Search Criteria: Research Area is "Immunology and Inflammation Research: Immunodeficiency Associated with Other Defects"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 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. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase in body weight, and probably results from it. Homozygotes have an ab
..... For more information please see the full descriiption on the strain data sheet | ||
| 000642 | BKS.Cg-m +/+ 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 descriiption on the strain data sheet | ||
| 002468 | KK.Cg-Ay/J | Level 2 |
| Ay and other mutations at the a locus conferring a completely yellow coat color are dominant to all a alleles that produce a darker coat. Hair pigment of Ay heterozygotes is yellow, but eyes are black. Heterozygotes usually become obese and infertile within a few months after birth. Increased adipose tissue mass is due to fat cell hypertrophy, and it has been hypothesized that the obesity results from the observed reduction in hypothalamic norepinephrine and dopamine. Heterozygotes are more susceptible to several kinds of tumors than are normal mice, possibly due, at least in part, to a general increase in cell proliferation that also manifests as a slight increase in lean body mass and skeletal length. Further spleen cells from heterozygotes cause a significantly lower graft vs. host reaction. Mice homozygous for the yellow spontaneous mutation (Ay) die before implantation, or shortly thereafter. The time of death and
..... For more information please see the full descriiption on the strain data sheet | ||
| 000697 | B6.Cg-m +/+ Leprdb/J | Level 3 |
| 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 4 to 8 weeks. Affected mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. On the C57BL/6 background there is compensatory hyperplasia of the islet B-cells, and continued hyperinsulinemia throughout an 18- to 20-month life span. Wound healing is delayed and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (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 diabet
..... For more information please see the full descriiption on the strain data sheet | ||
| 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. | ||
| 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. | ||
| 000629 | C57BL/6J-Lystbg-J/J | Level 4 |
| Mice homozygous for the beige-J spontaneous mutation (Lystbg-J) are identical to the original beige mutation (Lystbg). The phenotype closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syn
..... For more information please see the full descriiption on the strain data sheet | ||
| 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. | ||
| 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. | ||
| 003641 | B6.129S4-C3tm1Crr/J | Repository- Live |
| Mice homozygous for the C3 (complement component C3) targeted mutation are viable and fertile. Homozygous mutants exhibit an increased susceptibility to lethal infection by Group B streptococci. Reductions in peritoneal mast cell degranulation, production of tumor necrosis factor alpha, neutrophil infiltration and bacterial clearance have also been reported in these mice. Homozygotes also demonstrate a profound defect in antibody response to T cell dependent antigens. They show a diminished level of peanut agglutin+ germinal centers and a failure in isotype switching despite normal B cell signalling in vitro. | ||
| 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 descriiption 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. | ||
| 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 descriiption 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 descriiption on the strain data sheet | ||
| 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 descriiption on the strain data sheet | ||
| 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 descriiption on the strain data sheet | ||
| 006906 | B6.Cg-Lepob Ldlrtm1Her/J | Repository- Live |
| Independently, the C57BL/6-Lepob homozygotes (Stock No. 000632) model the increasingly prevalent metabolic disorder seen in humans (hyperglycemia, hyperinsulinemia, and hyperlipidemia), while LDLR-deficient mice (Stock No. 002207) are predisposed to atherosclerosis. When mutant mice are homozygous for both mutant alleles, they exhibit exacerbated hyperlipidemia and extensive atherosclerotic lesions in the aorta. The mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, and hypercholesterolemia. | ||
| 000524 | B6.WK-Lama2dy-2J/J | Repository- Live |
| Mice homozygous for the dystrophia-muscularis spontaneous mutations (Lama2dy and Lama2dy-2J) are characterized by progressive weakness and paralysis beginning at about 3 1/2 weeks of age. The hindlimbs are affected first, later the axial and forelimb musculature. Death usually occurs before 6 months of age, and mutant mice are usually sterile. Skeletal muscle shows degenerative changes with proliferation of sarcolemmal nuclei, increase in amount of interstitial tissue, and size variation among individual muscle fibers. In the dorsal and ventral roots of the peripheral nerves, both spinal and cranial, Schwann cells fail to separate and ensheathe axons so that groups of closely apposed naked axons, normally seen only in early stages, persist into adulthood. In the rest of the PNS, the basement membrane of Schwann cells is interrupted by gaps, the internodal gap in the nodes of Ranvier is lengthened, and there is delayed onset of myelination with fewer
..... For more information please see the full descriiption on the strain data sheet | ||
| 006495 | B6;129-Trp53bp1tm1Jc/J | Repository- Live |
| Homozygous "53BP1"-deficient mice are viable and fertile, but exhibit retarded growth and generate reduced litter sizes. Protein from the targeted gene is not detected in the testes (by immunoblot) or in mouse embryonic fibroblasts (MEFs) (by immunofluorescence). Homozygotes are immunocompromised, hypersensitive to whole-body irradiation, and develop thymic lymphomas with higher frequency (8%) compared to wildtype by 4-7 months of age. MEFs from homozygous mutant mice have a defective DNA damage response with impaired Chk2 activation. These mutant mice may be useful in studies of the immune system, cancer, tumor suppression, and DNA damage response pathways. | ||
| 005217 | B6;129S1-Tlr3tm1Flv/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Northern blot analysis detects a truncated gene product (mRNA), which is not functional. Unlike wildtype macrophages, macrophages derived from these animals fail to produce inflammatory cytokines, IFN-alpha or IFN-beta when challenged with poly(I:C), polyinosine-polycytidylic acid, a synthetic dsRNA analog. Splenocytes isolated from homozygotes do not respond to viral dsRNA and have diminished IL-6 production. Mice homozygous for the mutation are resistant to poly(I:C) induced shock and produce lower levels of IL-12. This mutant mouse strain may be useful in studies of the toll-like receptor pathway of innate immune response. | ||
| 000231 | B6C3Fe a/a-Csf1op/J | Repository- Live |
| Mice homozygous for the osteopetrosis spontaneous mutation (Csf1op) are viable and exhibit osteopetrosis. The osteoclasts are the primary cell type affected in homozygous mutant mice. This results in a generalized macrophage deficiency, monocytopenia, and defective bone remodeling. Homozygous mutant mice also have abnormal calcium regulation, impaired dental growth and female mice fail to lactate. Total leukocyte counts are reduced and marrow cells are decreased to one-tenth of normal control mice. Homozygous mutant mice have a deficient microglia and macrophage response, and therefore may be useful tools to study the role of glia in neurological disease if mated to transgenic models of neurodegenerative disease. | ||
| 001573 | B6C3Fe a/a-MitfMi/J | Repository- Live |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice heterozygous for the MitfMi mutation have less iris pigment than wildtype and often have white spotting on the belly, head, and tail. Homozygous mutant mice have small eyes and are devoid of pigment in the eyes, inner ear, and skin. Homozygotes are deaf at an early age. There is a decrease of mast cells in the spleen and gut. Most homozygotes die around weaning but some may live for several months. There is a deficiency of secondary bone resorption (osteopetrosis) and the incisors fail to erupt. Immunological defects include decreased macrophage chemotactic responses, impaired proliferative responses to B cell and T cell mitogens, diminished responses in vitro to T-dependent and T-independent antigens and reduced NK cell activity. | ||
| 004824 | BTBR.V(B6)-Lepob/WiscJ | Repository- Live |
| Mice homozygous for the obese spontaneous mutation, (Lepob commonly referred to as ob or ob/ob) exhibit obesity 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 number and size of adipocytes. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase body weight and is probably the result of it. Homozygotes do have an abnormally low threshold for stimulation of pancreatic islet insulin secretion even in very young preobese animals. As is the case with mice carrying the diabetes mutation (Leprdb
..... For more information please see the full descriiption on the strain data sheet | ||
| 002134 | C57BL/6J-Mitfmi-vit/J | Repository- Live |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the vitiligo spontaneous mutation Mitfmi-vit are only mildly affected compared to other Mitf alleles. Homozygous mutant mice have a lighter initial coat color than normal with extensive white spotting. After eight weeks of age, the mice producing increasing numbers of white hairs with each hair cycles resembling human vitiligo. Homozygotes exhibit uneven pigmentation of the retina and slow, progressive photoreceptor cell loss, eventually leading to blindness. | ||
| 000643 | DW/J Mlphln Pou1f1dw/J | Repository- Live |
| Mice homozygous mice for the dwarf spontaneous mutation (Pou1f1dw) are characterized by severe dwarfing, sterility, and hypothyroidism. Adult dwarf mice are about one-fourth to one-third the size of wildtype mice. There is a lack of growth hormone, prolactin and thyroid stimulating hormone producing cells in the anterior pituitary leading to severe endocrine deficiency of these hormones. Homozygous mutant mice show a transient loss in cortical thymocytes associated with the primary defect in anterior pituitary. | ||
| 006654 | FVB.BKS(D)-Leprdb/ChuaJ | Repository- Live |
| The phenotype of this congenic "FVB-db" strain varies from that previously published on other genetic backgrounds. Specifically, obese FVB-db mice show long-term hyperglycemia that is primarily due to severe insulin resistance. The hyperglycemia in the fed state persists despite escalating insulin secretion and a massive increase in pancreatic beta-cell mass. Obese FVB-db mice show evidence of mesangial matrix expansion, a hallmark of diabetic nephropathy. Whereas the original C57BLKS/J-db mice are hyperglycemic due to the development of hypoinsulinemia and loss of beta-cell mass, the hyperglycemia of FVB-db appears to be due to severe insulin resistance with continual increases in insulin secretory capacity from beta-cell mass expansion. As the phenotype varies by genetic background, these mutant mice, along with db mutants on other genetic backgrounds (see Stock No. 000642, For more information please see the full descriiption on the strain data sheet | ||
| 004848 | NOD.Cg-Rag1tm1Mom Prf1tm1Sdz/SzJ | Repository- Live |
| Mice that are homozygous for both targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities when housed under specific pathogen free conditions. These double homozygote mutant mice have no mature T or B lymphocytes, no detectable NK cell cytotoxic activity, and lack serum immunoglobulin. The number of nucleated spleen cells is significantly reduced in double mutant mice, when compared to the single homozygote, NOD.129S7(B6)-Rag1tm1Mom/J (Stock No. 003729). Although an increased number of DX5+CD122+ NK cells are found in the spleens of double mutants, these NK cells have impaired cytotoxic activity. The disruption of Prf1 ablates NK cell cytotoxic activity resulting in increased engraftment levels over that observed with Stock No. 003729. All mutant mice develop thymic lymphomas. This double mutant mouse strain may be useful in studies involving engraftment of human hematolympho
..... For more information please see the full descriiption on the strain data sheet | ||
| 001618 | STOCK Oca2p/Oca2p Prop1df/J | Repository- Live |
| Mice homozygous for the Ames dwarf spontaneous mutation (Prop1df) resemble mice homozygous for the Snell's dwarf mutation (Pit1dw). Homozygous Ames dwarf mutant mice show growth retardation after the first postnatal week, and weight at 2 months is only about one-half normal. Females and most males are sterile. There is no detectable growth hormone or prolactin. Ames dwarf mice have a secondary immune deficiency presumably resulting from the lack of growth hormone. | ||
| 000641 | 129P1/ReJ-Lama2dy/J | Repository-Cryopreserved |
| Mice homozygous for the dystrophia-muscularis spontaneous mutations (Lama2dy and Lama2dy-2J) are characterized by progressive weakness and paralysis beginning at about 3 1/2 weeks of age. The hindlimbs are affected first, later the axial and forelimb musculature. Death usually occurs before 6 months of age, and mutant mice are usually sterile. Skeletal muscle shows degenerative changes with proliferation of sarcolemmal nuclei, increase in amount of interstitial tissue, and size variation among individual muscle fibers. In the dorsal and ventral roots of the peripheral nerves, both spinal and cranial, Schwann cells fail to separate and ensheathe axons so that groups of closely apposed naked axons, normally seen only in early stages, persist into adulthood. In the rest of the PNS, the basement membrane of Schwann cells is interrupted by gaps, the internodal gap in the nodes of Ranvier is lengthened, and there is delayed onset of myelination with fewer
..... For more information please see the full descriiption on the strain data sheet | ||
| 000709 | 129P3/J-Leprdb-3J/J | Repository-Cryopreserved |
| Mice homozygous for the diabetes 3J spontaneous mutation (Leprdb-3J) become identifiably obese around 3 to 4 weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at 4 to 8 weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. Homozygous mutant mice on the 129P3/J background exhibit severe obesity but the diabetes phenotype is much reduced. | ||
| 000593 | B6 x B6CBCa Aw-J/A-Grid2Lc T(2;6)7Ca MitfMi-wh/J | Repository-Cryopreserved |
| Mice homozygous for the MitfMi spontaneous mutation are characterized by decreased macrophage chemotactic responses, impaired proliferative responses to B cell and T cell mitogens, diminished responses in vitro to T-dependent and T-independent antigens and reduced NK cell activity. | ||
| 002048 | B6 x C57BLKS-m Leprdb Myo15sh2-J/J | Repository-Cryopreserved |
| Mice homozygous for the shaker 2 Jackson spontaneous mutation (Myo15sh2-J) are viable and fertile, showing only a slight reduction in both compared to wildtype mice. The shaker 2 Jackson remutation is not visibly different from the original shaker 2 (Myo15sh2, Stock No. 000109). Homozygous mutant mice of both alleles display a phenotype very similar to the behavior and pathology to shaker-1 (Myo7ash1) with the exception that the abnormalities are observed a little earlier in shaker 2 mice. This strain is also carrying the misty (m) and diabetes (Leprdb) spontaneous mutations. | ||
| 000631 | B6.129P1-Lama2dy/J | Repository-Cryopreserved |
| Mice homozygous for the dystrophia-muscularis spontaneous mutations (Lama2dy and Lama2dy-2J) are characterized by progressive weakness and paralysis beginning at about 3 1/2 weeks of age. The hindlimbs are affected first, later the axial and forelimb musculature. Death usually occurs before 6 months of age, and mutant mice are usually sterile. Skeletal muscle shows degenerative changes with proliferation of sarcolemmal nuclei, increase in amount of interstitial tissue, and size variation among individual muscle fibers. In the dorsal and ventral roots of the peripheral nerves, both spinal and cranial, Schwann cells fail to separate and ensheathe axons so that groups of closely apposed naked axons, normally seen only in early stages, persist into adulthood. In the rest of the PNS, the basement membrane of Schwann cells is interrupted by gaps, the internodal gap in the nodes of Ranvier is lengthened, and there is delayed onset of myelination with fewer
..... For more information please see the full descriiption on the strain data sheet | ||
| 002463 | B6.129S-Itga4tm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Itga4tm1Hyn targeted mutation die during embryonic development. Homozygous mutant embryos fail to fuse the allantois with the chorion during placentation. There is a defect in the epicardium and coronary vessels results in in utero cardiac hemorrhage; also known as CD49D, VLA-4. | ||
| 008434 | B6.129S2-Seletm1Hyn/J | Repository-Cryopreserved |
| 003643 | B6.129S4-C4btm1Crr/J | Repository-Cryopreserved |
| Mice homozygous for the C4 (complement component C4) targeted mutation are viable and fertile. Homozygous mutants exhibit an increased susceptibility to lethal infection by Group B streptococci(GBS). C4 homozygous mutants show a similar susceptibility to GBS lethal infection as do C3 null mice, suggesting that the classical, and not alternative, pathway is primarily involved in antibody-independent humoral immunity to GBS. Homozygotes also demonstrate a profound defect in antibody response to T cell dependent antigens. They show a diminished level of peanut agglutin+ germinal centers and a failure in isotype switching despite normal B cell signalling in vitro. | ||
| 004197 | B6.129S6-Rac2tm1Mddw/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, and normal in size but exhibit phagocytic immunodeficiency. No endogenous gene product (mRNA or protein) was detected by Northern blot analysis, RT-PCR or Western blot analysis. The Rac proteins are a subclass of the Rho family of GTPases, and are involved in actin cytoskeletal organization in cell movement, cell proliferation, kinase signaling pathways, and in superoxide production in phagocytic cells. Neutrophils and mast cells derived from homozygous mice display abnormal actin-based functions: cytoskeleton remodeling ability, adhesion, migration, degranulation, and phagocytosis. Diminished superoxide production in response to some agonists, and reduced total number of leukocytes and neutrophils in peritoneal exudate is observed. As result of functional deficiencies in neutrophil and mast cell populations, these mutant mice are more vulnerable to invasive infection. Slowed growth of mast cells, accompanying redu
..... For more information please see the full descriiption on the strain data sheet | ||
| 001737 | B6.A-H2-T18a.HRS-Hrhr/J | Repository-Cryopreserved |
| Mice homozygous for the hr mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of statified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. In an attempt to offer alleles on
..... For more information please see the full descriiption on the strain data sheet | ||
| 000017 | B6.C3Fe-Avy/J | Repository-Cryopreserved |
| Homozygous (Avy/Avy) and heterozygotes (Avy/A and Avy/a) show considerable variation in appearance, ranging from clear yellow, to mottling with dark patches, to a completely agouti-like coat. The variation is strongly influenced by the agouti-locus genotype and strain genome of the dam. Homozygotes and heterozygotes tend to become obese, and the degree of obesity is correlated with the amount of yellow in the coat. Avy resembles Ay in causing greater tumor susceptibility and lower graft vs. host reactivity and higher hepatic malic enzyme activity. Homozygotes have a reduced humoral response to tetanus toxoid and decreased rates of carbon clearance as well as impaired mononuclear phagocyte function. The greater tumor susceptibility as well as several altered immune responses occur in Avy/a mice of mottled phenotype but not in those of agouti phenotype. | ||
| 000158 | B6.Cg-MitfMi-wh/MitfMi/J | Repository-Cryopreserved |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes white mutant mice show slight microphthalmia but normal skeleton. Mice heterozygous for the microphthalmia (MitfMi) mutation have less iris pigment than wildtype and often have white spotting on the belly, head, and tail. Homozygous mutant mice have small eyes and are devoid of pigment in the eyes, inner ear, and skin. Homozygotes are deaf at an early age. There is a decrease of mast cells in the spleen and gut. Most homozygotes die around weaning but some may live for several months. There is a deficiency of secondary bone resorption (osteopetrosis) and the incisors fail to erupt. Immunological defects include decreased macrophage chemotac
..... For more information please see the full descriiption on the strain data sheet | ||
| 000184 | B6.Cg-MitfMi-wh/Mitfmi-rw/J | Repository-Cryopreserved |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the red-eyed white spontaneous mutation Mitfmi-rw have some pigmentation around the neck and have small red eyes. Compound heterozygotes of white and red-eyed white (MitfMi-wh/Mitfmi-rw) are mostly white with tan spots and red eyes. | ||
| 000157 | B6.Cg-MitfMi-wh/Mitfmi-sp/J | Repository-Cryopreserved |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes white mutant mice show slight microphthalmic but normal skeleton. Both homozygous and heterozygous mice for the microphthalmia-spotted spontaneous mutation (Mitfmi-sp) are not detectably different form wild-type mice in color but have slightly less tyrosinase activity in the skin. Compound heterozygotes (MitfMi-wh/Mitfmi-sp) are light yellow with dorsal and ventral white spots and pigemented eyes. | ||
| 000057 | B6.Cg-MitfMi-wh/J | Repository-Cryopreserved |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a diluted coat color, light ears, a white belly spot, and in rare cases a dorsal spot. In addition, they display abnormalitites of both the cochlear and vestibular portions of the inner ear. | ||
| 000699 | B6.Cg-m Leprdb/+ +/J | Repository-Cryopreserved |
| 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 4 to 8 weeks. Affected mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. On the C57BL/6 background there is compensatory hyperplasia of the islet B-cells, and continued hyperinsulinemia throughout an 18- to 20-month life span. Wound healing is delayed, and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (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 diabe
..... For more information please see the full descriiption on the strain data sheet | ||
| 000772 | B6.DW-Pou1f1dw/J | Repository-Cryopreserved |
| Mice homozygous mice for the dwarf spontaneous mutation (Pou1f1dw) are characterized by severe proportional dwarfing, sterility, and hypothyroidism. Adult dwarf mice are about one-fourth to one-third the size of wildtype mice. There is a lack of growth hormone, prolactin and thyroid stimulating hormone producing cells in the anterior pituitary leading to severe endocrine deficiency of these hormones. Homozygous mutant mice show a transient loss in cortical thymocytes associated with the primary defect in anterior pituitary. | ||
| 003807 | B6;129S-Seletm1Hyn Selltm1Hyn Selptm1Hyn/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Sele, Sell and Selp genes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities at birth. As mice mature, however, they become susceptible to mucocutaneous infections that eventually lead to death. No Sele, Sell or Selp gene products (mRNA or protein) are detected. Leukocytes from these mice exhibit a deficiency in the ability to interact with, and roll along, the venular wall endothelium. This deficiency in the crucial first step of leukocyte recruitment to surrounding tissues in response to infection or injury contributes to an elevated leukocyte count in the peripheral blood. Delays in neutrophil and eosinophil recruitment to the peritoneum in response to thioglycollate and ragweed allergen, respectively, have been observed, specifically. These mice are suitable for use in research applications studying leukocyte homeostasis, infectious diseases and inflam
..... For more information please see the full descriiption on the strain data sheet | ||
| 003806 | B6;129S-Seletm1Hyn Selltm1Hyn/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Sele and Sell genes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Sele or Sell gene products (mRNA or protein) are detected. A slightly diminished response in neutrophil recruitment to the peritoneum in response to thioglycollate is observed, as is a diminished ability to interact with the venular endothelium resulting in increased "rolling" along the vessel wall. These mice are suitable for use in research applications studying leukocyte homeostasis, infectious diseases and inflammation. | ||
| 002916 | B6;129S2-Seletm1Hyn Selptm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for both the Seletm1Hyn Selptm1Hyn mutations are viable and fertile. They are characterized by leukocytosis, spontaneous bacterial infections, dermatitis and defective leukocyte recruitment in many models of inflammation. | ||
| 002915 | B6;129S2-Seletm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Seletm1Hyn targeted mutation are viable and fertile. Homozygous mutant mice show only subtle defects in leukocyte recruitment, unless P-selectin (Selp) is also ablated or blocked with antibody. | ||
| 006482 | B6;129S6-Lig4tm1Fwa/Kvm | Repository-Cryopreserved |
| 000350 | B6By.Cg-KitW-v MitfMi-wh T/J | Repository-Cryopreserved |
| 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. Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a dilut
..... For more information please see the full descriiption on the strain data sheet | ||
| 000604 | B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J | Repository-Cryopreserved |
| 000209 | B6C3Fe a/a-Dh/J | Repository-Cryopreserved |
| A spontaneous mutation on chromosome 1 of the dominant hemimelia gene, Dh, causes a defect in the embryonic splanchnic mesoderm and induces congenital absence of the spleen and widespread visceral and skeletal abnormalities. Mice homozygous for the Dh mutation die shortly after birth. Heterozygotes may exhibit tibial hemimelia, polydactyly, and extra fused toes. Rear leg(s) may be held at an odd angle with bent rear ankles. Heterozygotes have enlarged lymph nodes and elevated numbers of circulating lymphocytes, granulocytes and thrombocytes. They show reduced serum IgM and IgG2 and impaired humoral antibody response as well as decreased numbers of lymph node mast cells. The Pde6brd1 allele contributed to this strain by C3FeLe.B6-a causes blindness and is segregating in this strain. | ||
| 000182 | B6C3Fe a/a-Eef1a2wst/J | Repository-Cryopreserved |
| Mice homozygous for the wasted spontaneous mutation (Eef1a2wst) can be recognized at 20 days of age by tremor and uncoordinated body movements. Homozygous mutant mice develop progressive paralysis and do not survive beyond 30 days. They have marked lymphoid hypoplasia in the spleen, thymus, lymph nodes, and peripheral blood. Wasted mice have a severely reduced number of IgA plasma cells in the entire large and small intestines, but the number of such cells in the spleen and the level of serum IgA are normal. Neuronal degeneration occurs in the brain and spinal cord. Spinal cord abnormalities are preceded by gliosis following along a rostrocaudal gradient. Thoracic/abdominal muscles exhibit a progressive denervation of muscle fibers, with progressive asynchronous retraction of motor nerve terminals. (Newbery HJ, et al. 2005) | ||
| 000304 | B6C3Fe a/a-Krt71Ca Scn8amed-J/J | Repository-Cryopreserved |
| Mice homozygous for the motor end plate disease-Jackson spontaneous mutation (Scn8amed-J) have a phenotype that resembles the original mutation (Scn8amed). Homozygous motor end plate disease mutant mice show progressive skeletal muscle weakness beginning 8 to 10 days postnatally and usually die within 2 weeks of onset. Other disease characteristics include progressive atrophy of skeletal muscle, marked terminal sprouting of motor nerves along with slower conduction velocity and prolonged refraction, and eventually failure of muscle fibers to show end-plate potentials or action potentials in response to nerve stimulation. Heterozygotes may show mild manifestations of the disease during the first 2 weeks of life but symptoms disappear with age. Both homozygotes and heterozygotes exhibit immunological aberrations. | ||
| 000956 | B6CB-Mitfmi-rw/J | Repository-Cryopreserved |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the red-eyed white spontaneous mutation Mitfmi-rw have some pigmentation around the neck and have small red eyes. | ||
| 000504 | B6EiC3Sn a/A-Cacnb4lh/J | Repository-Cryopreserved |
| Mice homozygous for the lethargic spontaneous mutation (Cacnb4lh) are first recognizable at 15 days by their lethargic behavior with gait instability and occasional seizures. The seizures resemble human petit mal seizures. No pathological changes were found in the CNS or in skeletal muscles, but peripheral motor nerves show reduced conduction velocity and prolonged distal latency. There is early thymic involution at 3 to 4 weeks in Cacnb4lh homozygotes, accompanied by decreased lymphocyte count, decreased cell-mediated immunity, and increased levels of serum IgG1. The defects in the immune system tend to disappear by 2 months of age in mice that survive. In addition to neurological and immunological defects, homozygous lethargic mice show pituitary-adrenal hypercorticism. Homozygotes are smaller and weaker than their normal littermates and often die before 2 months old. Survivors of both sexes may breed, but their reproductivity is low. | ||
| 000700 | BKS.Cg-m Leprdb/+ +/J | Repository-Cryopreserved |
| 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 4 to 8 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. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Leprdb/+) also have increased metabolic efficiency and
..... For more information please see the full descriiption on the strain data sheet | ||
| 001192 | BKS.Cg-meaJ Leprdb +/+ + m/J | Repository-Cryopreserved |
| Mice homozygous for the meander tail-J spontaneous mutation (meaJ) have variably shortened and kinked tails. At about 2 weeks an unsteadiness of gait, often amounting to a tremor, appears. Homozygous mutant mice are smaller and less vigorous than wiltype controls but are fertile. The anterior lobe of the cerebellum is disorganized. Purkinje cells are scattered, some cellular layers never form, and Bergmann glial processes are absent. The cytoarchitecture of the posterior lobe is normal, and the transition from normal to disorganized areas is sharply demarcated. This mutation occurred in the BKS.Cg-Leprdb +/+ m strain so it is also segregating for the diabetes (Leprdb) and misty (m) mutations. See strain description for BKS.Cg-Leprdb +/+ m (Stock No. 000642) for more information. | ||
| 000696 | BKS.V-Lepob/J | Repository-Cryopreserved |
| Mice homozygous for the obese spontaneous mutation (Lepob, commonly referred to as ob or ob/ob) are first recognizable at about 4 weeks old. Homozygous mutant mice increase in weight rapidly and may reach three times the normal weight of wildtype controls. In addition to obesity, mutant mice exhibit hyperphagia; a diabetes-like syndrome of hyperglycemia, glucose intolerance, and elevated plasma insulin; subfertility; and increased hormone production from both pituitary and adrenal. They are also hypometabolic and hypothermic. The obesity is characterized by both an increased number and size of adipocytes. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase body weight and is probably the result of it. Homozygotes do have an abnormally low threshold for stimulati
..... For more information please see the full descriiption on the strain data sheet | ||
| 004647 | C.129P2-Lbptm1Jack/J | Repository-Cryopreserved |
| 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) activity is detected by ELISA analysis of serum. Homozygous mice are unresponsive to intraperitoneal injections of lipopolysaccharide (LPS)(200ng) even when pre-treated with galactosamine. Serum concentrations of TNF-alpha remain low after LPS challenge. Gram-negative bacteria infection induced by intraperitoneal injections of Salmonella typhimurium is fatal to mutant mice due to an impaired inflammatory response. This mutant mouse strain may be useful in studies of immune responses to bacterial infection. | ||
| 008438 | C.129S2(B6)-Seletm1Hyn Selptm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for both the Seletm1Hyn Selptm1Hyn mutations are viable and fertile. They are characterized by leukocytosis, spontaneous bacterial infections, dermatitis and defective leukocyte recruitment in many models of inflammation. 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. | ||
| 008435 | C.129S2(B6)-Seletm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Seletm1Hyn targeted mutation are viable and fertile. Homozygous mutant mice show only subtle defects in leukocyte recruitment, unless P-selectin (Selp) is also ablated or blocked with antibody. 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. | ||
| 005629 | C.129S2-Fcer1atm1Knt/J | Repository-Cryopreserved |
| 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. This mutant mouse strain may be useful in studies of anaphylaxis, and immunological response to allergens. | ||
| 006134 | C.129S4(B6)-Cxcl10tm1Adl/J | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 003798 | C3Fe.Cg-Scn8amed/J | Repository-Cryopreserved |
| 000200 | C3FeB6 A/Aw-J-Ankank/J | Repository-Cryopreserved |
| The progressive ankylosis allele (ank) is a spontaneous recessive mutation that causes a severe phenotype of joint calcification and degeneration. Few homozygotes survive beyond 5 months of age, although the adults can breed. Generally no more than 2 litters are produced by homozygotes of either sex. At 4 or 5 weeks of age, homozygotes can be identified by their inability to grasp a wire cage lid with their front paws when suspended above it. The joints swell with a milky fluid, and undergo a process proceeding through mononuclear inflammatory infiltration, hydroxyapatite deposition and increased calcification, hyperplasia, and fibrous and bony ankylosis. (for details see Mahowald et al., 1989; Hakim et al., 1984; Sweet and Green, 1981.) The front feet are affected before the hind feet and the phenotype is more severe in the most distal joints of the limbs. Hyperplasia and degeneration of the joint tissues, and ankylosis occur progressively, decreasing mobility and resulting i
..... For more information please see the full descriiption on the strain data sheet | ||
| 000510 | C3H/HeJ-Pou1f1dw-J/J | Repository-Cryopreserved |
| Mice homozygous mice for the dwarf Jackson spontaneous mutation (Pou1f1dw-J) have a phenotype very similar to mice homozygous for the original dwarf mutation (Pou1f1dw). Homozygous mutant mice are characterized by severe proportional dwarfing, sterility, and hypothyroidism. Adult dwarf mice are about one-fourth to one-third the size of wildtype mice. There is a lack of growth hormone, prolactin and thyroid stimulating hormone producing cells in the anterior pituitary leading to severe endocrine deficiency of these hormones. Homozygous mutant mice show a transient loss in cortical thymocytes associated with the primary defect in anterior pituitary. | ||
| 000120 | C3H/HeSn-Rab27aash/J | Repository-Cryopreserved |
| Ashen mice have a lightened coat color that is gray on a non-agouti background similar to that of dilute (Myo5ad) or leaden (ln) mutants. Lane and Womack reported that on an agouti background the yellow pigment is more dilute in ashen mice resulting in a grayer agouti than that found in dilute or leaden mice, but Wu et al. subsequently reported that dilute and ashen mice have identical degrees of coat color dilution. This pigment dilution results from defective trafficking of melanosomes that are normally found throughout the dendrites of melanocytes. Similar to that seen in leaden mutants, ashen melanosomes are clumped around the nucleus and sparse in the dendrites where normally they are released. Melanosome trafficking from the melanocyte cell body to the ends of the dendrites results from a microtubule-based bidirectional transport. MYO5A is essential for retaining the melanosomes in the ends of the dendrites and preventing their retrograde transport back t
..... For more information please see the full descriiption on the strain data sheet | ||
| 000099 | C3HeB/FeJ-Avy/J | Repository-Cryopreserved |
| Homozygotes (Avy/Avy) and heterozygotes (Avy/A and Avy/a) show considerable variation in appearance, ranging from clear yellow, to mottling with dark patches, to a completely agouti-like coat. The variation is strongly influenced by the agouti-locus genotype and strain genome of the dam. Homozygotes and heterozygotes tend to become obese, and the degree of obesity is correlated with the amount of yellow in the coat. Avy resembles APy in causing greater tumor susceptibility and lower graft vs. host reactivity and higher hepatic malic enzyme activity. Homozygotes have a reduced humoral response to tetanus toxoid and decreased rates of carbon clearance as well as impaired mononuclear phagocyte function. The greater tumor susceptibility as well as several altered immune responses occur in Avy/a mice of mottled phenotype but not in those of agout
..... For more information please see the full descriiption on the strain data sheet | ||
| 000519 | C57BL/6J-Dsg3bal/J | Repository-Cryopreserved |
| 000758 | C57BL/6J-Hbbp Hrrh-7J/J | Repository-Cryopreserved |
| Rhino mice have spleen cells with a defective response to T-dependent antigens and they develop an autoimmune disease characterized by hypergammaglobulinemia, immunoglobulin deposits in basement membrane of skin, spleen, liver, and kidney, and presence of antinuclear antibodies which occur in young mice and increase with age. These mice have increased numbers of Thy1 positive epidermal dendritic cells. Like homozygous hairless mice, rhino mice are hairless by 5 weeks and their skin becomes wrinkled and thickened. | ||
| 002611 | C57BL/6J-Mitfmi-bws/J | Repository-Cryopreserved |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. | ||
| 000574 | CBA-Pdss2kd/J | Repository-Cryopreserved |
| Mice homozygous for the kidney disease spontaneous mutation (Pdss2kd) develop autoimmune nephrosis recognizable at about 10 weeks of age by increased proteinuria and followed by excessive drinking, loss of weight, anemia, and death usually by 5 to 7 months. The process is mediated by an antigen-specific, H2k-restricted effector cell. The phenotype resembles human nephronophthisis. | ||
| 000707 | CBA.Cg-m Leprdb/+ +/J | Repository-Cryopreserved |
| Leprdb/Leprdb mice on the CBA strain background are characterized by exocrine pancreatic necrosis and kidney lesions in aging mice. In contrast to the obesity observed in other strain backgrounds, five month old homozygous males exhibit weight loss in comparison to controls. Homozygous males develop severe hyperglycemia exhibiting blood sugar levels of +/-475 mg/dl by three months of age and increasing to +/- 517 mg/dl by five months. Five month old homozygous males do not exhibit hyperinsulinemia, however homozygous females reach levels of +/-540 uU/ml. Homozygous males do not survive beyond six months. (Leiter EH, et al, 1981) Because of the sterility of Leprdb homozygotes, misty has been incorporated into stocks for maintenance of the diabetes mutation. The repulsion double heterozygote (Leprdb +/+ m) facilitates identification of heterozygotes for breeding, while the coupling double heterozygote,
..... | ||
| 003589 | D.B/20Ei-Lama2dy-6J/J | Repository-Cryopreserved |
| Mice homozygous for the dystrophia-muscularis spontaneous mutations are characterized by progressive weakness and paralysis beginning at about 3 1/2 weeks of age. The hindlimbs are affected first, later the axial and forelimb musculature. Death usually occurs before 6 months of age, and mutant mice are usually sterile. Skeletal muscle shows degenerative changes with proliferation of sarcolemmal nuclei, increase in amount of interstitial tissue, and size variation among individual muscle fibers. In the dorsal and ventral roots of the peripheral nerves, both spinal and cranial, Schwann cells fail to separate and ensheathe axons so that groups of closely apposed naked axons, normally seen only in early stages, persist into adulthood. In the rest of the PNS, the basement membrane of Schwann cells is interrupted by gaps, the internodal gap in the nodes of Ranvier is lengthened, and there is delayed onset of myelination with fewer myelinated axons and shorter internode length. In an att
..... | ||
| 002922 | D2.HRS-Hrhr/J | Repository-Cryopreserved |
| 000681 | DW.C3-Mlph+ Pou1f1+/J | Repository-Cryopreserved |
| This DW/J congenic strain is wildtype for both the leaden (+Mlph-ln) and dwarf ( +Pit1-dw) mutations and thus serves as a control strain for DW/J-Pit1dw/+ Mlphln/Mlphln, Stock No. 000643. | ||
| 000673 | HRS/J | Repository-Cryopreserved |
| Mice homozygous for the hr spontaneous mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of stratified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. HRS/J mice, fed an ather
..... For more information please see the full descriiption on the strain data sheet | ||
| 001103 | HRS/J-Hrhr Esdb/+ Esdb/J | Repository-Cryopreserved |
| Mice homozygous for the hr mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of statified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. | ||
| 001200 | LLC.A/CkcJ | Repository-Cryopreserved |
| 004673 | NOD.129(B6)-Rag1tm1Mom Cd80tm1Shr/JbsJ | Repository-Cryopreserved |
| The NOD.129(B6)Rag1tm1MomCd80tm1Shr/JbsJ homozygous mice fail to produce T or B cells. Mice homozygous for both Rag1tm1Mom and Cd80tm1Shr are viable and fertile and exhibit no signs of diabetes due to the absence of lymphocytes. On the NOD background Cd80tm1Shr alone exacerbates diabetes onset when compared to standard NOD controls. When injected with proteolipid protein in Complete Freund's Adjuvant, NOD mice homozygous for the Cd80tm1Shr/JbsJ mutation alone develop similar though slightly milder, experimental autoimmune encephalomyelitis (EAE) when compared with NOD controls. NOD.129(B6)-Rag1tm1MomCd80tm1Shr/JbsJ are valuable for unraveling the co-stimulatory pathways of T cell activation as it relates to autoimmune diseases and organ transplantation. | ||
| 004222 | NOD.129P2(B6)-Il4tm1Cgn/DvsJ | Repository-Cryopreserved |
| Complete Freund's adjuvant (CFA) induced suppression of diabetes in NOD mice has been associated with a shift to Th2 cytokine production. NOD mice deficient in IL4 were created to investigate the role of IL4 in this shift. Mice homozygous for the Il4tm1Cgn targeted mutation are viable and fertile. T and B cell development is normal but IgG1and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced. IL4 deficient NOD mice develop IDDM with the same incidence as standard NOD/Lt controls, and there is no change between IL4 deficient and wildtype NOD in disease protection conferred by treatment of bacillus Calmette-Guerin vaccine (BCG) or CFA. Both IL4 deficient and wildtype NOD mice are significantly protected from insulitis by treatment of CFA but not by treatment of BCG. (Serreze et al 2001) | ||
| 004762 | NOD.129S4-Cd86tm1Shr/JbsJ | Repository-Cryopreserved |
| The NOD.129S4-Cd86tm1Shr/JbsJ homozygous mice fail to produce functional protein in T cells. Mice carrying this allele are protected from diabetes. Some homozygote mice have delayed onset peri-insulitis, which does not progress to severe insulitis. Beginning at 20 weeks of age, homozygous mice begin developing spontaneous autoimmune peripheral polyneuropathy marked by symmetrical mild hind limb paralysis. By 32 weeks of age 100% female and 30% males are severely affected with hind limb paralysis and moderate foreleg paralysis. Histological evaluation shows severe inflammation and mononuclear infiltrates in the peripheral nervous system. Skeletal muscle of severely affected mice showed focal neurogenic atrophy, but no cellular infitration. No detectable lesions were found in the brain or spinal cord. This phenotype has not been observed on C57BL/6 or 129 backgrounds (Salomon et al, 2001). NOD.129S4- Cd86tm1Shr /JbsJ provides a useful model for studyin
..... For more information please see the full descriiption on the strain data sheet | ||
| 003505 | NOD.B6-Prf1tm1Sdz/J | Repository-Cryopreserved |
| Mice homozygous for the Prf1tm1Sdz targeted mutation are viable and fertile. Homozygous mutant mice on an autoimmune type 1 diabetes prone NOD background have normal numbers of CD4- CD8+ T cells in the spleen. CD4- CD8- expressing T lymphocytes were also normal. NOD mice show a progressive infilitatraion of mononuclear cells into pancreatic islets beginning around 5 weeks of age. NOD wildtype and PRF1 deficient mice show similar development of insulititis. However, disease incidence was decreased from 77% in wildtype females to 16% in homozygotes. The onset of disease was also delayed from a median of 19 weeks to 39.5 weeks of age. These results show the importance of perforin-mediated cytotoxic T cells in development of autoimmune diabetes. (Kagi et al., 1994; Kagi et al., 1997.) | ||
| 004266 | NOD.Cg-Il10tm1Cgn/DvsJ | Repository-Cryopreserved |
| Mice homozygous for the Il10tm1Cgn targeted mutation are viable and fertile when housed under SPF conditions. This mutant develops type 1 diabetes at the same rate as the NOD/Lt parental strain. The Il10 tm1Cgn mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions. | ||
| 005273 | NOD.Cg-Rag1tm1Mom Cd86tm2Shr Cd80tm1Shr/JbsJ | Repository-Cryopreserved |
| Mice homozygous for the Cd80tm1Shr and Cd86tm2Shr mutations are deficient in both CD80 and CD86. NOD mice defiecient for CD80, CD86 and Rag1 are viable and fertile, fail to produce T or B cells, and exhibit no signs of diabetes due to the absence of lymphocytes. In an immunocompetent NOD background, the Cd86tm2Shr and Cd80tm1Shr mutations exacerbate diabetes onset as well as a variety of other autoimmune diseases including thyroiditis, sialitis, exocrine pancreas disease and neuropathy when compared to normal NOD controls. These mice have also been observed, by the donating investigator, to be Treg-deficient. NOD.129(B6)-Rag1tm1Mom Cd86tm2ShrCd80tm1Shr/JbsJ are valuable for unraveling the co-stimulatory pathways of T cell activation and Treg function as they relate to autoimmune diseases and organ transplantation. | ||
| 000266 | RHJ/Le | Repository-Cryopreserved |
| Rhino mice have spleen cells with a defective response to T-dependent antigens and they develop an autoimmune disease characterized by hypergammaglobulinemia, immunoglobulin deposits in basement membrane of skin, spleen, liver, and kidney, and presence of antinuclear antibodies which occur in young mice and increase with age. These mice have increased numbers of Thy1 positive epidermal dendritic cells. Like homozygous hairless mice, rhino mice are hairless by 5 weeks and their skin becomes wrinkled and thickened. | ||
| 002335 | SKH2/J | Repository-Cryopreserved |
| Mice homozygous for the hr spontaneous mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of stratified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. Black juvenile hair coa
..... For more information please see the full descriiption on the strain data sheet | ||
| 001253 | STOCK MitfMi-wh +/+ Wnt7apx/J | Repository-Cryopreserved |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. MIce homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a diluted coat color, light ears, a white belly spot, and in rare cases a dorsal spot. In addition, they display abnormalitites of both the cochlear and vestibular portions of the inner ear. Mice homozygous for the postaxial hemimelia spontaneous mutation (Wnt7apx) have skeletal defects of the forelimbs. Digits 5, 4, and sometimes 3, are missing and there is a reduction or absence of the ulna. There is always a large oval foramen in the scapula. The hindlimbs are usually unaffected, but digit 5 may be absent, and occasionally the fibula is r
..... For more information please see the full descriiption on the strain data sheet | ||
| 004964 | STOCK Sftpa1tm1Kor/J | Repository-Cryopreserved |
| 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 lung tissue from homozygous mice. Homozygotes are more susceptible (pneumonia and sepsis) to group B streptococcal, P. aeruginosa, and H. influenzae infections due to impaired bacteria clearance. Alveolar macrophages have impaired superoxide radical production. Administration of surfactant protein A increases phagocytosis of bacteria by macrophages. When experimentally infected with respiratory syncytial virus or influenza A, homozygotes have increased viral titer, pulmonary inflammatory cell infiltration and cytokine levels. This mutant mouse strain represents a model that may be useful in studies of host defense against respiratory pathogens and innate immune function.
In an attempt to offer alleles on well-characterized or mul
..... | ||
| 000302 | STOCK a/a MitfMi-wh +/+ Itpr1opt/J | Repository-Cryopreserved |
| Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a diluted coat color, light ears, a white belly spot, and in rare cases a dorsal spot. In addition, they display abnormalities of both the cochlear and vestibular portions of the inner ear. Mice homozygous for the opisthotonus spontaneous mutation (Itpr1opt) display a characteristic upward arching of head and tail. Homozygous mutant mice can be recognized at about 10 days of age by their loss of balance when standing or moving. Typical behavior of 15 to 20 day old homozygotes consists of falling over and struggling to get up. Agitation and s
..... For more information please see the full descriiption on the strain data sheet | ||
| 000147 | WLHR/LeJ | Repository-Cryopreserved |
| WLHR/Le is a balanced stock with wabbler-lethal (wl) and hairless (hr) spontaneous mutations maintained in repulsion on Chromosome 14. Homozygous wabbler-lethal mutant mice are first recognizable at 12 days of age and usually die at about four weeks. They have an abnormal wobbly gait and a pronounced tremor when walking. In an extensive study of behavioral development of this mutant, homozygous wabbler-lethal mice were shown to be deficient in nearly all behaviors tested. Histological examination showed myelin degeneration widely distributed throughout the CNS, particularly in the vestibulocerebellar and spinocerebellar systems. Electron microscopy showed widespread axonal (Wallerian) degeneration in the medulla with secondary myelin dissolution. Similar abnormalities were present to a lesser extent in the basal ganglia, spinal cord, and cerebellum and in the optic nerve. Homozygous hairless mutant mice have a higher incidence and earlier onset of leukemia, reducible by v
..... For more information please see the full descriiption on the strain data sheet | ||
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IMPORTANT NOTE: Price information is on the strain data sheet which can be viewed by clicking on the strain name.
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002574 | NOD.129P2(B6)-Il4tm1Cgn/Dvs | Research Strain |
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How to Register Interest
Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Under Development
Select the strain name to link to the strain data sheet.
New Strains Under DevelopmentThe Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
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It is VERY IMPORTANT that you register interest in strains Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.
- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
These strains are designated as: "Under Development for Distribution Colony"- Strains that will be made available through the Cryopreservation Repository.
These strains are designated as: "Under Development for Cryopreservation Repository"
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