin challenged mouse embryonic fibroblasts (MEFs). MEFs and renal proximal tubular epithelial cells have decreased apoptosis in response to endoplasmic reticulum stress induced by the toxin, tunicamycin. Pancreatic islets cells are more resistant to nitric oxide induced apoptosis. MEFs exhibit a delayed onset of unfolded protein response (UPR) target gene expression when treated with tunicamycin. This mutant mouse strain may be useful in studies of apoptosis and pathogenesis due to endoplasmic reticulum stress. | ||
| 004754 | B6.129S-Il1rntm1Dih/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and do not display any gross physical or behavioral abnormalities. By 6 weeks of age homozygous mice have lower body weight. Homozygous females may have reduced litter sizes. No gene product (mRNA) is detected by Northern blot analysis of lung tissue after lipopolysaccharide (LPS) challenge. Mice homozygous for the mutation are less susceptible to experimental Listeria monocytogenes infection, but are more susceptible to LPS endotoxin challenge. After LPS challenge IL-1 levels are decreased. Basal serum amyloid protein and serum IL-6 levels are higher. Hepatic acute phase protein inflammatory response and mortality to subcutaneous turpentine abscess induction are increased. When fed a high fat diet containing cholate for 12 weeks, homozygotes exhibit a 3-fold decrease in total cholesterol (non-HDL). Heterozygotes fed the same diet exhibit an intermediate decrease in total cholesterol. Immunohistochemical analysis of h ..... For more information please see the full phenotype on the strain data sheet | ||
| 005439 | B6.129S-Mecp2tm1Hzo/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and fertile. A truncated gene product (protein) is detected by immunohistochemical analysis of brain tissue. By 6 weeks of age, male mutant mice begin to exhibit tremors, progressive motor dysfunction, oily disheveled fur, hypoactivity, myoclonic seizures, and kyphosis. Approximately 10% of male mutants die between 10 and 12 months of age. Heterozygous female mice exhibit a milder phenotype. All mutant male mice and 62% of female heterozygotes exhibit a repetitive clasping movement of their forelimbs and exhibit tremors. The Donating Investigator reports that the myoclonic seizures, kyphosis and reduced survival were observed in aged male mutants on a 129/SvEv genetic background. This mutant mouse strain may be useful in studies of Rett Syndrome. The Howard Hughes Medical Institute and the National Institutes of Health supported the creation of this model. Importation of this model was supported by the Rett Syndrome Rese ..... | ||
| 010525 | B6.129S-Notch2tm3Grid/J | Repository- Live |
| These mice possess loxP sites on either side of exon 3 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 3 deleted in the cre-expressing tissue(s).
When bred to a strain with early embryonic Cre recombinase expression (see Stock No. 003755 for example), this mutant mouse strain may be useful in studies of the Notch pathway during development. When bred to a strain expressing Cre recombinase in embryos, in particular, cardiac neural crest cells (see Stock No. 005549 for example), this mutant mouse strain may be useful in studies of vascular smooth muscle development and the cardiovascular defects associated with Alagille syndrome ..... | ||
| 009411 | B6.129S-Pstpip1tm1Spg/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. Studies of spleen, thymus and embryonic fibroblasts indicate that expression is eliminated. Preliminary information suggests these mice have various defects in immune cells, predominantly T lymphocytes which appear to be hyperresponsive to antigen receptor stimulation. | ||
| 010919 | B6.129S-Themistm1Gasc/J | Repository- Live |
| These Themis-/- mice contain a mutation designed to disrupt the gene function of endogenous mouse Themis. Homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Thymocytes from these mice show defective positive selection resulting in fewer mature single positive thymocytes, and show impaired negative selection. This may be due to defective T cell antigen receptor (TCR) signal transduction and/or a so-far undefined signaling or metabolic defect. The defect in positive selection results in altered thymus structure, with the medulla being smaller and more fragmented than wild-type medulla. A greater percentage of Themis-/- T cells have CD4+CD25+Foxp3+ regulatory and CD62LloCD44hi memory phenotypes than do wild-type T cells. These mice may be useful for studying positive selection of thymocytes and early events in the TCR signaling cascade. | ||
| 005540 | B6.129S-Tnftm1Gkl/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does not affect the degree of obe ..... For more information please see the full phenotype on the strain data sheet | ||
| 013542 | B6.129S1(Cg)-Dnm2tm1.1Pdc/J | Repository- Live |
| These mice possess loxP sites on either side of exon 2 of the Dnm2 (dynamin 2) gene. Mice that are homozygous for this floxed allele are viable, fertile, and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this floxed strain is useful in eliminating expression of Dnm2 in a tissue-specific fashion (documented in cultured fibroblasts). Germline deletion results in embryonic lethality. This strain may be useful in further characterizing the role of this gene in endocytosis. | ||
| 014097 | B6.129S1(Cg)-Gdnftm1.1Neas/J | Repository- Live |
| These Gdnfflox mutant mice possess loxP sites flanking exon 3 of the glial cell line derived neurotrophic factor (Gdnf) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. GDNF is expressed in muscle and is required for the development of gamma motor neurons (γMNs). When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exon 3 deleted in the cre-expressing tissues. When these Gdnfflox mice are bred to mice carrying a muscle-specific Myf5Cre tissues (see Stock No. 007893), mutation or muscle-spindle-specific Egr3Cre mutation, disruption of Gdnf results in a loss of γMNs with preservation of the spindle, sensory innervation, and functional sensorimotor connectivity. This strain may b ..... For more information please see the full phenotype on the strain data sheet | ||
| 013787 | B6.129S1-Abcc6tm1Jfk/J | Repository- Live |
| Mice that are homozygous for this targeted mutation develop patchy, progressive mineralization of the dermis, kidneys, eyes, arteries, heart and subcutaneous tissues, mimicking the human disease symptoms of pseudoxanthoma elasticum. Mineralization of connective tissue capsule surrounding vibrissae is detectable at 5 weeks of age. Mineralization is associated with collagen fibrils and elastic fibers. Oxidative stress, as indicated by lipid peroxidation and protein oxidation, is higher in liver tissue and serum of mutant mice when compared to wildtype controls. Antioxidant diet reduces the oxidative stress levels in knock out mice, but does not prevent ectopic mineralization. The severity of mineralization can be altered by mineral intake as a diet with elevated magnesium levels prevents pathological connective tissue mineralization in mutants. Serum matrix gla protein (MGP) levels are reduced in homozygotes and the protein is under-carboxylated with diminished activity. Fetuin-A ..... For more information please see the full phenotype on the strain data sheet | ||
| 004525 | B6.129S1-Bcl2l11tm1.1Ast/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No full length gene product (protein) is immunodetected in spleen cells from homozygous mutant mice. Homozygous mice have lympho-myeloid hyperplasia and reduced platelet number. Lymphocytes are insensitive to certain apoptotic stimuli. Both homozygous and heterozygous mice exhibit progressive systemic autoimmune disease. This mutant mouse strain may be useful in studies of apoptosis, degenerative and autoimmune diseases, including lupus erythematosus and autoimmune kidney disease. | ||
| 006233 | B6.129S1-Casp3tm1Flv/J | Repository- Live |
| On this C57BL/6 congenic background, homozygotes are viable, fertile, and reach adulthood, but females reported display suboptimal mothering instincts. Functional endogenous protein and mRNA are absent from all tissues tested. Homozygous mice are resistant to in vivo cerebral ischemia/reperfusion and in vitro oxygen-glucose deprivation. Ovaries from female homozygotes show aberrant atretic follicles associated with a granulosa cell-intrinsic defect in apoptosis as well as defective corpus luteum regression. Homozygous mice are congenitally deaf with hair cell defects in the Organ of Corti. Optic lens formation/morphology also is abnormal with cataracts at the anterior lens pole. Of note, these mice lack the embryonic/perinatal-lethal brain pathology observed in mutant mice on the 129 and mixed B6;129 genetic backgrounds. These mutant mice may be useful in studies of apoptosis, ovarian follicle and corpus luteum development, and eye and ear development. | ||
| 002692 | B6.129S1-Il12atm1Jm/J | Repository- Live |
| Mice homozygous for the Il12atm1Jm targeted mutation on a normally resistant 129/Sv genetic background are unable to restrict the progression of Leishmania major infection, demonstrating the importance of this cytokine for developing such resistance. Homozygotes are unable to mount a delayed-type hypersensitivity (DTH) reaction but a TH2 response is induced. Also known as p35. Please refer to the Il12b-deficient related targeted mutations (Stock No. 002693 and 002694).
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 a ..... | ||
| 003248 | B6.129S1-Il12rb2tm1Jm/J | Repository- Live |
| Mice homozygous for the Il12rb2tm1Jm targeted mutation are viable and fertile. Homozygous mutant mice do not show an increased susceptibility to infections. 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. | ||
| 010616 | B6.129S1-Jag1tm1Grid/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, and normal in size. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis of homozygous embryos, aged embryonic day 10. Homozygotes have an embryonic lethal phenotype, with defective vasculature formation in the embryo and yolk sac and widespread hemorrhaging at embryonic day 10.5. Heterozygotes exhibit iris coloboma, irregular/off center pupils and corneal opacity. | ||
| 010546 | B6.129S1-Jag2tm1Grid/J | Repository- Live |
| Mice that are homozygous for this targeted mutation have a perinatal lethal phenotype, dying shortly after birth due to craniofacial defects (cleft palate, due to fusion of unelevated palatal shelves with the tongue). Embryos homozygous for the mutation and aged embryonic day 10.5-11.5, display a hyperplastic thick apical ectodermal ridge of the limb buds. Homozygous neonates have bilateral cleft of the secondary palate and syndactyly (fused digits) of both forelimbs and hindlimbs, although the hindlimbs are more affected. The number of inner ear hair cells is increased in mutants. Histological analysis reveals an increased number of inner ear hair cells and disorganized stereocilia bundles in mutants. Homozygotes exhibit abnormal thymic morphology and decreased gamma-delta T cell number. Heterozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Heterozygotes have abnormal inner ear morphology (increased number of hair c ..... For more information please see the full phenotype on the strain data sheet | ||
| 004319 | B6.129S1-Mapk8tm1Flv/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, normal in size, do not display any gross physical or behavioral abnormalities and are fertile but poor breeders. No gene product, protein or mRNA, is detected. Lymphocyte development, T cell to B cell ratio and CD4 to CD8 ratio are normal. Naive Th cells activated in vitro preferentially differentiate into Th2 cells. Mutant mice are susceptible to infection when challenged with the intracellular pathogen, Leishmania major. Primary murine embryonic fibroblasts prepared from mutant embryos are partially protected from UV-induced apoptosis. This mutant mouse strain represents a model that may be useful in studies related to signal transduction. | ||
| 006600 | B6.129S1-Mnx1tm4(cre)Tmj/J | Repository- Live |
| Mice heterozygous for this HB9cre targeted mutation are viable and fertile, with cre expression replacing HB9 (Hlxb9 or Mnx1) expression. Under control of the endogenous upstream elements, cre expression is directed to motor neurons. In heterozygotes, cre expression coincides with HB9 expression. Homozygous HB9cre mice die at or soon after birth, with expression of Cre recombinase likewise directed to motor neurons but no expression of endogenous HB9. When these HB9cre mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination in the resulting offspring leads to deletion of the flanked sequences in Mnx1/HB9 expressing cells; making them useful in neurodevelopmental studies of homeobox genes, motor neuron function and differentiation, and the central nervous system. | ||
| 005763 | B6.129S1-Nod2tm1Flv/J | Repository- Live |
| Homozygous mice are viable and fertile with normal lymphoid and myeloid cellularity and no intestinal inflammation up to 6 months of age. Homozygotes do not express the targeted gene in spleen or intestinal crypts. Null mice, as well as antigen presenting cells derived from them, lack the protective immunity (IgG1, interleukin-6, and NF-kappaB-related responses) normally afforded by endogenous protein recognition of its ligand, bacterial muramyl dipeptide (MDP). Mice homozygous for the mutation have increased susceptibility to oral (intragastric) bacterial challenge and diminished cryptdins. This mouse may be useful in studies of Crohn's disease and other inflammatory bowel diseases, innate immunity, signal transduction, and bacterial susceptibility. | ||
| 010620 | B6.129S1-Notch2tm1Grid/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. Due to alternative splicing, 2 in-frame gene products (mRNA) are detected by RT-PCR analysis of homozygous embryos. The mutant transcripts would produce proteins with one or two EGF repeats deleted. Levels of the mutant transcripts are similar to the wildtype transcript level. This targeted allele is a hypomorph. Homozygotes are neonatal lethal due to developmental defects in the kidney, heart and eye vasculature. Homozygous neonates exhibit hypoplastic kidneys, with vasculature lesions at the cortical surface, and lack mature glomeruli. Bilateral microphthalmia, with retrolenticular hyperplasia, is observed in homozygotes. At age embryonic day 11.5, some homozygous embryos exhibit delayed growth, pericardial effusion and widespread hemorrhaging. Homozygous embryos that survive past embryonic day 11.5 display myocardial hy ..... For more information please see the full phenotype on the strain data sheet | ||
| 006228 | B6.129S1-Nox3het-3J/GrsrJ | Repository- Live |
| Homozygotes completely lack otoconia, both in the utricle and the saccule, as early as embryonic day 14 and this persists in the adult. However, the rest of the inner ear appears morphologically normal and hearing is normal. Otoconia appear to be normal in heterozygotes. Homozygotes can be identified by a significant sideways tilting of the head. When dropped 30cm to a soft surface homozygotes fail to land on their feet. They also fail to orient and swim in water, but instead rotate underwater and require rescue. | ||
| 010621 | B6.129S1-Snai1tm2.1Grid/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous mice have an embryonic lethal phenotype, failing to develop past gastrulation. Homozygotes exhibit a phenotype similar to mice homozygous for the Snai1del1 allele, with abnormal mesoderm with cavities or lacunae, and lined with cells exhibiting a polarized, columnar epithelium morphology. | ||
| 010617 | B6.129S1-Snai2tm1Grid/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, subfertile, and smaller in size compared to wildtype controls. These mice express a beta galactosidase fusion protein with 120 amino acids from the first half of the endogenous protein. The beta galactosidase staining pattern mimics the endogenous gene expression pattern in the embryonic limb buds and extraembryonic tissue. Homozygous adults develop eye infections (suppurative conjunctivitis) due to swollen eyelids. When challenged with UV radiation exposure, homozygotes exhibit decreased inflammation, lower skin tumor burden and fewer spindle cell tumors compared to wildtype. | ||
| 006848 | B6.129S2(C)-Cxcr2tm1Mwm/J | Repository- Live |
| The donating investigator reports that homozygous mice are viable and fertile but few pups are produced, and they need a gnotobiotic facility to thrive. Homozygous mice have several abnormalities, including neurological defects, impaired wound healing, impaired angiogenesis, and altered growth of induced/implanted tumors. Homozygotes may also exhibit splenomegaly, lymphadenopathy, and increased susceptibility to various pathogens due to impaired neutrophil recruitment and decreased pathogen clearance during innate immune responses. These mutant mice may be useful in studies of inflammation and immunology and cancer biology.
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 becom ..... | ||
| 006144 | B6.129S2(C)-Itgaetm1Cmp/J | Repository- Live |
| Mice that are homozygous for this targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No endogenous gene expression is detected in intraepithelial lymphocytes by FACS analysis or on TGF-beta1-treated splenocytes by immunoprecipitation. Homozygous null mice exhibit reduced numbers of intestinal intraepithelial lymphocytes and lamina propria lymphocytes. These mice may be useful in studies of the immune system, including T cell function. 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. | ||
| 005977 | B6.129S2(C)-Stat6tm1Gru/J | Repository- Live |
| Homozygous mice are viable and fertile with no behavioral abnormalities. Homozygotes do not express the endogenous protein in thymus and peripheral lymphoid organs. In contrast to controls, IL-4 treated lymphocytes show no induction of MHC class II or IL-4 receptor genes and have severly impaired proliferative responses. Further, homozygous mice have a defective IgE response. While T-helper 1 (Th1) cell differentiation is unimpaired in homozygous splenocytes, Th2 cell differentiation is almost completely abrogated despite IL-4 or IL-13 incubation. Myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) is more severe in homozygous mice compared to wildtype. This mouse may be useful in studies of Th2 cell differentiation, Th2-mediated diseases, asthma, cytokine/chemokine function, signal transduction and transcription factors, and diseases of the central nervous system such as multiple sclerosis. | ||
| 006659 | B6.129S2(Cg)-Cxcr5tm1Lipp/J | Repository- Live |
| Homozygous (CXCR5-deficient) mice are viable and fertile. Multiple lymphoid organs lack detectable levels of targeted protein expression using flow cytometry, and RNA transcripts are also absent in spleen cells. Homozygous mutant mice exhibit a complex pattern of lymph node (LN) developmental defects (e.g. deficient in inguinal, iliac and parathymic LN, but apparently normal mesenteric LN) accompanied by impaired Peyer's patch development. In addition, CXCR5-deficient mice show a completely disorganized splenic microarchitecture, lacking segregated T- and B-cell areas within the splenic white pulp. These mutant mice (along with CCR7-deficient mice: Stock No. 006621) may be useful in immunological studies of chemokine receptors, including T- and B-cell function in primary and adaptive immune responses, entry of lymphocytes and dendritic cells into secondary lymphoid organs and their homing to T- and B-cell zones therein.
In ..... | ||
| 010512 | B6.129S2(Cg)-Fcer1atm1Knt/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. Cultured bone marrow-derived mast cells from homozygotes, that have been activated with interleukin-3, do not bind to monomeric IgE as analyzed by flow cytometry. Mice homozygous for the mutant allele are resistant to IgE induced passive cutaneous and systemic anaphylaxis and are more susceptible to IgG1-dependent passive and active systemic anaphylaxis 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. 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. | ||
| 013152 | B6.129S2(Cg)-Fut7tm1Jbl Fut4tm1Jbl/J | Repository- Live |
| In this strain the catalytic domains of the fucosyltransferase 4 (Fut4) gene and the fucosyltransferase 7 (Fut7) gene were replaced with neomycin resistance (neo) cassettes, abolishing gene function. Mice homozygous for both alleles are viable, fertile, and normal in size. These mice lack inflammation-dependent leukocyte recruitment; specifically neutrophils, eosinophils, monocytes, T cells and dendritic cells are unable to migrate to extravascular sites of acute and chronic inflammation. The peripheral nodes in these mice do not support normal B lymphocyte or naive T lymphocyte homing. FucTIV-null defects in leukocyte E- and P-selectin counterreceptor activity and HEV-born L-selectin ligand activity are reversed in the double null mutant mice. Neutrophils in the doubly null mice, unlike FucT-7VII null leukocytes, are virtually devoid of E- and P-selectin ligand activities. These mice also exhibit extreme leukocytosis characterized by decreased neutrophil turnover and in ..... For more information please see the full phenotype on the strain data sheet | ||
| 015828 | B6.129S2(FVB)-Pak4tm2.1Amin/J | Repository- Live |
| These Pak4 floxed mutant mice possess loxP sites flanking exons 2-4 of the p21 protein (Cdc42/Rac)-activated kinase 4 (Pak4) gene. Homozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Pak4 is a member of the group B family of PAK serine/threonine kinases and is expressed early in development in a variety of tissues. It is involved in the formation of filopodia in response to Cdc42, promoting neuronal growth. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2-4 deleted in cre-expressing tissues. This strain may be useful for studying the role of Pak4 in the development of extraembryonic tissue, embryonic vasculature, and the placenta. | ||
| 004743 | B6.129S2-Airetm1.1Doi/J | Repository- Live |
| Mice homozygous for the targeted allele are viable, normal in size and at birth do not display any gross physical or behavioral abnormalities. While a transcript may be generated from the targeted locus, a functional protein is not translated. Homozygous mice display a phenotype consistent with a broad defect in immunological tolerance induction. By four weeks of age histological analysis reveals lymphocytic infiltrates in some organs. Infiltrates become more prevalent as the mouse ages. Serum autoantibodies are detected by 3-6 months. Thymic medullary epithelial cell (MEC) number is doubled. Similarly, a near doubling in the numbers of activated/memory CD44hiCD62Llo T lymphocytes is observed. A loss or reduction in expression occurs for a substantial number of genes in MECs, an observation consistent with the targeted gene's role as a transcriptional activator. The Donating Investigator reports that homozygotes are not fertile (most homozygous females are sterile ..... For more information please see the full phenotype on the strain data sheet | ||
| 002778 | B6.129S2-Alox15tm1Fun/J | Repository- Live |
| Homozygous (12/15-LO-deficient) mutant mice are viable and fertile. 12/15-LO-deficient mice develop a myeloproliferative disorder (MPD) (similar to human chronic myelogenous leukemia (CML)) that progresses to transplantable leukemia. Chronic MPD stage homozygotes exhibit increased activation of the phosphatidylinositol 3–kinase (PI3-K) pathway, hyperphosphorylation/decreased nuclear accumulation of the transcription factor interferon consensus sequence binding protein (ICSBP), and increased expression of the oncoprotein Bcl-2; all of which are reversible upon treatment with a PI3-K inhibitor. The evolution of MPD to leukemia is associated with additional regulation of ICSBP at the RNA level. Peritoneal macrophages have altered arachidonic acid metabolism as well as a diminished ability to oxidize low density lipoprotein (LDL) following stimulation. These mutant mice may be useful in studying myeloproliferative disorders, chronic myelogenous leukemia, and other cancers. | ||
| 004155 | B6.129S2-Alox5tm1Fun/J | Repository- Live |
| Mice homozygous for the Alox5tm1Fun targeted mutation are viable and fertile. In general, homozygous mutant mice are selectively resistant to inflammatory insults. They are resistant to the lethal effects of platelet activating factor but reaction to endotoxin shock is normal. Phorbol ester induced inflammation is normal but arachidonic acid induced inflammation is reduced. | ||
| 002666 | B6.129S2-Cd28tm1Mak/J | Repository- Live |
| Mice homozygous for the Cd28tm1Mak targeted mutation exhibit normal development of T and B cells, but have an impaired response to lectins. Other characteristics of homozygous mutant mice include decreased IL2 receptor expression, reduced basal Ig levels, low titers of IgG1 and IgG2b but increased IgG2a, reduced activity of T helper cells and diminished Ig class switching after infection with vesicular stomatitis virus. Infection of mice with lymphocytic choriomeningities virus creates induced and delayed-type hypersensitivity response in cytotoxic T cells. | ||
| 002770 | B6.129S2-Cd40lgtm1Imx/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice show no overt phenotypic abnormalities. Percentages of B and T cell subpopulations is normal. Homozygotes do show selective deficiencies in humoral immunity (low basal serum isotype levels and undetectable IgE) as well as abnormal secondary antigen-specific responses to immunization with a thymus-dependent antigen. The phenotype of the mice resembles human X-linked hyper IgM syndrome. | ||
| 003239 | B6.129S2-Ciitatm1Ccum/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile when housed under specific pathogen-free conditions. Mice do not express conventional MHC class II molecules on the surface of splenic B cells and dendritic cells. In addition, interferon gamma stimulated peritoneal macrophages and somatic tissues from homozygous mutant mice do not express MHC class II molecules. The levels of invarient chain and H2m gene transcripts are substantially decreased in class II transactivator deficient mice. Homozygous mice have very few mature CD4 T cells in the periphery despite MHC class II expression in the thymus. | ||
| 005628 | B6.129S2-Emx1tm1(cre)Krj/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This strain expresses Cre recombinase from the endogenous Emx1 locus. Western blot analysis of cortical brain tissue does not detect reduced endogenous gene product (protein). When crossed with a strain containing a loxP-site flanked sequence, Cre-mediated recombination results in tissue-specific deletion of the flanked sequence. Recombination occurs in approximately 88% of the neurons of the neocortex and hippocampus, and in the glial cells of the pallium, mimicking the pattern of expression of the endogenous gene. Further, the donating investigator reports that Cre recombinase is also expressed in a subset of male germline cells, thus some offspring from a cre; floxed male will have the floxed allele recombined in all cells. This mutant mouse strain represents a model that may be useful in studies of forebrain development and f ..... For more information please see the full phenotype on the strain data sheet | ||
| 003584 | B6.129S2-H2dlAb1-Ea/J | Repository- Live |
| Mice that are homozygous null for MHC class II genes H2-Ab1, H2-Aa, H2-Eb1, H2-Eb2, H2-Ea are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. MHC class II gene products (mRNA or protein) are not detected. A dramatic decrease is observed in the number of CD4 positive T cells in thymus, spleen and lymph nodes. This strain should serve as a suitable recipient of xenogenic Class II MHC transgenes allowing the engineering of mouse models of human MHC Class II-associated diseases. 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. | ||
| 002762 | B6.129S2-Irf1tm1Mak/J | Repository- Live |
| Mice homozygous for the Irf1tm1Mak targeted mutation are viable and fertile with no major abnormalities. T cell development is impaired leading to significant reduction in TCR alpha beta + CD4- CD8+ T cells. Type I interferon gene induction is abnormal. | ||
| 002258 | B6.129S2-Ltatm1Dch/J | Repository- Live |
| Mice homozygous Ltatm1Dch targeted mutation are viable and fertile. Homozygous mutant mice show abnormal development of peripheral lymphoid organs with no detectable popliteal, inguinal, para-aortic, mesenteric, axillary, or cervical lymph nodes, and no detectable Peyer's patches. Morphological changes in the spleen white pulp were accompanied by alterations in T and B cell content. CD4+ and CD8+ T cells counts in peripheral blood are normal but there is a four-fold increase in B cells. Neutrophil, monocyte, and platelet counts are normal. The thymus contains normal numbers of CD4+CD8+, CD4+, CD8+, and CD4-CD8- T cells. Splenic T cells develop normal MHC class I and class II-restricted allocytotoxic responses. Also known as tumor necrosis factor beta, Tnfb. | ||
| 004321 | B6.129S2-Mapk9tm1Flv/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product, mRNA or protein, is detected. Mutant mice have normal T cell and B cell development, ratio of CD4+ and CD8+ T cells in the spleen, and numbers of peripheral B cells. Although differentiation of precursor CD4+ T cells into effector Th2 cells is normal, Th1 cell differentiation is impaired. Treatment with IFN-gamma and IL-12 during precursor CD4+ T cell differentiation results in normal Th1 cell development. Primary murine embryonic fibroblasts prepared from mutant embryos have decreased viability and increased genomic DNA fragmentation with UV irradiation. This mutant mouse strain represents a model that may be useful in studies related to signal transduction. | ||
| 007558 | B6.129S2-Oprk1tm1Kff/J | Repository- Live |
| Mice homozygous for this kappa-opioid receptor mutant allele (KOR-) are viable and fertile. KOR-selective ligand binding is absent on brain membranes from homozygous mice. In contrast to mutant mice deficient of delta- or mu-opioid receptors (Stock No. 007557 or 007559), KOR- homozygotes have normal mechanical pain thresholds, but greatly increased sensitivity to chemical visceral pain. KOR- homozygotes also exhibit normal spontaneous stress responses (unlike delta-opioid receptor null mice). Homozygous KOR- mice also show decreased ethanol self-administration and decreased THC-conditioned place aversion. These KOR mutant mice may be useful in studying biological activity of opioids, analgesics, spinally mediated thermal nociception and chemical visceral pain thresholds. 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. These mut ..... | ||
| 007559 | B6.129S2-Oprm1tm1Kff/J | Repository- Live |
| Mice homozygous for this mu-opioid receptor mutant allele (MOR-) are viable and fertile. MOR-selective ligand binding is absent on brain membranes from homozygous mice. Homozygous MOR- mice exhibit a lack of morphine analgesia, reward, and withdrawal. This is accompanied by decreased mechanical, thermal, and chemical pain thresholds. Homozygous MOR- mice also show decreased ethanol self-administration and decreased THC-conditioned place aversion. In contrast to mutant mice deficient of delta- or kappa-opioid receptors (Stock No. 007557 or 007558, respectively), MOR- homozygotes exhibit hypolocomotive spontaneous stress responses. Indeed, the reduced anxiety and depressive-like behavior observed in MOR- mutants is in stark contrast to kappa-opioid receptor deficient mice. These MOR mutant mice may be useful in studying the biological activity of opioids, analgesics, and responses to mechanical, chemical and thermal nociception at a supraspinal level. In an attempt to offer alleles ..... | ||
| 015829 | B6.129S2-Pak4tm1Amin/J | Repository- Live |
| In this strain, a neo cassette replaces exon 1 of the p21 protein (Cdc42/Rac)-activated kinase 4 (Pak4) gene, abolishing gene expression. Heterozygotes are viable, fertile, normal in size, and do not display any gross physical abnormalities. Homozygotes die by E11.5 due to fetal heart defects. Pak4 is a member of the group B family of PAK serine/threonine kinases and is expressed early in development in a variety of tissues. It is involved in the formation of filopodia in response to Cdc42, promoting neuronal growth. Improper folding of the caudal neural tubes of homozygous embryos results in the formation of two neural lumens. They also exhibit abnormalities in the development, migration and differentiation of neurons. Specifically, axonal outgrowth was impaired, and neurons failed to migrate to their proper locations. These mice may be useful for studying the role of Pak4 in embryonic and neuronal development. | ||
| 002508 | B6.129S2-Plattm1Mlg/J | Repository- Live |
| Homozygotes develop normally, are fertile and have a normal life span. There are no histological abnormalities. Pulmonary clot lysis is 21% that of normal wildtype siblings. Endotoxin induced venous thrombosis is increased over that seen in normal wildtype siblings. Fibrin dissolution by PLAT-deficient macrophages is unaffected. | ||
| 010945 | B6.129S2-Pms2tm1Lisk/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, but show an increased incidence of sarcomas and lymphomas. Sperm, tail and tumor cells from homozygous mice exhibit microsatellite instability. Male mice on the mixed C57BL/6 and 129S2 background are infertile with reduced numbers of spermatozoa. Spermatozoa exhibit misshapen heads, truncated, irregular flagella. This strain may be useful in the studies of spermatogenesis, cancer and DNA mismatch repair. | ||
| 014089 | B6.129S2-Rbfox1tm1.1Dblk/J | Repository- Live |
| These Fox1flox mutant mice possess loxP sites flanking exons 11-12 of the RNA binding protein, fox-1 homolog 1 (Rbfox1) gene. Mice that are homozygous for this allele are viable, fertile, and normal in size. Fox-1 is expressed in brain, heart, and skeletal muscle and regulates alternative splicing in vertebrates by binding specifically to (U)GCAUG sequences. When these mutant mice are bred to mice that express Cre recombinase, the resulting offspring will have exons 11-12 deleted in the Cre-expressing tissue, resulting in inactivation of Fox-1 gene function.
For example, when crossed to a strain expressing Cre recombinase in the central and peripheral nervous system (see Stock No. 003771), this mutant mouse strain may be useful in studies of neuronal excitation and seizures. | ||
| 002507 | B6.129S2-Serpine1tm1Mlg/J | Repository- Live |
| Mice homozygous for this mutation develop normally and are viable and fertile. Compared to wild type mice, pulmonary clot lysis is increased in the heterozygote and further increased in the homozygote. Endotoxin induced venous thrombosis is decreased compared to wild type mice. Thus, disruption of the Serpine1 gene induces a mild hyperfibrinolytic state. Hemostasis is normal in homozygous mutants. | ||
| 002944 | B6.129S2-Tap1tm1Arp/J | Repository- Live |
| Mice homozygous mice for the Tap1tm1Arp targeted mutation are viable and fertile. They are defective in the stable assembly and intracellular transport of class I molecules. They show severely reduced levels of class I surface molecules. They lack CD4-8+ T cells. This phenotype is similar to the mouse RMA-S cell line and human beings with TAP1 and TAP2 deficiencies. This strain should be housed under pathogen free conditions similar to the Prkdcscid/Prkdcscid mouse or any other immunodeficient strain. | ||
| 006141 | B6.129S2-Thbs1tm1Hyn/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile, with an approximate 20% decrease in embryo/neonate viability and a mild and variable lordotic curvature of the spine apparent from birth. Homozygous mice have an abnormal, but no full length transcript in multiple tissues. Western analysis confirmed the absence of the protein in platelets. Homozygotes exhibit an increase in the number of circulating white blood cells. During the first four to ten weeks of life, homozygotes exhibit patches of acute and organizing pneumonia. At later time points, there is considerable hyperplasia of the various epithelial cell lineages. Mutant mice also have an increased number of retinal endothelial cells and inappropriate remodeling and maturation of retinal vasculature following injury. On the FVB/N background, spontaneous tumor growth and vasculature are significantly increased compared to wildtype. Mutant mice may be useful in studies of inflammatory responses in the lungs, eye, and ..... For more information please see the full phenotype on the strain data sheet | ||
| 002620 | B6.129S2-Tnfrsf1btm1Mwm/J | Repository- Live |
| Mice homozygous for a Tnfrsf1btm1Mwm targeted mutation (formerly Tnfr2tm1Mwm, p75 deficient) are viable and fertile. Homozygous mutant mice show normal T-cell development and activity, but are resistant to TNF-induced cell death. Subcutaneous injections of TNF into homozygotes elicit much less tissue necrosis. | ||
| 002101 | B6.129S2-Trp53tm1Tyj/J | Repository- Live |
| Mice homozygous for the Trp53tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and sarcomas) at three to six months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors. | ||
| 008117 | B6.129S4(129S6)-Ssttm1Ute/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern blot, in situ hybridization or radioimmunoassay analysis of brain tissue. Homozygotes exhibit increased baseline plasma growth hormone, corticosterone and total ghrelin levels compared to wildtype. Mutant mice have impaired motor performance ability. Somatostatin-deficient mice have enlarged stomachs with an increased number of parietal cells and hyperchlorhydria. Hippocampal neprilysin activity is diminished. Compared to wildtype controls, amyloid beta 42 peptides levels are elevated in the hippocampus. This mutant mouse strain may be useful in studies of gastric homeostasis, learning and memory and endocrinology. | ||
| 012933 | B6.129S4(C)-Vhltm1Jae/J | Repository- Live |
| This strain contains loxP sites flanking the Vhl promoter and exon 1. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Cre-mediated recombination results in the deletion of the promoter and exon 1. Studies in which liver-specific inactivation of the Vhl gene was achieved by breeding this strain with albumin promoter driven-Cre mice (see Stock No. 003574 for example) resulted in hemizygous mice that exhibit cavernous hemangiomas of the liver, a rare component of the human von Hippel-Lindau (VHL) disease.
When bred to a strain expressing Cre recombinase in the myeloid cell lineage (see Stock No. 004781 for example), this mutant mouse strain may be useful in studies of myeloid cell mediated inflammation. When bred to a strain expressing Cre recombina ..... | ||
| 007668 | B6.129S4(Cg)-Arntltm1Weit/J | Repository- Live |
| Mice homozygous for this conditional (floxed) allele possess loxP sites flanking exon 8 of the targeted gene and are viable and fertile, with circadian behavioral rhythms indistinguishable from wildtype littermates. When bred to mice that express Cre recombinase, the resulting offspring will have the exon encoding the ARNTL (BMAL1) basic helix-loop-helix (bHLH) domain deleted in the cre-expressing tissue(s). These Bmal1-floxed mutant mice may be useful in generating conditional mutations (whole-mouse or tissue-specific) to study the role of circadian clock/circadian rhythm in physiological and behavioral regulation.
For example, when crossed to a strain expressing Cre recombinase in the retina (see Stock No. 005105), this mutant mouse strain may be useful in studies of the circadian clock of the retina. | ||
| 014156 | B6.129S4(Cg)-Cdk5tm1.1Lht/J | Repository- Live |
| These Cdk5 floxed mutant mice possess loxP sites flanking exons 1-5. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice that express Cre recombinase, resulting offspring lack detectable Cdk5 in the cre-expressing tissues. | ||
| 006955 | B6.129S4(FVB)-Insrtm1Khn/J | Repository- Live |
| Mice homozygous for this IRlox allele are viable and fertile. These mutant mice have loxP sites flanking exon 4 of the targeted gene. When bred to Cre-recombinase expressing mice, offspring will have a deletion of exon 4 in the cre expressing tissue(s). These "floxed" mice may be useful in studying insulin receptor function in several different tissues (including pancreas, liver, and skeletal muscle), as well as diabetes and glucose regulation.
For example, when crossed to a strain expressing Cre recombinase in the central and peripheral nervous system (see Stock No. 003771), this mutant mouse strain may be useful in studies of glucose homeostasis. When crossed to a strain expressing Cre recombinase in skeletal and cardiac muscle (see Stock No. 006475), this mutant mouse strain may be useful in studies of diabetes. When cr ..... | ||
| 009641 | B6.129S4-Adcyap1tm1Clw/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, but experience high postnatal mortality between postnatal week 1 and 2 due to thermoregulatory defect. The Donating Investigator reports that postnatal survival is improved if temperature is kept at 82.5 F. Homozygous males are fertile, homozygous females are subfertile. No gene product (protein) is detected by RIA (radioimmunoassay) analysis of hypothalamus, cerebral cortex, kidney, and stomach tissues in homozygotes. Homozygotes exhibit sustained hyperactivity, shortened circadian period and abnormal circadian phase shifting with 50% reduction in the magnitude of light cued phase shift. Homozygous mice lack the light stimulation increase of sympathetic nerve activity and plasma corticosterone that is observed in wildtype mice. Testicular aging is delayed in 15-month old male homozygotes; reactive oxygen species generation and apoptosis in the testis is reduced. Young male homozygotes (4 month old) exhibit decreased steroi ..... For more information please see the full phenotype on the strain data sheet | ||
| 015857 | B6.129S4-Arg1tm1Lky/J | Repository- Live |
| A targeting vector was designed to insert an internal ribosome entry site (IRES)-enhanced yellow fluorescent protein (eYFP) fusion protein, downstream of the endogenous stop codon of the arginase (Arg1) gene. These homozygous YARG mice are viable, fertile, and normal in size. Located in the cytoplasm of the liver and specifically in macrophages, arginase I converts L-arginine into L-ornithine and urea as the final step in the urea cycle. L-arginine can also be catabolized into nitric oxide (NO), a secreted free radical which causes tissues damage and is toxic to bacteria. Arginase I suppresses NO production by decreasing the amount of L-arginine available to the nitric oxide synthase (NOS) enzyme for conversion into NO and other reactive oxygen species (ROS). Nine days after infection with the helminth, Nippostrongylus brasiliensis, YARG mice exhibit accumulation of arginase I-expressing macrophages in the lung and peritoneum. As soon as two days afte ..... For more information please see the full phenotype on the strain data sheet | ||
| 002266 | B6.129S4-Bdnftm1Jae/J | Repository- Live |
| Mice heterozygous for the Bdnftm1Jae mutation show about half normal levels of Bdnf mRNA, but appear normal. Mice homozygous for the Bdnftm1Jae mutation are smaller than normal siblings and most die within the second postnatal week. They have defective coordination of movements and balance. They also exhibit head bobbing and spinning during periods of hyperactivity. There are rare survivors to adulthood. There is excessive degeneration in all sensory ganglia examined, including the vestibular ganglion. Motor neurons are not affected. BDNF can prevent death of central motor neurons and other neurons in vitro, but does not affect these in vivo. | ||
| 004999 | B6.129S4-Ccr2tm1Ifc/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis of spleen or thioglycollate elicited peritoneal exudate cells. These mutant mice have defective type 1 (Th1) immune responses. Mycobacteria bovis purified protein derivative induced lung granulomas are initially smaller in size and contain fewer macrophages than wildtype controls. Mutant mice also exhibit decreased IFN-alpha production after lung granuloma induction. When challenged with thioglycollate treatment homozygotes respond with reduced peritoneal macrophage recruitment. Macrophages derived from these animals fail to migrate in response monocyte chemoattractant protein- 1 (MCP-1). Homozygotes are resistant to experimental autoimmune encephalomyelitis (EAE), a macrophage-mediated inflammatory disease. This mutant mouse strain may be useful in studies of immune respons ..... For more information please see the full phenotype on the strain data sheet | ||
| 002704 | B6.129S4-Cd247tm1Lov/J | Repository- Live |
| Mice homozygous for the Cd3ztm1Lov targeted mutation are viable and fertile. Homozygous mutant mice exhibit impaired T-cell development and function. | ||
| 003610 | B6.129S4-Cd80tm1Shr Cd86tm2Shr/J | Repository- Live |
| Cd80/Cd86-mediated signaling is critical to germinal center formation and Ig class switching in vivo. Mice homozygous for both the Cd80 (B7-1) and Cd86 (B7-2) targeted mutations are viable, fertile and have a normal life span. Homozygous null Cd80/Cd86 mice fail to generate antigen specific IgG1 and IgG2a responses. During the postimmunization period (seven-10 days) they have smaller spleens devoid of germinal centers. Unimmunized null mice exhibit a three to five fold reduction in total serum immunoglobulin and IgG2a. Levels of IgG1 are also reduced five to 10 fold. Levels of IgM and IgG3 are elevated three to five fold. When immunized, antigen specific IgG1 and IgG2a isotype levels are 0.1% that of wild-type levels. Levels remain low even when immunization is performed with adjuvent. This strain is also resistant to myelin oligodendrocyte glycoprotein (MOG) 35-55 peptide-induced experimental autoimmune encephalomyelitis (EAE), a T cell-mediat ..... For more information please see the full phenotype on the strain data sheet | ||
| 003611 | B6.129S4-Cd80tm1Shr/J | Repository- Live |
| Cd80 (B7-1) null mice are viable and fertile. They possess normal numbers of B and T lymphocytes but exhibit a diminished mixed lymphocyte response. Following immunization, antigen specific IgG1, IgG2a and IgM isotypes are 25%-50% that of wild type levels. Survival of certain tissue allografts are slightly prolonged in Cd80 null mice. | ||
| 003609 | B6.129S4-Cd86tm1Shr/J | Repository- Live |
| Cd86 (B7-2) null mice are viable and fertile. Unimmunized mice have normal levels of serum immunoglobulin and normal numbers of B and T lymphocytes. Upon intravenous immunization without adjuvant, they fail to form germinal centers or undergo isotype switching and antigen specific IgG1 and IgG2a isotypes are found to be 5% that of wild type levels. When the immunization route is subcutaneous, IgG1 and IgG2a levels are the same as in wild type mice. | ||
| 002781 | B6.129S4-Cdkn1btm1Mlf/J | Repository- Live |
| Mice deficient in p27kip are viable and larger than normal littermates, with increased cellularity of all tissues. The thymus and spleen are particularly enlarged. Homozygous (nullizygous) adult mice have a shortened lifespan due to the growth of benign intermediate lobe pituitary tumors. Female mice are infertile, with a follicular phase ovulatory block. Large doses of exogenous gonadotropin induce ovulation, but both implantation and intrauterine embryonic development is impaired. The mice demonstrate haploid-insufficient susceptibility to the development of adenomas in the pituitary, intestine and lung adenomas following exposure to gamma irradiation or chemical carcinogens. | ||
| 010925 | B6.129S4-Clocktm1.1Rep/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 immunohistochemical and immunoprecipitation analysis of SCN (suprachiasma nucleus). Homozygotes exhibit a shorter circadian period of approximately 20 minutes, when kept in constant darkness. While under 12 hr light/12 hr dark (LD) cycle, homozygotes become active approximately 2 hours before the start of the dark cycle, indicating altered response to light cues. A four hour extended light period preceding constant darkness does not result in the expected activity rhythm phase delay. Re-entrainment with LD cycle followed by a 4 hour light pulse in the dark cycle does not cause activity rhythm phase advance. | ||
| 010490 | B6.129S4-Clocktm1Rep/J | Repository- Live |
| These mice possess loxP sites on either side of exons 5 and 6 of the targeted gene. Mice that are homozygous for this conditional 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 5 and 6 deleted in the cre-expressing tissue(s). When bred to a strain expressing Cre recombinase in the male germ line (see Stock No. 003328 for example), this mutant mouse strain may be useful in studies of circadian rhythm and behavior. | ||
| 010923 | B6.129S4-Csnk1dtm1.1Drw/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical abnormalities. Homozygotes die during late gestation and perinatally, with no homozygotes at weaning age. Homozygous embryos are smaller (approximately 30% less than control weight) than wild-type controls at embryonic day 18-19. A truncated non-functional gene product (protein), lacking residues 26 to 62, is detected by Western blot analysis and cotransfection assays of homozygotes. The truncated protein does not phosphorylate or degrade PER1, period homolog 1 (Drosophila), and PER2, period homolog 2 (Drosophila), proteins. After being kept in constant darkness for 10 days, heterozygotes exhibit a longer free-running period than wild-type controls. | ||
| 010487 | B6.129S4-Csnk1dtm1Drw/J | Repository- Live |
| These mice possess loxP sites on either side of exon 2 of the targeted gene. Mice that are homozygous for this conditional allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 deleted in the cre-expressing tissues. After Cre-mediated excision of exon 2, a mutant gene product (protein) is detected by Western blot analysis of liver tissue. This mutant protein is relatively unstable, does not interact with PER (Period) proteins, and does not have biological activity with respect to PER protein phosphorylation. This mutant mouse strain may be useful in generating conditional mutations for studying circadian rhythm and behavior. | ||
| 010924 | B6.129S4-Csnk1etm1.1Drw/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 liver. After being kept in constant darkness for 10 days, heterozygotes exhibit a longer free-running period than wild-type controls. The level of CSNK1D protein is increased in the liver. | ||
| 010489 | B6.129S4-Csnk1etm1Drw/J | Repository- Live |
| These mice possess loxP sites on either side of exons 2 and 3 of the targeted gene. Mice that are homozygous for this conditional allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 2 and 3 deleted in the cre-expressing tissue(s). This mutant mouse strain may be useful in generating conditional mutations for studying circadian rhythm and behavior. | ||
| 006087 | B6.129S4-Cxcl10tm1Adl/J | Repository- Live |
| Homozygous mice are viable, fertile, and have no overt morphological or developmental abnormalities. No endogenous gene expression is observed in bone marrow-derived macrophages before or after IFN-gamma stimulation. Homozygous mice have defective T cell responses, including impaired proliferation and IFN-gamma secretion following antigenic challenge (129Sv background). In experimental models of T helper-1 (Th1)-mediated immune responses, homozygous-deletion leads to diminished immune function; contact hypersensitivity is reduced (129Sv background) and diminished threshold for disease expression in experimental autoimmune encephalomyelitis (EAE, human model of multiple sclerosis) (C57BL/6 background). After injection with a neurotropic coronavirus MHV, null mice (on a B6;129Sv background) exhibit impaired viral clearance, decreased CD4+/CD8+ infiltration into the brain, and are protected from viral-induced demyelination. Similarly, homozygous mice (on a C57BL/6 ba ..... For more information please see the full phenotype on the strain data sheet | ||
| 012932 | B6.129S4-Ftmttm1Mdf/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis of testes from homozygotes. Homozygotes do not exhibit any overt phenotype. | ||
| 005246 | B6.129S4-Grin1tm2Stl/J | Repository- Live |
| These mice possess loxP sites flanking approximately 12kb of sequence of the targeted gene that encodes the entire transmembrane domain and C-terminal region. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to a strain expressing Cre recombinase in the CA3 region of the hippocampus (see Stock No. 006474 for example), this mutant mouse strain may be useful in studies of associative memory recall. When bred to a strain expressing Cre recombinase in the CA1 region of the hippocampus (see Stock No. 005359 for example), this mutant mouse strain may be useful in studies of nonspacial memory. | ||
| 010959 | B6.129S4-Grk5tm1Rjl/J | Repository- Live |
| Grk5 (G protein-coupled receptor kinase 5) targeted mutant mice exhibit supersensitivity (lost desensitization) of brain and lung airway M2 muscarinic receptors. Aged homozygotes develop amyloid-like plaques and exhibit some cognitive defects. Although the gene is normally expressed in heart and lymphocytes, cardiac M2 muscarinic receptor function and lymphocyte chemotaxis in response to SDF-1 are normal. Homozygotes are viable and present no gross anatomical differences nor striking behavioral abnormalities. Western blot analysis demonstrates a loss of expression in brain, lymphocytes, lung and heart. | ||
| 010961 | B6.129S4-Grk6tm1.1Mca/J | Repository- Live |
| These Grk6 (G protein-coupled receptor kinase 6) targeted mutant mice exhibit supersensitive locomotor responses to psychostimulant drugs and dopamine D2 agonists. CXCL12-induced chemotaxis of B and T lymphocytes from homozygous mice is reduced in vitro, whereas neutrophils show enhanced accumulation at sites of inflammation. In the dextran sulfate model of colitis, homozygotes develop more severe disease and fail to recover normal colonic function after withdrawal of the irritant. | ||
| 002867 | B6.129S4-Icam1tm1Jcgr/J | Repository- Live |
| Mice homozygous for the Icam1tm1Jcgr targeted mutation are viable and fertile. The phenotype is similar to C57BL/6J-Icam1tm1Bay (Stock No. 002127) but are reported to be less leaky. Characteristics include longer lifespan and nephritis with no apparent lung involvement. | ||
| 002952 | B6.129S4-Il2ratm1Dw/J | Repository- Live |
| Mice homozygous for the Il2ratm1Dw targeted mutation are are characterized by a lymphoproliferative disorder, hemolytic anemia, and an inflammatory bowel disease beginning at approximately 9 weeks of age; also known as p55 gene chain, Ly43, CD25. | ||
| 003174 | B6.129S4-Il2rgtm1Wjl/J | Repository- Live |
| Mice homozygous for the Il2rgtm1Wjl targeted mutation are viable and fertile. Mutant mice have hypoplastic thymuses with a 10-fold reduction in the absolute number of lymphocytes. They have a limited number of mature splenic B and T cells, lack NK cells and Peyer's patches, and development of gut-associated intraepithelial lymphocytes is diminished. In vitro studies show defects in NK activity, IL4-directed Ig class switching of thymocytes, and thymocyte mitogenic responses. | ||
| 003991 | B6.129S4-Itgamtm1Myd/J | Repository- Live |
| Mice that are homozygous for the Itgamtm1Myd targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No Itgam protein is detected in homozygous mutant neutrophils. Homozygous null animals have a diminished ability to clear thioglycollate-induced neutrophils, have reduced mast cell numbers in the dorsal skin and peritoneal wall/cavity, and are less susceptible to cerebral ischemia/reperfusion injury. Neutrophils from these animals are deficient at spreading, phagocytosing complement-opsonized particles, and in several Fc-mediated functions. They also exhibit impaired oxidative burst and a diminished responsiveness in LPS- and taxol-mediated gene expression. | ||
| 008102 | B6.129S4-Ltb4r1tm1Adl/J | Repository- Live |
| Mice homozygous for this BLTR (BLT1)-deficient allele are viable and fertile. Northern blot analysis of neutrophils, macrophages, lymph nodes, lungs, and
spleens isolated from homozygous mice show absence of the normal transcript and presence of the expected larger transcript (due to the insertion of the neomycin resistance cassette in exon 2 of the targeted gene), albeit at lower levels than the wild type transcript. Homozygous disruption of this allele confers impaired leukocyte function (chemotaxis, recruitment, firm adhesion). For example, homozygotes exhibit substantially diminished recruitment of eosinophils in a model of peritonitis, effector T cells in a model of allergic pulmonary inflammation, and neutrophils in a model of rheumatoid arthritis. As the G protein-coupled receptor BLTR/BLT1 is expressed on myeloid leukocytes (including neutrophils, macrophages, eosinophils, T cell lymphomas, and effector T cells (TH1 CD4+ cells, TH2 CD4+ cells, and effecto ..... For more information please see the full phenotype on the strain data sheet | ||
| 006122 | B6.129S4-Mbl1tm1Kata Mbl2tm1Kata/J | Repository- Live |
| Mice homozygous for both mannose-binding lectin (MBL)-A and MBL-C targeted mutations (termed MBL-null) are viable, fertile, and normal in size with no obvious developmental defects. Histological examination of multiple organs from 6-10 week old mice shows no abnormalities. MBL-null mice have no endogenous gene expression in liver (the principal site of MBL synthesis) and no protein detectable in serum. While the classical complement pathway is unaffected in MBL-null mice, the lectin-dependent complement pathway is non-functional. MBL-null mice have increased mortality following intravenous injection of S. aureus associated with abnormal serum levels of TNFalpha and IL-6 (decreased at 2h, elevated at 24h post injection). Cyclophosphamide-induced febrile neutropenic MBL-null mice inoculated with S. aureus have greatly increased susceptibility to abscess formation in kidney, liver, and lung (but not spleen). These same treated mice also have persistent bacteremia despite a r ..... For more information please see the full phenotype on the strain data sheet | ||
| 003755 | B6.129S4-Meox2tm1(cre)Sor/J | Repository- Live |
| This strain expresses Cre recombinase under the control of the endogenous Meox2 promoter. Expression of Cre recombinase is observed in epiblast-derived tissues as early as embryonic day 5. The insertion creates a null allele for the Meox2 gene. Homozygous mice are viable on this background but exhibit an overall reduction in muscle mass and the absence of specific muscles resulting in abnormal limb posture and reduced motility. This phenotype is variable. As many as 80% of homozygotes are severely affected, fail to thrive and die before weaning. Some homozygotes (10%) exhibit clefting of the secondary palate. These mice can be utilized as a deleter strain for loxP flanked DNA and provide an alternative to tetraploid embryo analysis. | ||
| 011009 | B6.129S4-Mtortm1.2Koz/J | Repository- Live |
| Mice homozygous for this mTORfl allele are viable and fertile, with loxP sites flanking exons 1-5 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have the sequences encoding the putative transcription start site and the coding sequence through coding exon 5 deleted in the cre-expressing tissue(s). These mTORfl mutant mice may be useful in generating conditional mutations for studying mTOR and mTOR complex signaling; including regulation of cell growth, cell proliferation/differentiation, cell survival, cancer, tumor cell motility and metastasis, the RTK-PI3K-mTOR signaling axis, stem cell development, cytokine signaling, and T cell lineage commitment.
For example, when bred to a strain expressing Cre recombinase in adult striated muscle fibers and embryonic striated muscle cells of the somites and heart (see Stock No. 006149 for example), ..... | ||
| 007893 | B6.129S4-Myf5tm3(cre)Sor/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Myf5 locus. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs skeletal muscle and the dermis, and in several ectopic locations. Homozygotes for this allele have a perinatal lethal phenotype and die at birth. Homozygotes display abnormal rib development and some fusions of the cervical or thoracic vertebrae. This mutant mouse strain represents a model that may be useful in studies of skeletal development.
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 p ..... | ||
| 002213 | B6.129S4-Ngfrtm1Jae/J | Repository- Live |
| Mice homozygous for the Ngfrtm1Jae mutation are viable and fertile. They display a decreased cutaneous innervation by calcitonin gene-related peptide- and substance P-immunoreactive sensory fibers. Because of this decreased innervation they develop ulcers on their toes by four months of age. The toes become inflamed and progressively infected. There is also reduced sensitivity to heat in the extremities of these mice. Pineal glands lack sympathetic innervation and innervation to sweat glands on foot pads is either reduced or absent. Deficits in the peripheral nervous system were examined by looking at cellular responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. p75-deficient DRG and SCG neurons displayed a two- to three-fold decreased sensitivity to NGF at embryonic day 15 and postnatal day three, respectively. These ages coincide with the peak of naturally occurring cell death. p75-deficient ..... For more information please see the full phenotype on the strain data sheet | ||
| 002986 | B6.129S4-Nos1tm1Plh/J | Repository- Live |
| Mice homozygous for the Nos1tm1Plh targeted mutation are viable and fertile; however, they have enlarged stomachs and reduced stroke size. Hyperglycemic-euglycemic clamp studies demonstrate that homozygotes exhibit insulin resistance at the level of peripheral tissues. Homozygous males are reported to be more aggressive than normal wildtype siblings although this has not been confirmed in The Jackson Laboratory colony. These mice may be useful model for stroke research. | ||
| 008519 | B6.129S4-Nos1tm2Plh/J | Repository- Live |
| In this targeted mutation exon 6, which encodes the heme-binding domain, is deleted. Mice that are homozygous for the targeted mutation are viable only when maintained on a liquid diet and are not fertile. Some truncated gene product (mRNA) containing exon 2 but completely lacking exon 6 is detected by RR-PCR of brain. Nitric oxide synthase activity is only 0.3% of wildtype levels in the brain. Homozygotes have smaller total body and gonad weight and develop pyloric stenosis. Female homozygotes have fewer ovarian corpora lutea and increased hypothalmic gonadotropin-releasing hormone and circulating luteinizing hormone. Homozygous males have decreased follicle stimulating hormone levels and do not display mating behavior. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of hypothalamo-pituitary axis and neuroendocrine regulation of ..... For more information please see the full phenotype on the strain data sheet | ||
| 006582 | B6.129S4-Park2tm1Shn/J | Repository- Live |
| Homozygous mice are viable and fertile, and exhibit grossly normal brain morphology. Western blot analysis using antibody specific to C-terminal sequences indicates the absence of full length gene product. RT-PCR shows that exon 2 splices to exon 4, skipping exon 3 entirely, resulting in a frame shift and a premature stop codon in exon 5. While EGFP transcripts are present, little parkin-EGFP fusion protein is detectable by Western analysis. Homozygous mice have increased extracellular dopamine concentration in the striatum. Further, medium-sized striatal spiny neurons require greater currents to induce synaptic responses, suggesting a reduction in synaptic excitability in the absence of the endogenous gene. Homozygotes also exhibit deficits in behavioral paradigms sensitive to dysfunction of the nigrostriatal pathway. The numbers of dopaminergic neurons in the substantia nigra, however, are normal up to the age of 24 months, in contrast to the substantial loss of nigral neurons charac ..... For more information please see the full phenotype on the strain data sheet | ||
| 007669 | B6.129S4-Pdgfratm11(EGFP)Sor/J | Repository- Live |
| Mice homozygous for this knock-in targeted mutation have an embryonic lethal phenotype, with half of the embryos failing to survive past embryonic day 12.5 and the remainder failing to survive beyond embryonic day 15.5. These mice express the H2B-eGFP fusion gene from the endogenous Pdgfra locus. Fluorescence is detectable at embryonic day 4.5 in polar trophectoderm cells and at embryonic day 6.5 in the extraembryonic ectoderm. Expression of H2BGFP mimick the expression pattern of the endogenous gene. Homozygotes exhibit abnormal placenta development and placenta vasculature. This mutant mouse strain may be useful in studies of 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). | ||
| 010493 | B6.129S4-Per3tm1Drw/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 whole brain minus cerebellum and hypothalamus, whole hypothalamus, and anterior hypothalamus containing SCN, from homozygotes. Immunoprecipitation analysis of brain lysates from homozygotes does not detect any gene product (protein). Abberant gene products (mRNA) are detected by Northern blot analysis and RT-PCR, and have rhythmic expression. Under conditions of constant darkness, homozygous males exhibit a shorter free running period. A subset of mice exhibit progressive shortening of the period length in extended constant darkness. This mutant mouse strain may be useful in studies of circadian rhythm and sleep patterns.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic backg ..... | ||
| 016132 | B6.129S4-Perptm2Att/J | Repository- Live |
| 015860 | B6.129S4-Pglyrp2tm1Lky/J | Repository- Live |
| These PGRP-L mice contain a targeting vector designed to insert an enhanced green fluorescent protein (EGFP) immediately downstream from the initiation sequence of the peptidoglycan recognition protein, 2 (Pglyrp2) gene, abolishing gene expression. Homozygous mice are viable, fertile, normal in size and do not display any gross physical abnormalities. PGRP-L, the longest member of a family of innate immune recognition molecules, recognize peptidoglycan components of bacterial cell walls. Expressed mainly in liver, PGRP-L is secreted and multimerizes in the serum. Peritoneal macrophages from these PGRP-L-deficient mice showed a decrease in interleukin 6 (IL6) and tumor necrosis factor alpha (TNFα) production when stimulated with E. coli or lipopolysaccharide (LPS), but comparable amounts when stimulated with S. aureus, C. albicans, gram-positive or -negative peptidoglycans, suggesting a redundant pathway is involved. These mice may be useful for visualizing PGRP-L expre ..... For more information please see the full phenotype on the strain data sheet | ||
| 010671 | B6.129S4-Pkd1tm2Ggg/J | Repository- Live |
| These mice possess loxP sites on either side of exons 2 through 4 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 2 through 4 deleted in the cre-expressing tissue(s).
For example, when crossed to a strain with widespread Cre recombinase expression (see Stock No. 003553), this mutant mouse strain may be useful in studies of polycystic kidneys. | ||
| 006440 | B6.129S4-Ptentm1Hwu/J | Repository- Live |
| These mice possess loxP sites flanking exon 5 of the targeted gene. Mice homozygous for the"floxed" allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele.
For example, when crossed to a strain expressing Cre recombinase in astrocytes (see Stock No. 012887), this mutant mouse strain may be useful in studies of neurogenesis. When crossed to a strain expressing Cre recombinase in the central nervous system (see Stock No. 004600), this mutant mouse strain may be useful in studies of glia differentiation and cerebellar development. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to ..... | ||
| 006243 | B6.129S4-Timp1tm1Pds/J | Repository- Live |
| Homozygous females and hemizygous males (the gene is X-linked) are viable and fertile. No endogenous transcript is detected in lung tissue from affected mice by Northern blot analysis.. Homozygous mice have increased resistance to corneal and pulmonary infection with P. aeruginosa, and have altered immune, hematopoietic, and vascular permeability in bleomycin-induced lung injury trials. Homozygotes also show increased and continued progression of aneurysm formation compared with wild-type mice in induced thoracic aortic aneurysm (TAA) models. Mice with this X-linked targeted mutation may be useful in studies of cornea and pulmonary infection, pulmonary injury and aneurysm, as well as of P. aeruginosa resistance in individuals with unresolved, antibiotic-resistant pulmonary infections, such as those often observed in cystic fibrosis patients.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genet ..... | ||
| 010672 | B6.129S4-Tnfrsf11btm1Eac/J | Repository- Live |
| Mice homozygous for this osteoprotegerin (OPG)-mutant allele are viable and fertile. While a smaller transcript is made from the disrupted allele, the spliced product is predicted to be out of frame and result in a nonfunctional protein. OPG-deficient mice exhibit dysregulation of osteoclast production leading to drastic changes in the bone architecture; homozygotes develop severe osteoporosis, gross deformations in bone structure, decreased bone density, and altered long bones physical dimension. Hematopoietic, B lymphocyte, and dendritic cell functions are also dysregulated.
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. | ||
| 012838 | B6.129S4-Tnfrsf4tm1Nik/J | Repository- Live |
| In Ox40-/- mice, the targeted mutation replaces exons 1-4 of the tumor necrosis factor receptor superfamily, member 4 (Tnfrsf4 or Ox40) locus with a floxed neomycin (neo) resistance cassette, abolishing gene function. Homozygous mice are viable, fertile, and normal in size. Ox40-/- CD4+ T cells Ox40-/- CD4+ T cells demonstrate defects in clonal expansion associated with impaired survival of activated cells. These mice may be useful for studying the importance of the CD134 molecule in T cell differentiation and responses. | ||
| 006133 | B6.129S4-Vdrtm1Mbd/J | Repository- Live |
| Heterozygous mice are phenotypically indistinguishable from wildtype siblings. As originally characterized on a mixed B6;129 genetic background, homozygous mice are viable and fertile with normal survival until approximately 14 months. RNA isolated from the intestine and kidney show a truncated deletion of the second zinc finger coding region followed by a premature termination codon, resulting in the absence of receptor protein. Homozygous mice exhibit an identical phenotype as the human disease hereditary vitamin D-dependent rickets type II (HVDDR). As early as 21 days of age, mutant mice demonstrate hypocalcemia, hypophosphatemia, hyperparathyroidism, increased serum parathyroid hormone, abnormal blood mineral levels, and growth retardation. In addition, renin and plasma angiotensin II levels are increased. Homozygous mice are hypertensive and exhibit cardiachypertrophy. At 4 weeks of age, homozygous mice exhibit perioral and periorbital alopecia that progresses over the entire bod ..... For more information please see the full phenotype on the strain data sheet | ||
| 012564 | B6.129S5-Dhcr24tm1Fein/SbpaJ | Repository- Live |
| Homozygous mice on the C57BL/6 genetic background die within the first postnatal day with features of lethal restrictive dermopathy; including taut, wrinkle-free, shiny skin, severe defects in epidermal maturation/epidermal barrier function (impaired epidermal development), and increased presence of hyperproliferative immature keratinocytes (defective keratinocyte differentiation). The increased transepidermal water loss/increased epidermal water content is associated with increased aquaporin-3 (AQP3) expression throughout the epidermis. Mice heterozygous for this allele are viable and fertile, with no overt phenotype. As the Dhcr24 protein functions to catalyze the last step of cholesterol biosynthesis (the conversion of desmosterol to cholesterol), homozygous disruption of this locus results in desmosterolosis: almost no cholesterol in plasma and tissues with ~99% of total sterols in the form of desmosterol. lacZ expression from the mutant allele is not characterized.
<> ..... For more information please see the full phenotype on the strain data sheet | ||
| 013189 | B6.129S5-Mlst8tm1Lex/J | Repository- Live |
| In this strain, the allele replaces exons 2-8 of the mTOR (Mechanistic target of rapamycin) associated protein (LST8 homolog), Mlst8, gene with an internal ribosome entry site (IRES)-lacZ (β-galactosidase), and a neomycin resistance (neo) cassette, abolishing gene function. Heterozygous mice are viable, fertile, and normal in size, while homozygous mice die by e10.5. mLST8 forms the complex mTORC1 with mTOR and Rptor (regulatory associated protein of mTOR, complex 1), which is critical for the growth of the inner cell mass and trophoblast cell outgrowth during early embryonic development. mLST8 also forms the complex mTORC2 with mTOR and Rictor (Rptor independent companion of mTOR, complex 2), which is critical for midgestational embryonic development. Mlst8-/- embryos exhibit underdeveloped telencephalic and vitelline vesicles, defective yolk sac vasculature, internal hemorrhaging, and dilated blood vessels, particularly in the head. Although ..... For more information please see the full phenotype on the strain data sheet | ||
| 013190 | B6.129S5-MtorGt(OST92090)Lex/J | Repository- Live |
| This secretory trap mutation abolishes endogenous mTOR (Mechanistic target of rapamycin) gene function and expresses a neomycin (neo) resistance cassette/simian virus 40 (SV40) polyadenylylation signal fusion protein. Heterozygous mice are viable, fertile, and normal in size, while homozygous mice die by e6.5. mTOR forms the complex mTORC1 with mLST8 (mTOR associated protein (LST8 homolog)) and Rptor (regulatory associated protein of mTOR, complex 1), which is critical for the growth of the inner cell mass and trophoblast cell outgrowth during early embryonic development. mTOR also forms the complex mTORC2 with mLST8 and Rictor (Rptor independent companion of mTOR, complex 2), which is critical for midgestational embryonic development. The inner cell mass and trophoblast giant cells fail to expand in explanted mTOR-/- blastocysts. By day 4 the cells of the blastocysts stop growing and by day 7 the cells are detached and dying. These mice may be useful for studying mTOR complex sig ..... For more information please see the full phenotype on the strain data sheet | ||
| 013191 | B6.129S5-Rptortm1Lex/J | Repository- Live |
| In this strain, the allele replaces alternate exon 1 and common exon 2 of the regulatory associated protein of mTOR (Mechanistic target of rapamycin), complex 1 (Rptor) gene with an internal ribosome entry site (IRES)-lacZ(β-galactosidase), and a neomycin resistance (neo) cassette, abolishing gene function. Heterozygous mice are viable, fertile, and normal in size, while homozygous mice die by e6.5. Raptor forms the complex mTORC1 with mLST8 (mTOR associated Protein, LST8 homolog) and mTOR, which is critical for the growth of the inner cell mass and trophoblast cell outgrowth during early embryonic development. When Raptor-/- blastocysts are implanted, 25% can implant but all fail to expand and differentiate. In culture, by day 4 the cells of the blastocysts stop growing and by day 7 the cells are detached and dying. β-gal staining is evident in embryonic cells expressing Raptor. These mice may be useful for studying raptor-mTOR complex signaling ..... For more information please see the full phenotype on the strain data sheet | ||
| 016565 | B6.129S6(Cg)-Cdkn1atm1Led/J | Repository- Live |
| In this knockout strain, a neo cassette replaces exon 2 of the of the cyclin-dependent kinase inhibitor 1A (Cdkn1a or p21CIP1/WAF1) gene. Homozygotes are viable, fertile, and normal in size. P21CIP1/WAF1 is expressed, in a p53-dependent manner, during embryogenesis and postnatal development primarily in dividing cells. Although, actively dividing cells in these mice do not arrest in G1 phase of the cell cycle in response to DNA damage, these mice do not develop tumors as mice deficient in p53 do. These mice may be useful for studying cell cycle timing and arrest during cellular proliferation. | ||
| 013720 | B6.129S6(Cg)-Ntrk1tm2Ddg/J | Repository- Live |
| A targeting vector was designed to place a FLAG tag upstream of exon 1 of the neurotrophic tyrosine kinase receptor, type 1 (Ntrk1 or TrkA) gene. Mice homozygous for the TrkAFlag allele are viable, fertile, and normal in size. | ||
| 004936 | B6.129S6(Cg)-Spp1tm1Blh/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis of embryonic fibroblasts and kidney. Immunohistochemical analysis of kidney and bone tissue also fails to detect gene product (protein). Homozygotes exhibit disorganized ultrastructural wound matrix remodeling and defective macrophage infiltration and accumulation at sites of injury and infection. Experimentally induced hyperoxaluria results in renal tubule deposition of calcium oxalate crystals. Accelerated ectopic calcification mineralization in soft tissues occurs after subcutaneous implantation of glutaraldehyde-fixed aortic valve tissue. Mutant macrophage response to mycobacteria infection and pulmonary granulomatous response and inflammation are impaired. According to a recent publication (Hsieh et al 2006 Cancer Res 2006 66:7119-27), mutant mice treated with a skin ch ..... For more information please see the full phenotype on the strain data sheet | ||
| 008101 | B6.129S6(FVB)-Ptgs2tm1.1Fun/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 are not fertile. The protein gene product does not have cyclooxygenase activity while the peroxidase activity is normal as measured by LPS induction of macrophages derived from mutant mice. Mutant mice are more sensitive to collagen treatment resulting in reduction of platelet numbers (indicating enhanced thrombogenesis) and exhibit a higher frequency of sudden death due to thromboxane receptor agonist treatment. No prolonged bleeding time from LPS administration is observed. Prostaglandin E metabolite levels are diminished in urine. Three month old mutant mice have elevated systolic blood pressure (measured by the tail cuff method). Homozygotes exhibit undersize, pale kidneys with atrophic cortices, interstitial inflammation, hypoplastic glomeruli and glomerulosclerosis.
This mutant mouse strain may be useful in studies of ..... For more information please see the full phenotype on the strain data sheet | ||
| 007611 | B6.129S6(SJL)-Cdh2tm1Glr/J | Repository- Live |
| These mice possess loxP sites on either side of exon 1 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 1 deleted in the cre-expressing tissue(s). When bred to a strain with inducible Cre recombinase expression in cardiac cells (see Stock No. 005657 for example), this mutant mouse strain may be useful in studies of myocardium physiology. | ||
| 006237 | B6.129S6-Casp7tm1Flv/J | Repository- Live |
| Homozygous mice are viable and fertile with normal appearance, organ morphology, and lymphoid development. Endogenous protein expression is absent in all tissues tested (including brain, thymus, heart, lung, liver, spleen, kidney, and skeletal muscle). Mouse embryonic fibroblasts (MEFs) from homozygotes exhibit a slight survival advantage when treated with apoptosis inducers, but other cell subsets undergo normal apoptosis (including activated T cells death following T cell receptor stimulation, thymocyte apoptosis, and Fas-mediated B cell and hepatocyte cell death). These mutant mice may be useful in studies of mitochondrial events of apoptosis, especially when paired with other executioner caspase mutant models. | ||
| 013061 | B6.129S6-Ccr6tm1(EGFP)Irw/J | Repository- Live |
| Homozygous Ccr6-EGFP mice are viable and fertile; harboring an enhanced green fluorescent protein (EGFP) allele that both abolishes endogenous Ccr6 gene function and expresses EGFP from the Ccr6 promoter/enhancer elements. As such, robust EGFP fluorescence is directed to all mature B cells, subpopulations of splenic CD4+ and CD8+ T cells, CD4+ and CD4- myeloid dendritic cells (DC), some CD11c+ DC, and most CD11b+ myeloid DC. Fluorescence is detected at lower levels in epidermal Langerhans cells (LC). These mice exhibit abnormalities in Peyer's patches, decreased isolated lymphoid follicle development in the intestine, and reduced numbers of intestinal M cells. | ||
| 002269 | B6.129S6-Cd4tm1Knw/J | Repository- Live |
| Mice homozygous for the Cd4tm1Knw targeted mutation have a significant block in CD4+ T cell development; 90% of their circulating T cells are CD8+. Homozygous mutant mice also show a Class II restricted deficit in helper T cell activity and other T cell responses. | ||
| 016263 | B6.129S6-Ch25htm1Rus/J | Repository- Live |
| Stimulation of toll-like receptors has been shown to normally induce the expression of Ch25h (cholesterol 25-hydroxylase) in macrophages. Il2 (interleukin 2)-mediated stimulation of B cell proliferation is suppressed, activation-induced cytidine deaminase (AID) expression is repressed, and immunoglobulin class switch recombination is blocked, leading to markedly decreased IgA production.
The Ch25h gene was deleted in this targeted mutant strain. Homozygotes have excessive levels of IgA in their sera, mucosa, and the bronchial fluid of the lungs. This strain may be useful in studies of innate immune system regulation of adaptive immune responses. | ||
| 008240 | B6.129S6-Eif2ak4tm1.2Dron/J | Repository- Live |
| Mice homozygous for the GCN2.KO4 mutant locus (also called GCN2.KO4-, GCN2-, GCN2.KO4ex, or GCN2-KO) are viable, fertile and overtly indistinguishable from wild-type mice, with little if any mRNA expressed from the mutant locus. Homozygous GCN2-deficiency is associated with altered inflammatory responses and altered stress responses, including sensitivity to nutritional deficiencies and aberrant eating behavior. As GCN2 is a protein kinase that phosphorylates eIF2 (eukaryotic initiation factor 2) in response to environmental stresses (amino acid starvation, proteasome inhibition and UV irradiation) to reduce global translation and activate stress-related transcription factors (such as NF-kappaB) to alleviate cellular injury or alternatively induce apoptosis, these GCN2.KO4 mutant mice may be useful for such immunology, inflammatory, immunity cell biology, or neurobiology research.
Of note, mice with a conditional allele (loxP-flanked exon XII ..... | ||
| 013788 | B6.129S6-Fam3btm1Bkht/J | Repository- Live |
| Homozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by RT-PCR and Western blot analysis of pancreatic islets and small intestines from homozygotes. Male mice that are homozygous for the targeted mutation and 4 to 6 months of age exhibit higher blood glucose levels in glucose tolerance tests when compared to wildtype controls. Although, insulin sensitivity is normal in mutant mice, insulin levels are elevated after glucose stimulation (intraperitoneal glucose injection) due to decreased hepatic insulin clearance. Glucose intolerance is not observed in mutant female mice. Isolated pancreatic islets from male homozygotes have impaired glucose-stimulated insulin secretion and calcium signaling. Male homozygotes have reduced hepatic glucose production (HGP) and increased insulin-mediated HGP suppression conditions as determined by hyperinsulinemic-euglycemic clamp assays. Further ..... For more information please see the full phenotype on the strain data sheet | ||
| 015840 | B6.129S6-Itga8tm1.1Rdav/J | Repository- Live |
| Mice homozygous for this f(α8) conditional allele are viable and fertile, with loxP sites flanking the last two coding exons (exons 29-30) of the Itga8 gene (also called integrin alpha 8, alpha8-integrin, or α8-integrin). When bred to mice that express Cre recombinase, the resulting offspring will have the sequences encoding the transmembrane and the cytoplasmic domains deleted in the cre-expressing tissue(s). These f(α8) mutant mice may be useful in generating conditional mutations for studying the role of Itga8 transmembrane cell adhesion receptors in neuronal function in the developing and adult central nervous system, including intracellular signaling, behavior, synaptic plasticity, and memory formation.
For example, when f(α8) mice are bred to mice expressing Cre recombinase in forebrain neurons (see Stock No. 005359 for example), the double mutant offspring may exhibit impa ..... | ||
| 014633 | B6.129S6-Nr1h2tm1Djm/J | Repository- Live |
| In this strain a neomycin (neo) resistance cassette replaces exons 5-6 of the nuclear receptor subfamily 1, group H, member 2 (Nr1h2) gene, abolishing gene function. Homozygotes are viable, fertile, and normal in size. Also known as liver X receptor beta (Lxrβ), Nr1h2 binds to retinoid X receptors (RXRα, RXRβ, RXRγ; NR2B1, NR2B2, and NR2B3) and is activated by oxysterols to regulate the expression of genes involved in cholesterol metabolism. Homozygous Lxrβ-/- mice lose their ability to appropriately regulate cholesterol, lipid, and carbohydrate metabolism, and have defects in immune function. These defects are more severe when combined with the knockout of Lxrα (available as Stock No. 013761). These mice may be useful for studying lipid and cholesterol metabolism, and regulation of the immune response. | ||
| 013761 | B6.129S6-Nr1h3tm1Djm/J | Repository- Live |
| Homozygous Nr1h3 (nuclear receptor subfamily 1, group H, member 3) targeted mutation mice lose their ability to respond normally to dietary cholesterol. Mice maintained on cholesterol diets fail to induce transcription of the Cyp7a1 (cytochrome P450, family 7, subfamily a, polypeptide 1) gene, a rate-limiting enzyme in bile acid synthesis, and fail to induce expression of ABCG5 (ATP-binding cassette, sub-family G (WHITE), member 5) and ABCG8 (ATP-binding cassette, sub-family G (WHITE), member 8), ATP-binding cassette transporters that are required for cholesterol secretion into bile. Large amounts of cholesterol rapidly accumulate in the liver leading to impaired hepatic function. Impaired reverse cholesterol transport from peripheral tissues is also observed. The ability to regulate lipids and carbohydrates is also lost. Defects in innate immune responses by activated macrophages have also been described. Males are not infertile, but show a significantly higher number ..... For more information please see the full phenotype on the strain data sheet | ||
| 006852 | B6.129S6-Per2tm1Jt/J | Repository- Live |
| Mice homozygous for this "mPer2Luc" mutation are viable and fertile with no developmental or morphological differences compared to wildtype littermates. Expression of PERIOD2::LUCIFERASE (or mPER2::LUC) fusion protein during peak periods is similar to endogenous pPER2 patterns. Homozygous mice have normal entrainment and circadian behaviors. These mPer2Luc knock-in mice may be useful as a real-time reporter of circadian dynamics in different tissues. | ||
| 016238 | B6.129S6-Rbp7tm1Vgl/J | Repository- Live |
| Mice that are homozygous for this knockout 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 heart tissue extracts from homozygous mice. Homozygous lactating females have reduced levels of total retinyl ester in milk, with the largest reduction in retinyl palmitate levels. Total retinol levels in heart tissue are reduced in homozygotes at weaning, but not in homozygotes aged 11 or 17 weeks. Decreased levels of retinol and retinyl ester are detected in the mammary glands of homozygous females 11 weeks of age. At 17 weeks of age, only total retinol levels remain diminished. Postprandial retinoid turnover is not changed in mutant mice. Homozygotes fed a high fat diet have reduced hepatic steatosis, lower hepatic triglyceride levels, and decreased serum free fatty acids and efflux from adipose tissue compared to wildtype controls. On a ..... For more information please see the full phenotype on the strain data sheet | ||
| 012904 | B6.129S6-S100a4tm1Egn/YunkJ | 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. Parts of exon 2 and 3 of the endogenous gene were replaced by in-frame sequence encoding Green Fluorescent Protein. Fibroblasts isolated from heterozygotes are immunohistochemically positive for both FSP1 (S100A4) and GFP. Fibroblasts isolated from homozygotes are immunohistochemically positive for GFP. No gene product (protein) is detected in fibroblasts isolated from homozygotes by immunohistochemical analysis. | ||
| 005623 | B6.129S6-Shhtm2(cre/ERT2)Cjt/J | Repository- Live |
| This strain expresses a fusion product involving Cre recombinase and a mutant form of the human estrogen receptor ligand binding domain from the endogenous Shh locus. The mutant human estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen. Restricted to the cytoplasm, the Cre/ESR1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. Tamoxifen administration induces Cre recombinase expression in all cells that express the endogenous gene resulting in the deletion of the first 35 base pairs following the ATG. Homozygous mice are not viable or fertile. Heterozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of limb patterning and development. | ||
| 006878 | B6.129S6-Taglntm2(cre)Yec/J | Repository- Live |
| Mice homozygous for this SM22alpha-CreKI allele are viable and fertile. These mice have a Cre-recombinase gene inserted into the endogenous transgelin (SM22alpha) locus. The donating investigator reports that this mutation results in a loss of function of the targeted gene. Cre recombinase activity is shown in adult smooth muscle cells (such as arteries, veins, and visceral organs) and cardiac myocytes, but activity is not observed in the same embryonic tissues. It has been the experience of The Jackson Laboratory that optimal breeding is achieved by mating heterozygous females to homozygous males as female mortality post gestation has been noted in our colony. These SM22alpha-CreKI mice may be useful for Cre-lox technology applications in studying smooth muscle and cardiac gene function, as well as cardiovascular disease. | ||
| 004648 | B6.129S6-Tbx21tm1Glm/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. No gene product (mRNA or protein) is detected in isolated lymph node T cells by Northern or Western blot analysis. T cells from the homozygotes do not produce the TH1-type cytokine interferon gamma and secrete elevated levels of TH2-type cytokines in response to in vitro T cell receptor (TCR) cross-linking and in vivo protein antigen immunization. Additionally, mice homozygous for the targeted mutation on this genetic background are susceptible to Leishmania major infections. Without induced sensitization or challenge, female homozygotes display hyper-responsiveness (AHR) with resulting airway remodeling similar to characteristics of asthma. Histological analysis of lung tissue from female homozygous mice, aged 4 to 6 weeks, reveals eosinophil and lymphocyte infiltration of peribronchial and perivenular tissue, thickening of the subepithelial collagen layer, and increased num ..... For more information please see the full phenotype on the strain data sheet | ||
| 012565 | B6.129S7(129S4)-Ift20tm1.1Gjp/J | Repository- Live |
| These Ift20flox mice harbor loxP sites flanking exons 2-3 (encoding the first 71 codons including the start codon) of the intraflagellar transport 20 homolog (Chlamydomonas) locus. The primary cilium is a microtubule-based antenna-like structure that emanates from the surface of virtually all cells in the mammalian body. The primary cilium functions as a sensory organelle (mechano-, chemo-, photo-receptor) that receives signals from other cells/the environment, and transmits these signals to the nucleus to elicit a cellular response. Most types of eukaryotic cilia and flagella are assembled and maintained by the process of intraflagellar transport (IFT). During IFT, large protein complexes (IFT particles) are transported along the ciliary microtubules under the ciliary membrane. IFT particle proteins organize into at least three distinct complexes called complex A, complex B and the Golgi IFT complex. The unique role of Ift20 in both complex B as well as the Golgi IFT ..... For more information please see the full phenotype on the strain data sheet | ||
| 004133 | B6.129S7-Apptm1Dbo/J | Repository- Live |
| At birth, mice homozygous for the targeted allele are viable, and do not display any gross physical or behavioral abnormalities. No App gene product (mRNA or protein) is detected. Body weight is 15-20% less than that observed in wildtype age-matched control mice. By 14 weeks of age the mice exhibit evidence of reactive gliosis. Neurological evaluation reveals significantly reduced forelimb grip strength and decreased locomotor activity. This mutant strain offers a model useful in studies related to Alzheimer's disease. | ||
| 003173 | B6.129S7-Cd47tm1Fpl/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable, fertile, and display no obvious phenotypic abnormalities. Homozygous mutant mice display normal blood counts except for a reduction in the CD3+ fraction of peripheral lymphocytes. Integrin-associated protein (IAP; CD47) expression in heterozygous mice was approximately 40% of wildtype. Intraperitoneal injection of virulent Escherichia coli kills IAP-deficient mice, indicating a defect in the host defense pathway. This response appears to be secondary to both delayed polymorphonuclear leukocyte (PMN) migration to the site of infection and to defective activation at the site. Young CD47-null mice have enhanced physical performance and more efficient metabolism. They also display lower reactive oxygen species signaling leading to decreased blood vessel turgor and lower blood pressure. Skeletal muscle in young (3 month old) CD47-null mice exhibit increased densities of mitochondria (that function normally in terms of ..... For more information please see the full phenotype on the strain data sheet | ||
| 003232 | B6.129S7-Chrna7tm1Bay/J | Repository- Live |
| Mice homozygous for the Chrna7tm1Bay mutation are viable and fertile. Neuropathological and histochemical assessment of the brain reveals no abnormalities. High-affinity nicotine binding sites are present but there is an absence of high-affinity 125alpha-BGT sites. Homozygotes lack rapidly desensitizing, methyllycaconitine-sensitive, nicotinic currents that are present in hippocampal neurons. | ||
| 012468 | B6.129S7-Fyntm1Sor/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable, fertile and are grossly normal. Homozygous mutant mice exhibit defective T cell receptor signaling, a reduction in levels of tyrosine-phosphorylated proteins, failure to flux calcium in response to TCR cross-linking, and a reduction in production of calcium-related IL2. THY-1-induced proliferation is also reduced in thymocytes but not in splenic T cells. Neurological defects include blunted long-term potentiation (LTP), impaired special learning, and altered hippocampal development. 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. | ||
| 008039 | B6.129S7-Gja1tm1Dlg/J | Repository- Live |
| Mice homozygous for this Cx43flox conditional allele are viable and fertile, with loxP sites flanking exon 2 of the targeted gene. Presence of the loxP sites has no reported affect on expression of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have exon 2 deleted in the cre-expressing tissue(s). These Cx43flox mutant mice may be useful in generating conditional mutations for studying the role of connexin and gap junctions in various tissues and systems, including the cardiovascular system. | ||
| 002192 | B6.129S7-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.
If breeding heterozygous mice together, recovery of homozygous offspring is significantly reduced. For unknown reasons, homozygous mutant mice are prone to convulsions. If breeding or creating homozygous mice, they should be handled carefully and quietly to avoid poor breeding, loss of litters, or premature death. | ||
| 003245 | B6.129S7-Il1r1tm1Imx/J | Repository- Live |
| Mice homozygous for the Il1rtm1Imx targeted mutation fail to respond to IL1. They display normal acute phase response to systemic LPS challenge, but have defective responses to local turpentine induced inflamation. Homozygotes display increased frequency and severity of S. aureus septic arthritis. | ||
| 002295 | B6.129S7-Il7rtm1Imx/J | Repository- Live |
| Mice homozygous for the Il7rtm1Imx targeted mutation are viable and fertile. Newborn and young adult homozygous mutant mice have dramatically reduced thymic and splenic lymphoid cellularity in both B and T cell compartments. T cell development is affected prior to surface expression of CD4 and CD8 and prior to the initiation of T cell receptor beta chain rearrangement. B cell development is through pre-pro-B cells (Cd43+ HSAdull). The phenotype in the mouse resembles human interleukin-2 receptor gamma deficiency (XSCID). IL2Rgamma has been shown to be a necessary component of the IL7R providing the biochemical basis for this condition. | ||
| 005257 | B6.129S7-Itgaltm1Bll/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by flow cytometry analysis of isolated neutrophils. Homozygotes exhibit peripheral leukocytosis due to an increased number of neutrophils. Isolated neutrophils do not exhibit increased adhesion to purified ICAM-1 or to endothelial cells. Neutrophil extravasation in response to TNF-alpha is diminished in mutant mice. Isolated neutrophils show decreased attachment strength to endothelial cells as revealed by shear stress detachment tests. This mutant mouse strain may be useful in studies of leukocyte adhesion deficiency type I (LADI), and neutrophil adhesion and extravasation. | ||
| 002128 | B6.129S7-Itgb2tm1Bay/J | Repository- Live |
| Mice homozygous for the Itgb2tm1Bay mutation are viable and fertile. Homozygous mutant mice show an increased neutrophil count, and a decreased inflammatory response to peritonitis. Responses to delayed-type hypersensitivity and rejection of transplanted tissue are impaired. PLEASE NOTE: The Itgb2tm1Bay allele is not a null mutation; it is a hypomorphic mutation which results in the expression of very low levels of Itgb2 protein. This strain serves as a model for the moderate form of human CD18 deficiency. | ||
| 015813 | B6.129S7-Kittm1Rosay/J | Repository- Live |
| Mice that are heterozygous for this alelle are viable, normal in size and do not display any gross behavioral abnormalities. Heterozygotes exhibit white patches at the end of the tail, the belly and paws. Homozygotes exhibit an embryonic lethal phenotype. Mutant allele expression levels (mRNA) are similar to endogenous Kit expression in multiple tissues as detected by qPCR analysis (brain, heart, liver, lung, kidney, stomach, small intestine, colon). High expression levels are detected in lung. copGFP fluorescence is detected in KIT immuno-positive gastrointestinal interstitial cells of Cajal (ICC) by immunohistochemical and flow cytometric analysis.
When crossed with mice homozygous for the Lepob allele (see Stock No. 000632), loss in the intramuscular and myenteric populations of ICC in the intestine and colon can be visualized with confocal microscopy. | ||
| 006883 | B6.129S7-Ldlrtm1Her Sod2tm1Leb/J | Repository- Live |
| Independently, mice that are homozygous for this MnSOD mutation (Sod2tm1Leb) allele exhibit postnatal lethality and exhibit anemia, degeneration of neurons in the basal ganglia and brainstem, progressive motor disturbances, and myocardial injury. Individual LDLR homozygous mutants are predisposed to atherosclerosis. When mutant mice are homozygous for both alleles, they die in utero. Mice heterozygous for the Sod2 mutation and homozygous for the LDLR are viable and fertile. The mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, and hypercholesterolemia, and oxidative stress. | ||
| 002289 | B6.129S7-Selptm1Bay/J | Repository- Live |
| Mice homozygous for the Selptm1Bay mutation are viable and fertile. Homoyzgous mutant mice show a deficit in leukocyte rolling and delayed neutrophil extravasation in response to intraperitoneal injections of thioglycollate. Neutrophil count is elevated (2-3-fold). Circulating lymphocyte and monocyte counts are normal. 60-70% reduction in neutrophil emigration into the peritoneum during Streptococcus pneumoniae-induced peritonitis is reduced 60-70%. It can be used as model for human leukocyte adhesion deficiency I syndrome (characterized by elevated levels of circulating leukocytes and impaired leukocyte extravasation to sites of inflammation or infection). | ||
| 002973 | B6.129S7-Sod2tm1Leb/J | Repository- Live |
| Mice homozygous for the Sod2tm1Leb targeted mutation die within 21 days after birth. They exhibit severe wasting and are clearly much smaller, weaker,and less coordinated than their wildtype and heterozygous littermates. Homoyzotes exhibit several novel pathogenic phenotypes including severe anemia, degeneration of neurons in the basal ganglia and brainstem, progressive motor disturbances, and myocardial injury. | ||
| 013106 | B6.129S7-Sox9tm2Crm/J | Repository- Live |
| These Sox9flox mutant mice possess a loxP site upstream of exon 2, a neomycin resistance (neo) cassette followed by another loxP site downstream of exon 3 of the SRY-box containing gene 9 gene, Sox9. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, the resulting offspring will have exons 2-3 deleted in the cre-expressing tissue, resulting in inactivation of Sox9 gene function. Breeding these Sox9flox mice to strains that express Cre recombinase ubiquitously results in severe bone defects and perilethality. This strain may be useful for studying cell fate determination including endochondral bone formation, limb development and patterning, joint formation, and hair and stem cell differentiation | ||
| 003568 | B6.129S7-Trp63tm2Brd/J | Repository- Live |
| Mills 1999 Nature 398:708 describes the homozygous phenotype on a mixed B6-Tyrc-Brd;129S7(129S5) background. Further, they not distinguish between the two targeted alleles (pTV6H(90)-generated p63Brdm1 [Trp63tm1Brd] or pTV12E(60)-generated p63Brdm2 [Trp63tm2Brd]) as both "produced an identical phenotype." Homozygous mice are born alive, but die several hours after birth. No transcripts have been detected in homozygotes. They have striking developmental defects, exhibiting truncated forelimbs, absent hindlimbs, and transparent skin with a complete lack of hair follicles. Both the gross and histological appearance of internal organs is normal. Functional permeability of the skin is dramatically increased; homozygous mice lose thirty times more water than normal littermates. It is presumed that death occurs from dehydration. Heterozygous mice are viable, fertile, and do not exhibit any overt developm ..... For more information please see the full phenotype on the strain data sheet | ||
| 002222 | B6.129S7-Twist1tm1Bhr/J | Repository- Live |
| Homozygotic embryos for the Twist1tm1Bhr targeted mutation die at 11.5. The most prominent phenotype is a failure of cranial neural tube closure. At embryonic day 8.5 the cranial neural folds are elevated but not fused. At embryonic day 9.5 exencephaly is evident (the cranial neuroepithelium is everted and exposed). There is also abnormal somite morphology and abnormal limb bud development. | ||
| 004855 | B6.129X-Mmp12tm1Sds/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. Homozygous females have reduced litter sizes (~60% of wildtype). No gene product (mRNA or protein) is detected by Northern or Western blot analysis of peritoneal macrophages and fluid. Casein substrate gel zymographic analysis of thioglycollate-stimulated cultured macrophages and peritoneal fluid reveals there is no lytic activity. In whole lung extracts, no elastase activity was detected by zymography. Immunohistochemistry of lung tissue does not detect macrophage elastase. Macrophages from homozygous mice are unable to penetrate artificial basement membrane matrix. Addition of plasminogen to cultured macrophages does not increase elastase activity. When challenged with chronic exposure to cigarette smoke, mutant mice do not develop emphysema. IL-13 induced tissue inflammation is reduced in homozygotes. This mutant mouse strain may b ..... For more information please see the full phenotype on the strain data sheet | ||
| 007579 | B6.129X1(Cg)-Fgfr2tm1Dor/J | Repository- Live |
| Mice homozygous for this Fgfr2flox allele possess loxP sites flanking exons 8-10 of the targeted gene and are viable and fertile. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have sequences encoding the alternatively spliced Ig domain IIIb, as well as the IIIc and TM domains, deleted in the cre-expressing tissue(s). These Fgfr2-flox mutant mice may be useful in generating conditional mutations to study the role of fibroblast growth factor receptors in vertebrate development; including early embryogenesis, regional specification of the brain, limb morphogenesis, and normal bone, craniofacial, and lens development.
For example, when crossed to a strain expressing Cre recombinase in the central nervous system, especially astrocytes (see Stock No. 004600), this mutant mouse strain may be useful in studies of astroglial migration. When crossed to ..... | ||
| 012843 | B6.129X1(Cg)-Slc32a1tm1.1Bgc/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 perinatal lethal phenotype due to respiratory failure. No gene product (mRNA) is detected by RT-PCR analysis of brain tissue from homozygous embryos aged E16.5. Beta-galactosidase staining pattern mimics the endogenous gene expression pattern. Neonate homozygotes exhibit lack of movement, hunched posture, cleft secondary palate, umbilical hernia, and bumps of displaced brown fat deposits in the dorsal cervical area. The Donating Investigator reports that adult heterozygous males on the C57BL/6J background have seizures starting approximately at age 6 months. | ||
| 012839 | B6.129X1(Cg)-Tnfrsf4tm2(cre)Nik/J | Repository- Live |
| In Ox40-cre mice, the targeted mutation inserts an internal ribosome entry site (IRES)-Cre recombinase into exon 3 of the tumor necrosis factor receptor superfamily, member 4 (Tnfrsf4 or Ox40) locus, abolishing gene function. Homozygous mice are viable, fertile, and normal in size. Cre recombinase expression is observed when Ox40 is induced during T cell activation. Ox40-cre induction is strong in activated CD4+ T cells (approximately 70% of memory CD4+ T cells have undergone Ox40-cre-mediated recombination in these mice). It is weaker and variable in activated CD8+ T cells. Regulatory CD4+ T cells constitutively express OX40 and thus ~90% of them have undergone Cre recombination in Ox40-cre mice. A minority (~15%) of the thymic precursors of naive CD4+ T cells express sufficient Ox40-cre to undergo Cre recombination. Ox40-cre is also expressed in the male (but not female) germline and this must be considered carefully when establishing breeding schemes. These mi ..... For more information please see the full phenotype on the strain data sheet | ||
| 012453 | B6.129X1(FVB)-Lrrk2tm1.1Cai/J | Repository- Live |
| Homozygous (Lrrk2-/-) mice are viable and fertile with no reported developmental or gross physical abnormalities. Exon 2 is deleted from the targeted Lrrk2 allele resulting in a premature stop codon in exon 3. No full length LRRK2 protein is detected in brain tissue. Lrrk2-/- mice show no apparent elevation of reactive astrocytosis or somatic accumulation of alpha-synuclein, both of which correlate with neurodegeneration in Parkinson's Disease patients. Deletion of Lrrk2 promotes the extension of neurites by suppressing the phosphorylation of the ezrin, radixin, and moesin (ERM) family of proteins and decreasing the content of F-actin in filopodia. These mice may be useful for studying Parkinson's disease pathogenesis and neurodegeneration. | ||
| 007214 | B6.129X1(FVB)-Nr1h4tm1Gonz/J | Repository- Live |
| Mice that are homozygous for the targeted Nr1h4 allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Nr1h4 protein product is detected in liver tissue although an aberrant transcript appears to be generated. Homozygous mice display a proatherogenic serum lipoprotein profile characterized by elevated levels of serum and hepatic cholesterol and triglycerides. Serum bile acids are also elevated. When fed a diet supplemented with 1% cholic acid, severe wasting, hypothermia and increased mortality is observed. Wildtype mice fed a similar diet display no ill effects. Levels of fecal bile excretion are reduced in homozygotes. This mutant mouse strain represents a model that may be useful in studies related to bile acid and lipid homeostasis. 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 ..... | ||
| 002994 | B6.129X1-Baxtm1Sjk/J | Repository- Live |
| Mice homozygous for the Baxtm1Sjk mutation are viable but display lineage-specific aberrations in cell death. Thymocytes and B cells from homozygous mutant mice display hyperplasia. Ovaries contain unusual atretic follicles with excess granulosa cells while Bax-deficient males are infertile. There is an accumulation of atypical premeiotic germ cells and no mature haploid sperm found in seminiferous tubules. Multinucleated giant cells and dysplastic cells accompany massive cell death. Used in conjunction with strain B6.129-Bak1tm1Thsn/J (see Stock No. 004183), to generate the double knock-out Bak/Bax, a model for demonstrating severe defects in the regulation of apoptosis during development and tissue homeostasis.
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| 014172 | B6.129X1-Camkk2tm1Tch/J | Repository- Live |
| Mice that are homozygous for this knockout mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator reports that mutant mice have reduced osteoclast differentiation and function. Cortical neurons isolated from double mutant mice carrying the Camkk2tm1Tch and Camkk1tm1Tch (see Stock No. 006606) alleles exhibit shortened axons and dendrites. | ||
| 006112 | B6.129X1-Elanetm1Sds/J | Repository- Live |
| Homozygous mice are viable, fertile and phenotypically normal in the absence of inflammatory stress. Homozygotes do not express the targeted gene in bone marrow myeloid cells. Homozygous mice have increased susceptibility to sepsis, morbidity, and mortality following intraperitoneal injection of Gram-negative (e.g. (K. pneumoniae and E. coli), but not Gram-positive (e.g. (S. aureus), bacteria. Despite this, mutant mice are not at increased risk to spontaneous infection. Although neutrophil, T cell, and macrophage migration/recruitment to the site of infection is unaffected in homozygous mutant mice, neutrophils show impaired bactericidal activity. Further, homozygous mice treated with a broad-spectrum inflammatory stimulus (zymosan) have impaired leukocyte firm adhesion and transmigration as well as reduced pro-inflammatory cytokine production. Upon exposure to cigarette smoke, homozygous mice are protected from the accumulation of neutrophils and macrophages in th ..... For more information please see the full phenotype on the strain data sheet | ||
| 003982 | B6.129X1-Fcgrttm1Dcr/DcrJ | Repository- Live |
| 006148 | B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J | Repository- Live |
| Mice that are homozygous for the R26-stop-EYFP mutant allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mice contain an Enhanced Yellow Fluorescent Protein gene (EYFP) inserted into the Gt(ROSA)26Sor locus. Expression of EYFP is blocked by an upstream loxP-flanked STOP sequence. When bred to mice with a cre recombinase gene under the control of a promoter of interest, the STOP sequence of the targeted gene is deleted in the tissue of interest, and EYFP expression is observed. These mutant mice may be useful in monitoring the Cre expression in living tissues, and tracing the lineage of such cells in embryos, young, and adult mice at desired time points.
These R26-stop-EYFP have also been used as a fluorescent reporter by the Allen Institute for Brain Science. For their characterization information, see images at the Allen Institute for Brain Science website (> ..... | ||
| 013181 | B6.129X1-H2-Ab1tm1Koni/J | Repository- Live |
| These iabneo floxed mutant mice possess a loxP-flanked neomycin resistance (neo) cassette upstream of the exon 1, and a single loxP site downstream of exon 1 of the histocompatibility 2, class II (MHC-II) antigen, beta 1 (H2-Ab1) locus. 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, some of the resulting offspring will have exon 1 deleted in cre-expressing tissues. When bred with mice expressing Cre-recombinase driven by a cd19 promoter, iab deficiency results in the loss of MHC-II from the surface most B cells. This results in severely impaired T cell-dependent primary B cell antibody response upon immunization while exhibiting delayed kinetics in B cell germinal centers and memory B cell development. When bred with mice expressing Cre-recombinase driven by endoth ..... For more information please see the full phenotype on the strain data sheet | ||
| 013547 | B6.129X1-Hip1tm4Tsr/J | Repository- Live |
| In the Hip1LSP-H/P strain, a floxed-STOP cassette causes termination of the endogenous huntingtin interacting protein 1 (Hip1) gene and a human HIP1/PDGFbR (H/P) cDNA fused to another polyA site and a neomycin resistance (neo) cassette, replace endogenous exons 2-7. Heterozygous mice are viable, fertile, and normal in size. These mice exhibit gross micro-ophthalmia and cataracts. When bred to mice that express Cre recombinase, offspring will have the floxed-STOP cassette deleted in the cre-expressing tissue(s), resulting in H/R fusion protein overexpression in cre-expressing cells. The overexpression of H/P mimics the human chromosomal translocation, t(5;7)(q33;q11.2), leading to constitutively active PDGFbR signalling and chronic myelomonocytic leukemia (CMML) development in humans. For example, H/P is able to transform hematopoietic cells to factor-independent growth in culture. When Hip1LSP-H/P mice are bred to mice tha ..... For more information please see the full phenotype on the strain data sheet | ||
| 004265 | B6.129X1-Mpotm1Lus/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. No Mpo gene product (mRNA or protein) is detected. Mutant mice exhibit total white blood cell counts and differentials similar to wildtype mice. Neutrophils and monocytes in periperhal blood and bone marrow have no endogenous peroxidase activity. Superoxide production levels in peritoneal exudate cells of mutant mice are similar to levels found in wildtypes mice. Hypochlorous acid production is undetectable in both isolated leukocytes and peritoneal exudate cells. Mutant mice display impaired fungicidal activity due to myeloperoxidase deficiency. When maintained under hyperlipidemic conditions, mutant mice develop atherosclerotic lesions 50% larger than those seen in control mice. | ||
| 007181 | B6.129X1-Notch1tm2Rko/GridJ | Repository- Live |
| Mice homozygous for this "floxed" Notch1 allele (fN1) are viable and fertile. These mice possess loxP sites on either side of exon 1 of the targeted gene. When bred to mice with a Cre recombinase gene, exon 1 of the targeted gene is deleted in the cre expressing tissue(s). These conditional knockout mice may be useful in generating tissue-specific mutants for studying the development of a wide range of tissues: for example, when crossed to a strain expressing Cre recombinase primarily in the nervous system (see Stock No. 003771), this mutant strain may be useful in studies of apoptosis in neural development.
When crossed to a strain expressing a differential Cre mediated reporter protein labeling: Notch1 signaling in actively cycling stem/progenitor cells (see Stock No. 006953), this mutant strain may be useful in studies of loss of Notch1 heterozyg ..... | ||
| 008712 | B6.129X1-Twist2tm1.1(cre)Dor/J | Repository- Live |
| Dermo1-cre (Twist2-cre) mutant mice harbor a Cre recombinase "knock-in" allele that also abolishes endogenous Twist2 gene function. Heterozygotes are viable and fertile, while homozygotes (twist-2-/-) die a few days after birth. Under control of the upstream promoter/enhancer elements, cre expression is observed in a pattern consistent with the wildtype gene; Cre recombinase activity is reported in mesoderm as early as embryonic day 9.5, in mesodermal tissues such as branchial arches and somites, and in condensed mesenchyme-derived chondrocytes and osteoblasts. When heterozygotes are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequences in Dermo1-expressing tissues of the offspring. Homozygous mice exhibit elevated expression of proinflammatory cytokines resulting in perinatal death from cachexia (wasting), as well as progressive growth retardation, impaired movement, th ..... For more information please see the full phenotype on the strain data sheet | ||
| 001148 | B6.AK-H2k/FlaEgJ | Repository- Live |
| 016883 | B6.B10(D2)-Grm6nob3/Boc | Repository- Live |
| Although retinal sections are histologically normal, electroretinogram assessment of homozygotes shows near-normal a-wave but absent both scotopic and photopic b-waves. The contrast sensitivity and spatial frequency thresholds are reduced. Retinal ganglion cell ON responses have a longer latency than normal and fewer retinal ganglion cells respond to the bright phase of a full-field stimulus. There are fewer OFF-center retinal ganglion cells that have an ON response to a full-field stimulus, which is distinct from findings in mice homozygous for the no b-wave 4 (nob4) allele. | ||
| 000537 | B6.BR-Agtpbp1pcd/J | Repository- Live |
| Mice homozygous for the Purkinje cell degeneration spontaneous mutation (Agtpbp1pcd) show a moderate ataxia beginning at 3 to 4 weeks. Homozygous mutant mice are somewhat smaller than normal but may live a fairly normal life span. Males have abnormal sperm and are sterile. Females are fertile but are poor breeders. There is rapid degeneration of nearly all Purkinje cells beginning at 15 to 18 days, and a slower degeneration of the photoreceptor cells of the retina and mitral cells of the olfactory bulb. Degeneration of Purkinje cells is followed by partial loss of granule cells. Discrete serotonin-immunoreactive fibers, which ascend to all three layers of the cerebellar cortex in normal controls, are of much higher density and form multidirectional contours in homozygotes. In the retina of homozygous mutant mice, pycnotic nuclei begin to appear in the photoreceptor cells between 18 and 25 days, and the outer rod segments become disorganized. Degeneration of the photor ..... For more information please see the full phenotype on the strain data sheet | ||
| 016187 | B6.BTBR-Tg(Per1-luc,Per1)1Jt/J | Repository- Live |
| This compound transgenic strain was created by co-injecting a BAC clone encoding the entire mouse Per1 locus and a transgenic vector in which the Per1 promoter drives expression of luciferase (Per1:luc). The expression of Per1:luc oscillates in the suprachiasmatic nuclei (SCN) as well as peripheral tissues in ex vivo cultures (unlike most other Per1:luc transgenic strains which have weak rhythms in peripheral tissues). | ||
| 000359 | B6.C-H2d/bByJ | Repository- Live |
| 006054 | B6.C-Tg(CMV-cre)1Cgn/J | Repository- Live |
| In this transgenic strain, deletion of loxP-flanked genes occurs in all tissues, including germ cells. The cre gene in this strain is under the transcriptional control of a human cytomegalovirus minimal promoter and is likely to be expressed before implantation during early embryogenesis. It also appears that the cre gene is X-linked since transgene transmission through males is restricted to female offspring. 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. | ||
| 002651 | B6.C3(Cg)-Rorasg/J | Repository- Live |
| Mice homozygous for the staggerer spontaneous mutation (Rorasg) show a staggering gait, mild tremor, hypotonia, and small size. The cerebellar cortex of homozygous mutant mice is grossly underdeveloped with a deficiency of granule cells and Purkinje cells. The remaining granule cells migrate inward from the external layer prematurely and then degenerate. Purkinje cells are much delayed in postnatal differentiation and lack the dendritic spines on which synapses with the parallel fibers from the granule cells normally occur. Staggerer mutant mice have been used as a source of an agranulate cerebellum in a number of investigations of the composition and function of granule cells. Kopmels et al. have reported a hyperproduction of IL1 biological activity and mRNA from LPS stimulated spleen cells of Rorasg/Rorasg mice on the C57BL/6J background relative to wild type siblings. In addition, homozygous mice exhibit an enhanced susceptibili ..... For more information please see the full phenotype on the strain data sheet | ||
| 003904 | B6.CBA-Tg(CETP)5203Tall/J | Repository- Live |
| Mice carrying the human CETP minigene under the control of its own promoter show a marked increase in CETP mRNA in liver when mice are fed a high fat, high cholesterol diet. Less dramatic increases are observed in spleen, small intestine and adipose tissues. Elevated plasma CETP protein levels are also observed. Mice carrying human CETP show reduced levels of plasma high density lipoprotein. This strain has been a useful model in studies related to cholesterol metabolism. | ||
| 004684 | B6.Cg Nos2tm1Lau-chtl/GrsrJ | 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. | ||
| 000021 | B6.Cg-Ay/J | Repository- Live |
| Mice homozygous for the yellow spontaneous mutation (Ay) die before implantation or shortly thereafter. The time of death and type of abnormality is, in part, determined by the genetic background on which the mutation is placed. Hair pigment in heterozygous mice is yellow, but eyes are black. Heterozygotes usually become obese and infertile after the first few months. Increased adipose tissue mass is due to fat-cell hypertrophy. It has been hypothesized that the obesity results from the observed reduction in hypothalamic norepinephrine and dopamine levels. Insulin resistance and hyperglycemia follow development of hyperinsulinemia in early adulthood, although the degree is less severe than on the KK/UpJ genetic background (Stock No. 002468). Heterozygotes are also more susceptible to several kinds of tumors than normal mice, and their spleen cells cause a significantly lower graft vs. host reaction. The level of ..... For more information please see the full phenotype on the strain data sheet | ||
| 006966 | B6.Cg-Akt2tm1.1Mbb/J | Repository- Live |
| Mice homozygous for this Akt2 (thymoma viral proto-oncogene 2) mutant allele are viable and fertile. Homozygotes develop insulin resistance, hyperglycemia, impaired glucose tolerance, abnormal glucose uptake in muscle tissue, increased pancreatic beta-cell mass, and diabetes. 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. | ||
| 007083 | B6.Cg-Cav1tm1Mls/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical abnormalities. Mutant mice exhibit exercise intolerance when challenged and are slightly hyperphagic. No gene product (protein) is detected by Western blot analysis in adipose, lung and heart tissues or in cultured mouse embryonic fibroblasts (MEFs). A decrease in the level of co-expressed caveolin-2 protein is immunodetected. At age 4-5 months, mutant mice are often smaller than their wildtype littermates. By one year of age, mutant mice weigh 5 to 7 grams less than wildtype, and are resistant to diet-induced obesity. Progressive adipose pathology results in reduced white adipose tissue with abnormally small adipocytes and enlarged, hyperplastic brown adipose tissue. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Isolated aortic tissue segments have a diminished vasoconstriction ..... For more information please see the full phenotype on the strain data sheet | ||
| 006366 | B6.Cg-Dicer1tm1Bdh/J | Repository- Live |
| These mice contain loxP sites on either side of exon 23. Homozygous mice are viable and fertile with no gross phenotypic or behavioral abnormalities. Expression of the targeted allele is indistinguishable from wild-type despite the frt-flanked neomycin cassette. Cre-mediated recombination (resulting in deletion of exon 23) in the germline leads to developmental arrest at embryonic day 7.5 (E7.5). Tissue specific deletion has been shown to result in loss of microRNA (miRNA) processing. Mutant mice can be used to generate cell/tissue-specific deletions of the endogenous gene for applications in embryonic development, translation, protein processing and miRNA/siRNA regulation of gene expression. For example, when crossed to a strain expressing Cre recombinase in mesenchyme (see Stock No. 005584), this mutant mouse strain may be useful in studies of limb morphogenesis. When bred to a strain expressing Cre recombi ..... | ||
| 004993 | B6.Cg-F2rl1tm1Mslb/J | Repository- Live |
| Homozygous mice are viable and fertile with no spontaneous abnormal phenotype. No endogenous gene expression is observed in liver, airway epithelium, smooth muscle, or vasculature of the lungs. Ovalbumin-induced allergic inflammation of the airway is significantly diminished in mutant mice, showing reduced eosinophil, neutrophil, and lymphocyte infiltration into bronchoalveolar lavage fluid. IgE levels in serum of ovalbumin sensitized homoyzgous mice are reduced 4-fold compared to wild-type. This targeted mutant mouse may be useful in studies of asthma, allergic inflammation of the airway, inflammatory bowel disease, injury/trauma, G protein-coupled receptors, signal transduction, and a wide variety of immunological or inflammatory diseases. | ||
| 000305 | B6.Cg-Fbn1Tsk +/+ Pldnpa/J | Repository- Live |
| Mice homozygous for the pallid spontaneous mutation Pldnpa and nonagouti (a) have pink eyes and a light, yellow-brown coat. The Pldnpa/Pldnpa mice have a slightly lighter coat than strains that are homozygous for the pink-eyed dilution allele (Oca2p/Oca2p). Viability of homozygous mutant mice is slightly reduced. Some homozygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manganese, L-dopa, and L-tryptophane in the brain. Homozygotes have elevated basal and testosterone-induced levels of the kidney lysosomal enzymes b-glucuronidase, b-galactosi ..... For more information please see the full phenotype on the strain data sheet | ||
| 014632 | B6.Cg-Fbn1Tsk/J | Repository- Live |
| The Fbn1Tsk allele contains a 30 to 40kb genomic tandem duplication resulting in a larger than normal in-frame transcript. Homozygotes are embryonic lethal, failing to survive past somite formation (7-8 days of gestation). Heterozygotes are viable and fertile, exhibiting excessive growth and hyperplasia of connective tissue, cartilage, tendon sheaths and bone. Skin tightness, due to hyperplasic thickening of subcutaneous loose connective tissue and abnormal organization and distribution of skin microfibrillar arrays, develops by the first week after birth. Although the size of the skeleton is increased, body weight remains normal. Mutant mice exhibit polyuria during the light cycle. Collagens and glycosaminoglycans accumulate in the skin, heart, lungs and bladder. Hypertrophy is also observed in the enlarged heart (aortic adventitia). Mutant mice have enlarged thoracic size and lungs with abnormal alveolar walls, irregular shaped alveoli, and increased lung cap ..... For more information please see the full phenotype on the strain data sheet | ||
| 004919 | B6.Cg-Fcgrttm1Dcr Tg(CAG-FCGRT)276Dcr/DcrJ | Repository- Live |
| These FcRn-/- hFcRn (276) Tg mice harbor a null mutation of the FcRn α-chain (Fcgrttm1Dcr) and also express a human FcRn α-chain cDNA (FCGRT) under the control the human cytomegalovirus immediate early promoter enhancer with chicken beta-actin/rabbit beta-globin hybrid promoter (CAG).
Mice homozygous for the FcRn α-chain null allele lack FcRn α-chain mRNA or protein expression, fail to transport IgG across the neonatal gut, degrade IgG at an accelerated rate, are functionally IgG deficient, and also exhibit plasma albumin deficiency. While hFcRn (276) transgene expression corrects the relative albumin deficiency caused by the FcRn α-chain knockout, expression of the hFcRn (276) transgene is unable to bind and protect murine IgG from degradation in FcRn α-chain null mice. However, hFcRn (276) transgene expression corrects the rapid decay rate of infused human IgG in FcRn-/- hFcRn (276) Tg mice. Furthermore, human antibodies ..... For more information please see the full phenotype on the strain data sheet | ||
| 014565 | B6.Cg-Fcgrttm1Dcr Tg(FCGRT)32Dcr/DcrJ | Repository- Live |
| These mFcRn-/- hFcRn (32) Tg mice are homozygous for the null mutation of the FcRn α-chain (Fcgrttm1Dcr) and express a human FcRn α-chain (FCGRT) transgene. Founder line 32 is more efficient in prolonging the serum half-life of hIgG compared with founder line 276 (see STOCK no. 004919). In Petkova et al.(2006), it is shown that the antibody half life of Hu4D5-IgG1 antibodies in mFcRn-/- hFcRn (32) Tg/0 is similar to those observed in mFcRn-/- hFcRn (276) Tg/Tg mice (see STOCK no. 004919). (Hu4D5-IgG1 human antibodies are directed against human epidermal growth factor receptor 2). In studies by Petkova et al. (2006), mice were pre-treated with human IgG to partially saturate the human FcRn. Since human FcRn does not bind mouse IgG, these mice have low levels of mouse IgG. These humanized FcRn mice may be useful in studying the quantitati ..... For more information please see the full phenotype on the strain data sheet | ||
| 004088 | B6.Cg-Foxp3sf/J | Repository- Live |
| Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. Phenotypes associated with these mice include runting, scaly, crusty skin on the eyelids, ears and tails, dermal thickening, squinted eyes, cachexia, reddening and swelling of the genital papilla, and small testicles that are retained in the abdominal cavity. This disorder, which parallels X-linked autoimmunity-allergic disregulation syndrome (XLAAD) in humans, results in Coombs' test-positive anemia, hypergammaglobulinemia, a small, thin thymus, and lymphohistiocytic proliferation in the skin and lymphoid organs, with splenomegaly, lymphadenomegaly, and hepatomegaly. Foxp3sf/Y males generally die by 16-25 days of age. Transgenic expression of Foxp3 prevents scurfy disease in Foxp3sf/Y mice. Neonatal thymectomy of scurfy males ameliorates disease and increases lifespan; athymic nude (Foxn1nu/Foxn1nu) ..... | ||
| 006772 | B6.Cg-Foxp3tm2Tch/J | Repository- Live |
| Homozygous mice are viable and fertile with normal T and B cell development. These "Foxp3EGFP" mice co-express EGFP and the regulatory T cell-specific transcription factor Foxp3 under the control of the endogenous promoter. EGFP expression accurately identifies the Foxp3+ T cell population (more than 97% of Foxp3+ T cells were EGFP+), and Foxp3 mRNA expression strictly segregates with EGFP+ T cells. Due to X-inactivation in females, the number of EGFP+CD4+ T cells found in the peripheral blood of heterozygous females was approximately half that of hemizygote males. CD4+EGFP+ cells also exhibit normal regulatory T cell suppression of effector cell proliferation (following stimulation with anti-CD3 and anti-CD28 monclonal antibodies ). Some EGFP expression is noted in a small population of CD8+ thymocytes. These mutant mice may be useful in immunological studies, including studie ..... For more information please see the full phenotype on the strain data sheet | ||
| 014162 | B6.Cg-Fxntm1Mkn Fxntm1Pand/J | Repository- Live |
| These frataxin knock-in/knockout (KIKO) mice harbor one allele of the frataxin (GAA)230 expansion mutation (Fxntm1Pand) on one chromosome, and one allele of the frataxin exon 4-deleted mutation (Fxntm1Mkn) on the homologous chromosome. KIKO mice are viable and fertile. Analysis of frataxin levels in tissues from KIKO mice demonstrate a reduction of frataxin to 25-36% of wildtype controls. KIKO animals up to 1 year of age perform equivalent to wildtype controls on rotarod test. Total iron concentrations were similar in all tested tissues of KIKO and wildtype mice except in pancreas: KIKO mice demonstrate lower iron levels in pancreatic tissues. No iron deposits and only mild collagen staining around the vessels of the heart were observed in both year old KIKO mice and wildtype controls. In contrast to Friedreichs Ataxia patients, no detectable change in GAA repeat size was found over six studied generations. Moreover, no evidence of so ..... For more information please see the full phenotype on the strain data sheet | ||
| 012910 | B6.Cg-Fxntm1Mkn Tg(FXN)YG22Pook/J | Repository- Live |
| The YG22 transgenic founder line carries a single copy of the human FXN gene with one GAA trinucleotide repeat sequence of 190 repeats. High levels of human FXN gene product (mRNA and protein) are detected by RT-PCR and Western blot analysis. 40-50% of the endogenous mouse Fxn gene product (protein) is detected by Western blot analysis in mice heterozygous for the targeted mutation alone. Mice that are homozygous for the targeted allele and hemizygous for the transgene exhibit an age dependent, tissue specific expansion of the GAA repeat, with expansion accumulation in the CNS (particularly cerebellum), similar to the human pathology. The GAA triplet repeat exhibits intergenerational instability. Mice that are homozygous for the targeted allele and hemizygous for the transgene exhibit progressive retinal degeneration, impaired and decreased locomotor activity and coordination, and an increase in body weight. At 9 months of age, muscle strength is decreased. Al ..... For more information please see the full phenotype on the strain data sheet | ||
| 012253 | B6.Cg-Fxntm1Mkn Tg(FXN)YG8Pook/J | Repository- Live |
| Mice that are heterozygous for the targeted allele and hemizygous for the transgene are viable and fertile. High levels of human FXN gene product (mRNA or protein) are detected by RT-PCR and Western blot analysis. 40-50% of the endogenous mouse Fxn gene product (protein) is detected by Western blot analysis in mice heterozygous for the targeted mutation alone. The YG8 transgenic founder carries two tandem copies of the human FXN gene with two GAA triplet repeat sequences of 82 and 190 repeats. Mice that are homozygous for the targeted allele and hemizygous for the transgene exhibit an age dependent, tissue specific expansion of the GAA repeat, with expansion accumulation in the CNS (particularly cerebellum), similar to the human pathology. The GAA triplet repeat exhibits intergenerational instability.
This mutant mouse strain may be useful in studies of Friedreich's Ataxia. In an attempt to offer alleles on well-characterized or multiple genetic backgrou ..... | ||
| 012844 | B6.Cg-Gad1tm1.1Bgc/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 a lethal phenotype. Beta-galactosidase staining pattern mimics the endogenous gene expression pattern. All newborn homozygotes have cleft palate, and 85% of neonate homozygotes exhibit umbilical hernia. | ||
| 006965 | B6.Cg-Gt(ROSA)26Sortm1(rtTA*M2)Jae/J | Repository- Live |
| Homozygotes are viable, fertile, normal in size and do not display any behavioral abnormalities. These targeted mutant mice have widespread expression of an optimized form of reverse tetracycline-controlled transactivator (rtTA-M2) protein. This R26-M2rtTA strain may be useful for doxycycline-inducible studies which utilize rtTA/tet-O (tet-on/TRE) models. | ||
| 005670 | B6.Cg-Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/J | Repository- Live |
| Homozygous mutant mice are viable, fertile, normal in size and do not display any behavioral abnormalities. When these gene targeted mice are bred to transgenic strains expressing Cre recombinase, functional rtTA and EGFP activity is observed in the double mutant offspring in the tissues that express cre. These double mutant mice may be bred to transgenic strains carrying genes of interest under the regulation of tetracycline responsive elements (TRE; tetO) to generate triple mutant mice in which the tissue specificity of the cre-transgenic line and doxycycline inducibility of the rtTA/TRE-controlled transgenes can be combined to regulate expression of the target gene. 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 th ..... | ||
| 007914 | B6.Cg-Gt(ROSA)26Sortm14(CAG-tdTomato)Hze/J | Repository- Live |
| Ai14 mice hemizygous for this Rosa-CAG-LSL-tdTomato-WPRE::deltaNeo conditional allele are viable and fertile. A loxP-flanked STOP cassette prevents transcription of the downstream red fluorescent protein variant (tdTomato). When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissue(s); resulting in expression of tdTomato. Because this CAG promoter driven reporter construct was targeted for insertion into the Gt(ROSA)26Sor locus, tdTomato expression is determined by which tissue(s) express Cre recombinase. Ai14 mice are not expected to express tdTomato prior to introduction of Cre recombinase and tdTomato expression following exposure to cre is expected to be detectable by fluorescence and mRNA (in situ hybridization). These Ai14 mice are useful as a Cre reporter strain; expressing the red fluorescent protein variant, tdTomato, following Cre-mediated recombination.
For cha ..... | ||
| 012567 | B6.Cg-Gt(ROSA)26Sortm27.1(CAG-COP4*H134R/tdTomato)Hze/J | Repository- Live |
| Ai27D (or Ai27Δneo) mice heterozygous for the Rosa-CAG-LSL-hChR2(H134R)-tdTomato-WPRE conditional allele are viable and fertile. A loxP-flanked STOP cassette prevents transcription of the downstream hChR2(H134R)-tdTomato fusion gene. Because this CAG promoter driven reporter construct was targeted for insertion into the Gt(ROSA)26Sor locus, hChR2(H134R)-tdTomato expression is determined by which tissue(s) express Cre recombinase. When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissues; resulting in expression of the hChR2(H134R)-tdTomato fusion protein. The donating investigator reports that Ai27D mice do not express hChR2(H134R)-tdTomato prior to introduction of Cre recombinase. Fusion protein expression following exposure to cre can be detected by tdTomato fluorescence and mRNA (in situ hybridization) (and presumably by antibody staining (immunohistochemistry); althoug ..... For more information please see the full phenotype on the strain data sheet | ||
| 007903 | B6.Cg-Gt(ROSA)26Sortm3(CAG-EYFP)Hze/J | Repository- Live |
| Ai3 mice hemizygous for this Rosa-CAG-LSL-EYFP-WPRE conditional allele are viable and fertile. A loxP-flanked STOP cassette prevents transcription of the downstream enhanced yellow fluorescent protein (EYFP). When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissue(s); resulting in expression of EYFP. Because this CAG promoter driven reporter construct was targeted for insertion into the Gt(ROSA)26Sor locus, EYFP expression is determined by which tissue(s) express Cre recombinase. The donating investigator reports that Ai3 mice do not express EYFP prior to introduction of Cre recombinase and EYFP expression following exposure to cre can be detected by fluorescence, mRNA (in situ hybridization) and antibody staining (immunohistochemistry). Of note, the FRT sites flanking the mutation allow for additional targeted replacement of the reporter sequences through Flp-medi ..... For more information please see the full phenotype on the strain data sheet | ||
| 014648 | B6.Cg-Gt(ROSA)26Sortm37(H1/tetO-RNAi:Taz)Arte/ZkhuJ | Repository- Live |
| These mutant mice have a tetracycline inducible Taz specific short hair pin RNA (shRNA) driven by the endogenous mouse Gt(ROSA)26Sor promoter.
Expression of the shRNA is controlled by the transcription of the H1 RNA polymerase III promoter, which is coupled to a tet-operator (tetO) sequence. Expression of the shRNA is blocked by codon-optimized version of the tet repressor itetR, which is part of the allelic construct found in this mouse. Doxycycline (dox--a tetracycline analog) treatment decreases the affinity of the itetR for the tetO sequence, allowing transcription of the shRNA.
Dox-induced Taz gene silencing is detected in heart (to ~3.7% of wildtype), skeletal muscle (to ~11.2%), liver (to ~8.9%) and brain (to ~3.4%) by RT-PCR analysis. Gene product (mRNA) in transgenic mice without dox induction is reduced by 35% of wildtype control levels. Withdrawal of dox at 4 weeks partially reverses the reduction of Taz expression. Protein product ..... For more information please see the full phenotype on the strain data sheet | ||
| 007906 | B6.Cg-Gt(ROSA)26Sortm6(CAG-ZsGreen1)Hze/J | Repository- Live |
| Ai6 mice hemizygous for this Rosa-CAG-LSL-ZsGreen1-WPRE conditional allele are viable and fertile. A loxP-flanked STOP cassette prevents transcription of the downstream enhanced green fluorescent protein (ZsGreen1). When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissue(s); resulting in expression of ZsGreen1. Because this CAG promoter driven reporter construct was targeted for insertion into the Gt(ROSA)26Sor locus, ZsGreen1 expression is determined by which tissue(s) express Cre recombinase. The donating investigator reports that Ai6 mice do not express ZsGreen1 prior to introduction of Cre recombinase and ZsGreen1 expression following exposure to cre can be detected by fluorescence and mRNA (in situ hybridization). Bright fluorescence is observed mainly in cell bodies. Of note, the FRT sites flanking the mutation allow for additional targeted replacement of the report ..... For more information please see the full phenotype on the strain data sheet | ||
| 007909 | B6.Cg-Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/J | Repository- Live |
| Ai9 mice hemizygous for this Rosa-CAG-LSL-tdTomato-WPRE conditional allele are viable and fertile. A loxP-flanked STOP cassette prevents transcription of the downstream red fluorescent protein variant (tdTomato). When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissue(s); resulting in expression of tdTomato. Because this CAG promoter driven reporter construct was targeted for insertion into the Gt(ROSA)26Sor locus, tdTomato expression is determined by which tissue(s) express Cre recombinase. The donating investigator reports that Ai9 mice do not express tdTomato prior to introduction of Cre recombinase and tdTomato expression following exposure to cre can be detected by fluorescence and mRNA (in situ hybridization). Of note, the FRT sites flanking the mutation allow for additional targeted replacement of the reporter sequences through Flp-mediated recombination if ..... For more information please see the full phenotype on the strain data sheet | ||
| 006428 | B6.Cg-Hydinhyrh/J | Repository- Live |
| Mice homozygous for this spontaneous mutation have smaller bodies and develop hydrocephaly and rhinitis, dying by 3 weeks of age. | ||
| 001317 | B6.Cg-Igha Thy1a Gpi1a/J | Repository- Live |
| This congenic strain was made by mating together, not backcrossing, three individual congenic strains carrying differential alleles already on a C57BL/6J genetic background (B6.C-Igha, B6.PL-Thy1a, and B6.CAST-Gpi1a). This triple congenic is useful as a cellular marker in transplantation studies in conjunction with C57BL/6J inbred mice (Ighb, Thy1b, Gpi1b). Igh is a B cell specific marker, Thy1 is a T cell specific surface marker, and Gpi1 is an enzyme that is widely expressed in mouse tissues, cultured fibroblasts, and in several types of tumors. | ||
| 006908 | B6.Cg-Ikbketm1Tman/J | Repository- Live |
| Homozygous IKKepsilon mutant mice are viable and fertile. Homozygous deletion results in a complete loss of the endogenous kinase function in lung, spleen, and embryonic fibroblasts. These mice have increased susceptibility to viral infection due to defective inteferon (IFN) signaling. These IKKepsilon mutant mice may be useful in immunological studies involving IFN signaling and host responses to infection. | ||
| 016101 | B6.Cg-Il7rtm1Imx Tg(Lck-Il7r)1676Trma/J | Repository- Live |
| These transgenic mice express the mouse Il7r (interleukin-7 receptor) gene under the control of the proximal mouse Lck (lymphocyte protein tyrosine kinase) promoter, and are homozygous for the Il7rtm1Imx allele. Transgene expression is detected in the thymus, specifically in T cells and thymocytes. No transgene expression is detected in B cells, NK cells, monocytes or in bone marrow. Transgene expression is reduced in CD3-CD4-CD8- (triple negative) thymocytes. The phenotype of mice homozygous for the Il7rtm1Imx allele is substantially rescued by expression of the transgenic wildtype Il7r in the thymus. Transgenic IL-7Rα protein is expressed in most thymocytes at levels similar to those seen in wildtype controls. The number of thymic cells is restored to 74% of wildtype control number. Although T cell development is substantially restored, peripheral T cells express minimal IL-7Ra (reduced by >90%) and are poorly ..... For more information please see the full phenotype on the strain data sheet | ||
| 006338 | B6.Cg-Lgals3tm1Poi/J | Repository- Live |
| Homozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavoiral abnormalities. No gene product (mRNA or protein) is detected by in situ hybridization of tibia bones sections from embryonic day 16.4 mice or by immunohistological staining of fetal skin. Homozygotes have an impaired acute inflammation response. Initial inflammatory infiltrate cell recruitment is normal, but four days after intraperitoneal injection of thioglycollate, mutant mice have a four-fold lower number of recruited granulocytes. Mutant mice have impaired chondrocyte differentiation during long bone development. Fewer hypertrophic chondrocytes but more empty lacunae and condensed chondrocytes are found in the chondrovascular junction. Chondrocytes, cartilage matrix and lacunae are morphologically abnormal. Carbon tetrachloride-induced liver fibrosis results in reduced collagen deposition when compared to wildtype controls. Mutant mice also display defective myofibroblast ..... For more information please see the full phenotype on the strain data sheet | ||
| 013716 | B6.Cg-Lhfpl2vgim/GrsrJ | Repository- Live |
| 013121 | B6.Cg-Lootl/GrsrJ | Repository- Live |
| The loop tail like mutation is similar to the loop tail mutation of the Vangl2 gene in causing neurodevelopmental defects leading to short, curly tails and spina bifida. There is incomplete penetrance and prenatal and perinatal lethality. Some heterozygous with mild spina bifida survive to adulthood and have bred. Some heterozygous females have closed vaginas. | ||
| 012736 | B6.Cg-Mapk14tm1.1Dvb/J | Repository- Live |
| Mice heterozygous for the p38AF dominant-negative allele are viable and fertile, with two amino acid substitutions (T180A and Y182F) at activating phosphorylation sites of the p38MAPK locus. Homozygous embryos die around embryonic day 11.5 with placental and heart defects (similar to some p38 knockout mice). Mice heterozygous for the p38AF dominant-negative allele exhibit specifically attenuated p38MAPK signaling without any reported effects on other MAPK pathways. Heterozygous mice do not exhibit any accelerated tumorigenesis on this genetic background (in fact, heterozygous mice crossed into two different tumor-prone genetic backgrounds also show no increased tumorigenic potential). Heterozygous mice show reduced aging-dependent activation of multiple cell cycle inhibitors in multiple tissues without increasing cancer predisposition. Specifically, reduced inhibitors include the products of the Cdkn2a tumor suppressor locus (p16Ink4a and p19 For more information please see the full phenotype on the strain data sheet | ||
| 005491 | B6.Cg-Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J | Repository- Live |
| Mice that are homozygous for the targeted allele and hemizygous for the transgene are viable and fertile. Although no endogenous mouse MAPT is detected, all six isoforms (including both 3R and 4R forms) of human MAPT are expressed. Hyperphosphorylated MAPT is detected in cell bodies and dendrites by three months of age. Paired helical filaments of aggregated insoluble MAPT can be isolated from brain tissue as early as two months of age. These mutant mice may be useful in studies examining the relationship between human MAPT and Alzheimer's disease pathogenesis 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. | ||
| 007745 | B6.Cg-Mir155tm1.1Rsky/J | Repository- Live |
| Mice homozygous for this loss-of-function/reporter allele (bic/mir-155-/-) are viable and fertile. The lacZ reporter allows the detection of bic promoter transcriptional activity using fluorescence activated cell sorting (FACS). In homozygotes, miR-155 expression is undetectable in activated splenic B cells. In heterozygotes, approximately 60% of germinal center (GC) B cells express the lacZ reporter whereas the vast majority of the non-GC B cells do not. Homozygous mice exhibit a reduced fraction of GC B cells in the gut-associated lymphoid tissue (GALT; including Peyer's patches (PPs) and mesenteric lymph nodes (mLNs)). In addition, bic/miR-155-/- B cells exhibit deficient tumor necrosis factor (TNF) and lymphotoxin-α (LT-α) cytokine production. Homozygous mice show impaired T cell-dependent antibody responses, and their T cells show a TH2 cytokine bias (an increased percentage of interleukin-4 (IL-4) producing cells and a decreased percentage of interferon-γ (IFN-& ..... For more information please see the full phenotype on the strain data sheet | ||
| 016231 | B6.Cg-Msh2tm2.1Rak/J | Repository- Live |
| The Msh2LoxP allele has loxP sites flanking exon 12 of the mutS homolog 2 (E. coli) [Msh2] gene. Homozygous Msh2LoxP mice are viable and fertile with no observed abnormalities. When bred to mice that express Cre recombinase, the resulting offspring will have the sequences encoding a portion of the essential ATPase domain of MSH2 protein deleted in the cre-expressing tissue(s). These Msh2LoxP mice may be useful in generating tissue-specific MSH2 deletions for studying DNA mismatch repair (single-nucleotide and insertion/deletion mismatches), as well as tumor development.
For example, when Msh2LoxP mice are bred to a strain expressing Cre recombinase in embryonic tissues (EIIA-Cre; see Stock Nos. 003314 or 003724), the resulting mice with pan deletion of MSH2 exhibit high inciden ..... | ||
| 006096 | B6.Cg-Msr1tm1Csk/J | Repository- Live |
| Homozygotes are viable and fertile. Liver sections treated with antibodies against type I and type II macrophage scavenger class A receptors show no protein staining. Homozygous mice have less severe lesion development in Apoe-deficient atherosclerosis model. Peritoneal macrophages have reduced mLDL uptake in vitro. Homozygous mice have increased susceptibility to pathogens. These mice may be useful in studies of immunity and host defense, cholesterol transport in macrophages, macrophage-derived foam cells, and atherosclerosis. | ||
| 006097 | B6.Cg-Nfkb1tm1Bal/J | Repository- Live |
| Mice homozygous for the Nfkb1tm1Bal targeted mutation are viable and fertile. Homozygous mutant mice exhibit defective B cell responses, defective responses to infection, and also defects in basal and specific antibody production. These mice may be useful in studies of inflammation and immune responses and signal transduction. 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. | ||
| 006577 | B6.Cg-Park7tm1Shn/J | Repository- Live |
| Homozygous mice are viable and fertile. Western blot analysis using antibody specific to C-terminal sequences indicates the absence of full length gene product. Homozygous mice exhibit hypokinesia and nigrostriatal dopaminergic deficits: evoked dopamine overflow in the striatum is reduced (primarily as a result of increased dopamine uptake), nigral neurons (dopaminergic neurons) have abnormal action potential characteristics, and long term depression is absent in medium spiny neurons. Also, D2-receptor mRNA abundance and radioligand binding is normal. Dopaminergic neurons from substantia nigra pars compacta (SNpc) of homozygous mice exhibit significantly higher sensitivity to energy metabolism impairment and nigral dopaminergic neurons are particularly sensitive to Na+/K+ ATPase impairment. These mutant mice may be useful in studies of Parkinson's disease, dopaminergic physiology, nigrostriatal function, locomotor inactivity, and other neurobiological research. ..... | ||
| 006492 | B6.Cg-Pdgfratm8Sor/EiJ | Repository- Live |
| These mice possess loxP sites on either side of exon 1 and exon 4 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele.
For example, when bred to a strain expressing Cre recombinase in midbrain/dorsal spinal cord (see Stock No. 007807 or 009107 for example), this mutant mouse strain may be useful in studies of cranial and cardiac neural crest cells. | ||
| 003819 | B6.Cg-Per2tm1Brd Tyrc-Brd/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display gross physical or behavioral abnormalities. A mutant transcript, if translated, would generate a protein with an 87 amino acid deletion. When maintained in constant darkness, two phenotypic components are exhibited: a shortened circadian period and a loss of persistent circadian rhythmicity. When housed under constant light, homozygotes exhibit normal activity rhythm but a period length of less than 24 hours. By 9-12 months of age, homozygous females exhibit low reproductive success and produce small litters when compared to wildtype. These mice also carry the recessive Tyrc-Brd mutation that, when homozygous, results in albino coat color. This mutant mouse strain may be useful in studies related to the regulation of the sleep-wake cycle. | ||
| 000528 | B6.Cg-PhexHyp/J | Repository- Live |
| Hypophosphatemia (PhexHyp) is an X-linked semidominant mutation that causes defects in phospate metabolism. It is allelic with the gyro mutation (PhexGy) but hypophosphatemia mutant mice do not circle. Hemizygous males and heterozygous females can be recognized at 20 to 30 days of age by their shortened hindlimbs and tail. They have reduced body size which persists throughout life, and skeletal changes resembling rickets. Hemizygous males are more affected than heterozygous females. Viability is normal in both sexes, but heterozygous females show better fertility than hemizygous males. | ||
| 012358 | B6.Cg-Pvalbtm1.1(cre)Aibs/J | Repository- Live |
| Mice heterozygous for the Pvalb-2A-Cre allele are viable and fertile, with a viral 2A oligopeptide that mediates ribosomal skipping and a Cre recombinase gene inserted immediately downstream of the parvalbumin translational STOP codon. As such, Pvalb-2A-Cre mice have both endogenous gene and Cre recombinase expression directed to Pvalb-expressing cells by the endogenous promoter/enhancer elements of the parvalbumin locus. When Pvalb-2A-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Pvalb-expressing cells in the offspring. Specifically, the donating investigator reports cre activity in scattered interneuron populations in the cortex and hippocampus, as well as neuronal populations in other brain regions, resembling the Pvalb expression pattern. Additional reporter gene expression is seen in cortical layer 5 neurons, which are unlikely to be interneurons. ..... For more information please see the full phenotype on the strain data sheet | ||
| 012359 | B6.Cg-Pvalbtm1.1(tTA2)Hze/J | Repository- Live |
| Mice homozygous for the Pvalb-2A-tTA2 allele are viable and fertile, with a viral 2A oligopeptide that mediates ribosomal skipping and a synthetic modified tetracycline-regulated transactivator (tTA2S) gene just downstream of the parvalbumin translational STOP codon. As such, Pvalb-2A-tTA2 mice have both endogenous gene and tTA2 expression directed to Pvalb-expressing cells by the endogenous promoter/enhancer elements of the parvalbumin locus. When Pvalb-2A-tTA2 mice are bred with mice carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE, TetRE or tetO), expression of the target gene in the Pvalb-expressing cells may be conditionally abolished with administration of the tetracycline analog doxycycline (dox) in the double mutant offspring. Specifically, the donating investigator reports that Pvalb-2A-tTA2 activates tetO-regulated gene expression in scattered interneuronal populations in the cortex and hippo ..... For more information please see the full phenotype on the strain data sheet | ||
| 004369 | B6.Cg-Rag1tm1Mom Ins2Akita/J | Repository- Live |
| Mice homozygous for the Rag1 targeted mutation and heterozygous for the Akita spontaneous display the diabetes phenotype in the absence of B and T cells and unlike single Akita mice, double mutants do not reject allografts. Mice heterozygous for only the Akita spontaneous mutation are viable and fertile. (Homozygotes typically die by 12 weeks of age from extreme hyperglycemia.) Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. The diabetic phenotype is more severe and progressive in heterozygous males than in females. Obesity and insulitis do not accompany diabetes. This double mutant strain is ideally suited for use in allogeneic or xenogeneic islet or stem cell transplantation protocols because the mice are severely immunocompromised and spontaneously develop diabetes at a young age. | ||
| 013188 | B6.Cg-Rptortm1.1Dmsa/J | Repository- Live |
| These Rptorflox/flox mutant mice possess loxP sites flanking exon 6 of the regulatory associated protein of mTOR (Mechanistic target of rapamycin), complex 1 , Rptor, 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 C57BL6-Tg(AlbCre)21Mgn (Stock No. 003574) mice, which direct liver-specific expression of Cre, mice exhibit a decrease in liver size yet produce ketones for hours after feeding. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exon 6 deleted in the cre-expressing tissues. This strain may be useful for studying mTOR-dependent regulation of ketogenesis and other cellular processes in response to feeding and fasting. | ||
| 004201 | B6.Cg-Selplgtm1Fur/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No targeted allele product (mRNA or protein) is detected by Northern blot or immunoassay. Mutant mice exhibit mild neutrophilia. Impaired early neutrophil migration in thioglycolate-induced peritonitis is followed by a delayed recovery to nearly normal levels. Although early trauma-induced leukocyte adhesion and migration is greatly reduced and in vivo leukocyte rolling (leukocyte-endothelial cell interaction) in postcapillary venules is severely decreased, cytokine-induced/E selectin-mediated leukocyte rolling is only slightly reduced in the mutant mice. This mutant mouse strain represents a model that may be useful in studies of leukocyte adhesion and migration in the inflammatory response. | ||
| 005622 | B6.Cg-Shhtm1(EGFP/cre)Cjt/J | Repository- Live |
| This strain expresses a fusion product involving Enhanced Green Fluorescent Protein (EGFP) and Cre recombinase from the endogenous Shh locus. EGFP and cre expression are consistent with the endogenous gene. Fluorescence is detected in the distal posterior region of the limb buds of embryos aged embryonic day 10 to 12 and colocalizes with the endogenous gene product (mRNA).
The donating investigator reports that it is not uncommon for a mosaic expression pattern to be exhibited when the allele is inherited through the female germline. It is recommended that this allele be passed through the male germline when conducting experiments involving cre-induced recombination. Mice homozygous for the mutation develop a limited limb skeleton and lack digit 2. Homozygous mice are not viable or fertile. Heterozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
This mutant mouse strain may be useful in studie ..... For more information please see the full phenotype on the strain data sheet | ||
| 013717 | B6.Cg-Slc20a1tm1.2Cmg/J | Repository- Live |
| A targeting vector was designed to remove exons 3-4 of the solute carrier family 20, member 1 (Slc20a1 or inorganic phosphate transporter-1 PiT-1) gene, in the epiblast, yolk sac mesoderm, and amnion, abolishing gene function. Mice that are heterozygous for this PiT-1Δe3,4 allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities, while homozygotes display an embryonic lethal phenotype. PiT-1, a ubiquitously expressed transmembrane type III sodium-dependent transporter, is associated with vascular calcification in many diseases, including diabetes, chronic kidney disease (CKD), and Werner Syndrome. The yolk sacs of homozygous embryos reveal a decrease in the superficial vasculature and appear severely anemic by E10.5. By E12.5, the embryos display significant growth retardation and anemia, leading to hypoxia, nutrient deprivation, growth arrest, and lethality. These homozygous PiT-1& ..... For more information please see the full phenotype on the strain data sheet | ||
| 004103 | B6.Cg-Tac1tm1Bbm/J | Repository- Live |
| Mice that are homozygous null for the Tac1 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Tac1 protein products (substance P or neurokinin A) are not immunodetectable. These mice have significantly reduced nociceptive pain responses to moderate to intense stimuli. Neurogenic inflammation is absent. Mutant mice are resistant to kainate-induced seizures and neurotoxicity. These mice provide a useful tool for studying the contribution of tachykinin peptides to pain processing and inflammatory disease states. | ||
| 004132 | B6.Cg-Terctm1Rdp/J | Repository- Live |
| Early generation mice that are homozygous null for the Terc gene are phenotypically normal. No Terc transcript or telomerase activity is detected. If null mice are maintained as homozygotes, progressive adverse effects on the reproductive and hematopoietic systems are observed. By the fifth generation of homozygous intercrossing, fertility is significantly diminished. Testes size and weight is reduced by ~80%. Germ cells exhibit decreased rates in proliferation and increased rates of apoptosis resulting in a general state of germ cell depletion. Females exhibit smaller ovaries and diminished uterine horns. The proliferative capacity of hematopoietic cells derived from bone marrow and spleen is significantly compromised. Progressive generations of interbreeding the null mice results in progressive telomere shortening (4.8 +/- 2.4 kb per generation). Cells from the fourth generation onward possess chromosome ends lacking detectable telomere repeats, aneuploidy, and chromoso ..... For more information please see the full phenotype on the strain data sheet | ||
| 005023 | B6.Cg-Thy1a/Cy Tg(TcraTcrb)8Rest/J | Repository- Live |
| This transgenic strain carries a rearranged T cell receptor transgene specific for the mouse homologue (pmel-17) of human SILV (gp100), an enzyme involved in pigment synthesis that is expressed by the majority of malignant melanoma cells including B16 melanoma, as well as by normal melanocytes. The strain is also homozygous for the T lymphocyte specific Thy1a (Thy1.1) allele. CD8+ T cells express a Tcra-V1/Tcrb-V13- transgenic TCR that recognizes an epitope of pmel-17 corresponding to amino acids 25-33 of gp100 presented by H2-Db MHC class I molecules. Greater than 95% of the CD8+ T cells in transgenic mice expressed the transgenic TCR based on the expression of Vbeta13, amounting to about 20% of all splenocytes. T cells in blood and spleen generally expressed baseline levels of the activation/effector markers CD25, CD44, and CD69, indicating that most of the transgenic cells were in the naive state. These transgenic mice in conjunction with the poor ..... For more information please see the full phenotype on the strain data sheet | ||
| 007484 | B6.Cg-Tyrc-2J Tg(Tyr)3412ARpw Tg(Sry-EGFP)92Ei/EiJ | Repository- Live |
| On an albino background the X-linked transgene Tg(Tyr)3412ARpw permits visual identification of XX versus XY as early as embryonic day 10.5. This strain is segregating for Tg(Tyr)3412ARpw and homozygous for Tyrc-2J so the individuals not carrying Tg(Tyr3412)ARpw are albino. Because Tg(Tyr)3412ARpw inserted into the X Chromosome, breeding a carrier male with a noncarrier (wild-type) female results in embryos in which all XX individuals develop eye pigment, due to the Tg(Tyr)3412ARpw inherited from their father, while all XY individuals have non-pigmented eyes, having inherited a wild-type X Chromosome from their mother.
This strain is also homozygous for Tg(SryEGFP)92Ei. This reporter transgene consists of a 5 prime regulatory segment of the Sry gene driving EGFP. This transgene is expressed in the pre-support cell lineage (pre-sertoli and pre-granulosa cells) of the fetal genital ridge (Albrecht and Eicher, 2001) and in discrete areas the adult male but not ..... | ||
| 008548 | B6.Cg-oda/GrsrJ | Repository- Live |
| Homozygotes can be identified by two weeks of age on this nonagouti background by their diluted steel grey coat color, which includes dilited pigment in the ears, feet, and tail. Homozygotes are viable and fertile. | ||
| 006149 | B6.Cg-Tg(ACTA1-cre)79Jme/J | Repository- Live |
| Mice hemizygous for this HSA-Cre79 transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These HSA-Cre79 transgenic mice have the cre recombinase gene driven by the human alpha-skeletal actin (HSA or ACTA1) promoter. Cre activity is restricted to adult striated muscle fibers and embryonic striated muscle cells of the somites and heart. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in striated muscle-specific deletion of the flanked genome. Specifically, these HSA-Cre79 (or ACTA1-Cre) transgenic mice were originally used to breed with mice heterozygous for a deletion of exon 7 and a loxP-flanked exon 7 mutation on homologous chromosomes of the Smn1 gene (see Stock No. 006138 or Stock No. 006146). The resulting offspring ( ..... For more information please see the full phenotype on the strain data sheet | ||
| 005703 | B6.Cg-Tg(ACTFLPe)9205Dym/J | Repository- Live |
| This transgenic strain expresses a variant of the Saccharomyces cerevisiae FLP1 recombinase gene under the direction of the human ACTB promoter. The FLPe recombinase variant exhibits enhanced thermostability with recombination activity being four-fold and ten-fold that of wildtype FLP at 37oC and 40oC, respectively. Mice that are hemizygous for the transgenic allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Recombinase activity is detected in a wide variety of tissues (spinal cord, heart, gonad, adrenal) as early as embryonic day 10.5. This deleter strain is a suitable alternative to, and complement with the Cre-loxP system for in vivo genetic engineering.
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 coul ..... | ||
| 003574 | B6.Cg-Tg(Alb-cre)21Mgn/J | Repository- Live |
| This strain may be maintained as a hemizygote or homozygote and lacks any phenotype related to the transgenic allele. It has been well characterized and shown to be very efficient for performing liver-specific gene knockouts using Cre/loxP system. This line has been shown to be nearly 100% efficient in achieving liver-specific recombination when crossed with at least 5 different floxed alleles.
View cre expression characterization. | ||
| 006881 | B6.Cg-Tg(Aqp2-cre)1Dek/J | Repository- Live |
| Mice hemizygous for this AQP2-Cre transgene are viable and fertile. Transgenic cre activity, directed by the mouse aquaporin 2 promoter, is observed in kidney cells (collecting duct) and testes (sperm). When bred with mice containing a loxP-flanked sequence of interest, cre-mediated recombination will result in deletion of the flanked sequence. In such breedings, maternal inheritance of the transgene is recommended for kidney-specific recombinase activity as males express cre in sperm as well as kidney tissues. These AQP2-Cre mice may be used to generate conditional mutations in the renal collecting duct for studying nephrology, physiology, metabolism, or type II diabetes. In addition, cre expression in sperm may be useful in generating conditional mutations in multiple or all tissues in the resulting offspring. | ||
| 011104 | B6.Cg-Tg(Atoh1-cre)1Bfri/J | Repository- Live |
| In this strain, mouse Atoh1 (atonal homolog 1 (Drosophila)) regulatory sequences drives cre expression primarily in precursors of granule cell neurons of the cerebellum and dorsal hindbrain/spinal cord in the dp1 domain. When bred with mice containing sequences flanked by similarly oriented loxP sites, flanked sequences will be deleted in the Cre-expressing tissues of the offspring. | ||
| 016997 | B6.Cg-Tg(Axin2-rtTA2S*M2)7Cos/J | Repository- Live |
| These transgenic mice express an optimized reverse tetracycline-controlled transactivator, rtTAS*M2, or rtTA2S-M2, under the control of the mouse Axin2 expression cassette (which contains 2883 nucleotides upstream of exon 1, exon 1, intron 1 and part of exon 2). Transgene expression mimics the endogenous Axin2 expression pattern, and is detected in dorsal neural tube neuroepithelial cells, migrating neural crest cells, and branchial arch post-migratory neural crest cells. When mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (tetO), expression of the target gene may be regulated by the tetracycline analog, doxycycline (dox); in the presence of dox, transcription of the target gene is induced in cells where rtTA is expressed. Mice that are hemizygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. T ..... For more information please see the full phenotype on the strain data sheet | ||
| 005317 | B6.Cg-Tg(BAT-lacZ)3Picc/J | Repository- Live |
| Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These "BAT-GAL" transgenic mice are a reporter strain that express beta-galactosidase in the presence of activated beta-catenin. The transgene expresses the lacZ gene under the control of a regulatory sequence consisting of seven consensus LEF/TCF-binding motifs upstream of the Xenopus siamois gene minimal promoter. Transgenic mice display beta-galactosidase activity beginning at embryonic day 6.0 in the posterior side of | ||