Search Criteria: Strain Type is "Inbred Strain"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 001026 | BALB/cByJ | Level 1 |
| BALB/c mice are particularly well known for the production of plasmacytomas following injection with mineral oil, forming the basis for the production of monoclonal antibodies. Although not all BALB/c substrains have been examined for plasmacytoma induction, substrains derived from the Andervont (An) lineage (which includes BALB/cByJ) typically are susceptible, while those descended from BALB/cJ are resistant (see: Potter M ,1985). Mammary tumor incidence is normally low, but infection with mammary tumor virus by fostering to MMTV+ C3H mice dramatically increases tumor number and age of onset. BALB/c mice develop other cancers later in life including reticular neoplasms, primary lung tumors, and renal tumors. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in both BALB/cJ and BALB/cByJ substrains. BALB/cByJ has a deletion in the Qa2 subregion of the murine MHC. | ||
| 000651 | BALB/cJ | Level 1 |
| BALB/c mice are particularly well known for the production of plasmacytomas following injection with mineral oil forming the basis for the production of monoclonal antibodies. Although not all BALB/c substrains have been examined for plasmacytoma induction, substrains derived from the Andervont (An) lineage (which includes BALB/cByJ) typically are susceptible, while those descended from BALB/cJ are resistant (see: Potter M ,1985). Mammary tumor incidence is normally low but infection with mammary tumor virus by fostering to MMTV+ C3H mice dramatically increases tumor number and age of onset. BALB/c mice develop other cancers later in life including reticular neoplasms, primary lung tumors, and renal tumors. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in both BALB/cJ and BALB/cByJ substrains.
White et al. reported a variation in thioglycolate medium-induced peritoneal leukocyte recruitment in 4 analyzed s
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| 000659 | C3H/HeJ | Level 1 |
| C3H/HeJ mice are used as a general purpose strain in a wide variety of research areas including cancer, immunology and inflammation, sensorineural, and cardiovascular biology. C3H/HeJ mice and all other Jackson substrains are homozygous for the retinal degeneration 1 mutation (Pde6brd1), which causes blindness by weaning age. There is also a high incidence of hepatomas in C3H mice (reportedly 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females). Despite the lack of exogenous mouse mammary tumor virus (MMTV), virgin and breeding females may still develop some mammary tumors later in life. C3H/HeJ mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 00066
..... For more information please see the full phenotype on the strain data sheet | ||
| 000664 | C57BL/6J | Level 1 |
| C57BL/6 is the most widely used inbred strain. It is commonly used as a general purpose strain and background strain for the generation of congenics carrying both spontaneous and induced mutations. Although this strain is refractory to many tumors, it is a permissive background for maximal expression of most mutations. C57BL/6J mice are used in a wide variety of research areas including cardiovascular biology, developmental biology, diabetes and obesity, genetics, immunology, neurobiology, and sensorineural research. C57BL/6J mice are also commonly used in the production of transgenic mice. Overall, C57BL/6 mice breed well, are long-lived, and have a low susceptibility to tumors. Primitive hematopoietic stem cells from C57BL/6J mice show greatly delayed senescence relative to BALB/c and DBA/2J. This is a dominant trait. Other characteristics include: 1) a high susceptibility to diet-induced obesity, type 2 diabetes, and atherosclerosis; 2) a high incidence of microphthalmia and other a
..... For more information please see the full phenotype on the strain data sheet | ||
| 000656 | CBA/J | Level 1 |
| CBA/J inbred mice are widely used as a general purpose strain. CBA/J strain is the only CBA substrain that carries the Pde6brd1 mutation, which causes blindness by wean age. CBA/J mice are not histocompatible with the CBA/CaJ (Stock No. 000654) substrain (Green and Kaufer, 1965). The CBA/J inbred mouse strain is used to study granulomatous experimental autoimmune thyroiditis (G-EAT), are relatively resistant to diet-induced atherosclerosis (Paigen et al. 1990), and develop a mild hearing loss late in life, with most of the hearing loss occurring in the higher frequencies (Sweet et al. 1988). Renal tubulointerstitial lesions have been observed in this strain at a high frequency (Rudofsky 1978). Some CBA/J mice spontaneously develop exocrine pancreatic insufficiency syndrome (Eppig and Leiter 1977, Leiter et al. 1977). | ||
| 000671 | DBA/2J | Level 1 |
| DBA/2J is a widely used inbred strain that is valuable in a large number of research areas, including cardiovascular biology, neurobiology, and sensorineural research. Its characteristics are often contrasted with those of the C57BL/6J inbred strain (Stock No. 000664). DBA/2J mice show a low susceptibility to developing atherosclerotic aortic lesions (20 to 350 um2 atherosclerotic aortic lesions /aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). They also exhibit high-frequency hearing loss beginning roughly at the time of weaning/adolescence (between three to four weeks of age) and becoming severe by two to three months of age. This strain possesses three recessive alleles that cause progressive cochlear pathology initially affecting the organ of Corti. Decreasing anteroventral cochlear nucleus volume decreases and neuron loss parallel the progression of peripheral
..... For more information please see the full phenotype on the strain data sheet | ||
| 001800 | FVB/NJ | Level 1 |
| FVB/NJ was inbred for the Fv1b allele which confers sensitivity to the Friend leukemia virus B strain. Due to the prominent pronuclei in their fertilized eggs and the large litter size, FVB/NJ mice are commonly used for transgenic injection. Compared to many other inbred strains, FVB/NJ is highly susceptible to asthma-like airway responsiveness with significant generation of antigen-specific IgE. Despite having the H2q MHC haplotype, FVB/NJ are resistant to collagen-induced arthritis. This resistance stems from coding polymorphisms in Tcra-V11.1 and a genomic deletion of some Tcrb-V genes that includes Tcrb-V8.2. FVB/NJ have higher than average activity, anxiety, and basal body temperature, low stress-induced hyperthermia, and are homozygous for the Pde6brd1 allele, which results in early onset retinal degeneration. Although FVB/N typically do not develop spontaneous tumors, they are highly susceptible to chemic
..... For more information please see the full phenotype on the strain data sheet | ||
| 001976 | NOD/ShiLtJ | Level 1 |
| Diabetes in NOD/ShiLtJ mice is characterized by insulitis, a leukocytic infiltrate of the pancreatic islets. Marked decreases in pancreatic insulin content occur in females at about 12 weeks of age and several weeks later in males. Onset of diabetes is marked by moderate glycosuria and by a non-fasting plasma glucose higher than 250 mg/dl. Diabetic mice are hypoinsulinemic and hyperglucagonemic, indicating a selective destruction of pancreatic islet beta cells. Susceptibility to IDDM in NOD/ShiLtJ mice is polygenic, and environment, including housing conditions, health status, and diet, exerts a strong effect on penetrance. NOD/ShiLtJ females are more widely used than males because the onset of IDDM symptoms occurs earlier and with a higher incidence (90-100% by 30 weeks of age). NOD/ShiLtJ males develop IDDM at a frequency of between 40-60% by 30-40 weeks of age. Male mice are useful for certain applications, including pharmaceutical studies, "accelerated transfer" of IDDM, and some <
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..... For more information please see the full phenotype on the strain data sheet | ||
| 002448 | 129S1/SvImJ | Level 2 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains.(1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently, 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997.
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| 000691 | 129X1/SvJ | Level 2 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson et al. 1997.
In response to challenge, 129S1/SvImJ mice develop immune-mediated nephritis characterized by proteinuria, glomeru
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| 000646 | A/J | Level 2 |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to cortisone-induced congenital cleft palate. It has a high incidence of spontaneous lung adenomas, and lung tumors readily develop in response to carcinogens. A high percentage of mammary adenocarcinomas (a large proportion of acinar-type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. A/J mice fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid, and 15% fat) fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/c
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| 000648 | AKR/J | Level 2 |
| Originally inbred at the Rockefeller Institute, AKR mice are widely used in cancer research for their high leukemia incidence (60-90%) and in immunology as a source of the Thy1.1 (theta AKR) antigen. AKR/J mice are viremic from birth, and express the ecotropic retrovirus AKV in all tissues. The hair interior defect (hid) mutation, a strain characteristic of AKR mice, causes alterations in hair development that is only evident microscopically. Adrenocortical lipid depletion (ald) in AKR mice is caused by a mutation in sterol O-acyltransferase 1 (Soat1), and leads to a truncated SOAT1 protein. AKR/J mice are relatively resistant to aortic lesion formation on a semi-synthetic high fat diet and are hyporesponsive to diets containing high levels of fat and cholesterol. | ||
| 000635 | C3H/HeOuJ | Level 2 |
| C3H/HeOuJ mice are used as a general purpose strain in a wide variety of research areas including cancer and sensorineural, research. C3H/HeOuJ mice and all other C3H substrains at The Jackson Laboratory are homozygous for the retinal degeneration 1 mutation (Pde6brd1), causing blindness by weaning age. There is also a high incidence of hepatomas in C3H mice (reportedly 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females). Despite the lack of exogenous mouse mammary tumor virus (MMTV), virgin and breeding females may still develop some mammary tumors later in life. | ||
| 000658 | C3HeB/FeJ | Level 2 |
| 000665 | C57BL/10J | Level 2 |
| C57BL/10J is a substrain of C57BL, and shares a common origin with C57BL/6J (Stock No. 000664), which is one of the most widely used inbred strains. Coat color is black (non-agouti), a/a. The C57BL/10J substrain is similar to the C57BL/6J substrain, but allelic variants have been described at the H9, Igh2 and Lv loci. C57BL/10J mice have a long life-span (826 +/-29 days in males, 693 +/- 31 days in females). Overall tumor incidence is 33% in males and 31% in females, most of which is due to lymphoma. C57BL/10J mice are prone to dermatitis, which is a common problem in the C57BL strain. C57BL/10J mice are a valuable immunological research tool. They have a high lymphocyte phytohaemagglutinin response, a good immune response to ovalbumin, a poor response to DNP-keyhole limpet haemocyanin and are resistant to induction of passive cutaneous anaphylaxis (IgG1- and IgE- mediated). They are susceptible
..... 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. | ||
| 000654 | CBA/CaJ | Level 2 |
| The CBA inbred strain was initially bred for longevity and a low incidence of spontaneous mammary tumors (compared with C3H). Burdette and Strong reported that CBA mice were comparatively susceptible to tumor induction after a single subcutaneous injection of methylcholanthrene. The tumor types identified in this early work in CBA mice included spindle cell sarcoma, rhabdomyosarcoma, and epidermoid carcinoma. Strong and Smith reported finding benign hepatomas in aging CBA mice. Several groups confirmed this finding, and the majority of studies found a higher frequency of spontaneous hepatomas in males than in females.
CBA/Ca mice are commonly used for leukemogenesis research because this strain has a low spontaneous incidence of leukemia but has a relatively high inducibility of myeloid leukemia in response to benzene and radiation exposure. Multiple reports using CBA, its F1 hybrids, and other strains, have indicated that deletions in a specific segment of chromosome 2 are linked
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| 000670 | DBA/1J | Level 2 |
| DBA/1J mice are widely used as a model for rheumatoid arthritis: immunization with type II collagen leads to the development of severe polyarthritis mediated by an autoimmune response. The incidence of collagen induced arthritis varies by experimental protocol, but is less than 100%. Similar to the human condition, mice with collagen-induced arthritis display synovitis and erosions of cartilage and bone. In addition, susceptibility in both humans and mice is linked to the expression of specific MHC class II molecules. DBA/1J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions on an atherogenic diet. In response to challenge, DBA/1J mice develop immune-mediated nephritis characterized by proteinuria, glomerulonephritis and tubulointerstitial disease (Xie et al., 2004). | ||
| 001140 | DBA/1LacJ | Level 2 |
| Historical reports indicate DBA/1J and DBA/1LacJ mice immunized with type II collagen develop a severe polyarthritis mediated by an autoimmune response. Recent in-house studies suggest that the response to collagen induction in the DBA/1LacJ strain is not as robust as indicated by earlier studies. Arthritis models such as B10.RIII-H2r H2-T18b/(71NS)SnJ (Stock No. 000457) and BUB/BnJ (Stock No. 000653) can be used as alternatives to DBA/1LacJ. Similar to the human condition, mice with collagen-induced arthritis display synovitis and erosions of cartilage and bone. In addition, susceptibility in both humans and mice is linked to the expression of specific MHC class II molecules. DBA/1 mice show a low susceptibility to developing atherosclerotic aortic lesions (20 to 350 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on a
..... For more information please see the full phenotype on the strain data sheet | ||
| 000486 | MRL/MpJ | Level 2 |
| The MRL/MpJ mice are large but docile to the point that males rarely fight. They are the parent and control strain for for MRL/MpJ-Faslpr (Stock Nos. 000485, 006825). Despite carrying the normal Fas gene, MRL/MpJ mice also exhibit autoimmune disorders, but symptoms are manifested much later in life compared to those the MRL/MpJ-Faslpr mice. Starting at about three months of age, levels of circulating immune complexes rise greatly in the MRL-Faslpr mouse but not in the wildtype control, MRL/MpJ. Also beginning at 3 months Faslpr mice exhibit very severe poliferative glomerulonephritis, whereas in the MRL/MpJ controls usually only mild glomerular lesions are detected. MRL/MpJ inbred female typically die at 73 weeks of age and males die at 93 weeks. This compares to a lifespan of 17 weeks in the female and 22 weeks for males in the mouse homozygous for Faslpr. See MRL/MpJ-Faslpr<
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..... For more information please see the full phenotype on the strain data sheet | ||
| 000686 | SJL/J | Level 2 |
| SJL mice display a very high incidence of reticulum cell sarcomas resembling Hodgkin's disease by approximately one year of age. Sarcomas first appear in the Peyer's patches and mesenteric lymph nodes and later in the spleen, liver, thymus and other lymph nodes. Most of the tumors are mixed-cell types classified as type B reticulum cell neoplasms, but a few are type A histiocytomas. This strain is also characterized by extreme aggression in males and its susceptibility to experimental autoimmune encephalomyelitis (EAE) for multiple sclerosis research. SJL/J mice develop a spontaneous myopathy resulting from a splice-site mutation in the Dysferlin gene. This Dysfim allele has been shown to result in decreased levels of dysferlin protein in SJL/J mice and makes this strain a good model for limb girdle muscular dystrophy 2B. This spontaneous myopathy is characterized by a progressive loss of muscle mass and strength corresponding with an increase in muscle pathology incl
..... For more information please see the full phenotype on the strain data sheet | ||
| 005314 | TALLYHO/JngJ | Level 2 |
| TALLYHO mimics many characteristics of human non-insulin-dependent type 2 diabetes mellitus (NIDDM). Male TallyHo mice develop hyperglycemia, hyperinsulinemia, hyperlipidemia, moderate obesity, and enlargement of the islets of Langerhans. Onset of hyperglycemia is delayed compared to ob/ob (B6.V-Lepob) and db/db (BKS.Cg- m +/+ Leprdb) mice beginning between 10 and 14 weeks of age. Female mice display moderate hyperinsulinemia, hyperlipidemia, and obesity but do not manifest overt diabetes (i.e. hyperglycemia). Chromosomal mapping identified a major diabetes susceptibility locus on Chr 19, designated Tanidd1 for TH-associated NIDDM. Breeding and mapping data suggest Tanidd1 is a single recessively inherited gene primarily responsible for the hyperglycemia phenotype in TALLYHO mice. Tanidd1 interacts with other loci including Tanidd2 on Chr 13, Tanidd3 on Chr 15, Tabw (TallyHo-associa
..... For more information please see the full phenotype on the strain data sheet | ||
| 000666 | C57BL/10SnJ | Level 3 |
| C57BL/10SnJ is a substrain of C57BL, which is one of the most widely used inbred strains. Coat color is black (non-agouti) a/a. C57BL/10SnJ are similar to other C57BL substrains. | ||
| 000662 | C57BLKS/J | Level 3 |
| Although C57BLKS/J is estimated to have more than 70% of its genome derived from C57BL/6J, these strains are phenotypically distinct. Diet-induced atherosclerotic lesions are much more severe in C57BLKS/J than in C57BL/6J or many other inbred strains. Compared with a panel of inbred strains, C57BLKS/J was found to have low total cholesterol and low HDL cholesterol when fed a normal diet and high total cholesterol and HDL cholesterol in an atherogenic diet. Paigen et al. found high levels of plasma bile salts in C57BLKS/J females after eight weeks on an atherogenic diet. The mutations diabetes (Leprdb) and obese (Lepob) each express a much more severe phenotype on the C57BLKS/J background than on the C57BL/6J background. The Cpefat mutation causes severe obesity, hyperinsulinemia, and hyperglycemia on the C57BLKS/J background rather than the hyperinsulinemia, and mild obesity without hyperglycemia found on the HRS/J background
..... For more information please see the full phenotype on the strain data sheet | ||
| 000928 | CAST/EiJ | Level 3 |
| 000676 | LP/J | Level 3 |
| LP/J mice display a high susceptibility to audiogenic seizures. This strain is also reported to have a fairly high incidence of tumors that develop later in life, including mammary tumors, lymphoma, lung and soft-tissue sarcomas. LP/J mice are also homozygous for the spontaneous mutation piebald in the endothelin receptor type B gene (Ednrbs). The piebald spontaneous mutation is the result of a mutation in the endothelin receptor type B gene, Ednrb. Mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. They also have dark eyes. The white areas of the coat are completely lacking in neural crest-derived melanocytes, and there is a reduction in the number of melanocytes in the choroid layer of the eye is reduced. | ||
| 002423 | NON/ShiLtJ | Level 3 |
| Although closely related to NOD mice, NON mice contain a diabetes resistant MHC haplotype (H2nb1 = Kb, Anb1, Ek, Db). The name was derived from "Non-Obese Non-diabetic"; however, NON/ShiLtJ mice should not be considered "normal." They carry the retinal degeneration (Pde6b) mutation and exhibit certain tendencies toward autoimmune disease. This strain maintains a low plasma insulin level, which may account in part why certain loci from NON/ShiLt can enhance development of autoimmune type 1 diabetes in segregating hybrid mice following outcross to NOD/ShiLtJ. The NON strain-characteristic immunologic abnormalities include perivascular/periductular leukocyte infiltration into the pancreas and submandibular salivary glands, and T lymphocytopenia evident by 20 weeks of age in spleen. NON/ShiLt mice clearly harbor genes predisposing to type 2 diabetes, as evidenced by early impaired glucose tolerance in males and females, d
..... For more information please see the full phenotype on the strain data sheet | ||
| 002019 | NU/J | Level 3 |
| 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 d
..... For more information please see the full phenotype on the strain data sheet | ||
| 000680 | PL/J | Level 3 |
| PL/J mice show a moderate susceptibility to experimental allergic encephalitis (EAE) with late onset and high mortality. Reports of leukemia incidence vary from 50% in females and 19% in males to 80-90%. In addition to a low threshold to electroconvulsive seizures, PL/J mice are susceptible to handling and rhythmic tossing-induced seizures (Kitami et al. 2004). | ||
| 000689 | SWR/J | Level 3 |
| SWR/J mice are used widely in research as a general purpose strain. Aging mice exhibit a high incidence of lung and mammary gland tumors. They also develop extreme polydipsia and polyuria (nephrogenic diabetes insipidus) with increasing age. SWR/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE). Germline deletion of about 50% of T-cell receptor V beta-chain gene segments and a T-cell receptor V alpha polymorphism are responsible for the resistance of SWR/J mice to collagen type II-induced arthritis. SWR/J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions (1670 to 1690 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). SWR/J mice have been recommended for generation and propogation of transgenic mice because they are high responders to exogenous hormones, have large and prominant pronuclei with good resistance to l
..... For more information please see the full phenotype on the strain data sheet | ||
| 000690 | 129P3/J | Level 4 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently, 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson et al. 1997. | ||
| 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). | ||
| 000668 | C57L/J | Level 4 |
| C57L/J mice are used widely in research as a general purpose strain. Mice have a high incidence of Hodgkin's-like reticulum cell neoplasm at 18 months of age and pituitary tumors in old multiparous females. C57L/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE). In addition, C57L/J mice are highly susceptible to developing atherosclerotic aortic lesions (4500 to 8000 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat) (Paigen et al. 1990). On a lithogenic diet, C57L/J mice develop gallstones as a result of abnormal regulation of cholesterol synthesis (Xua et al. 2004). C57L/J mice carry no detectable endogenous ecotropic MuLV DNA sequences. | ||
| 002050 | NOR/LtJ | Level 4 |
| NOR/LtJ mice are insulitis resistant and diabetes free. NOR/LtJ mice still exhibit peripheral T-lymphocyte accumulation and defective peritoneal macrophage responses characteristic of NOD/LtJ mice. NOR/ShiLtJ mice are matched at the diabetogenic H2g7 complex to NOD/ShiLtJ. | ||
| 001058 | NZW/LacJ | Level 4 |
| NZW mice have a normal lifespan but do develop anti-DNA antibodies, high serum levels of retroviral gp70 antigen, and nephritis later in life. F1 hybrids of NZB/BlNJ and NZW/LacJ (Stock No. 100008) are widely used as a model for autoimmune disease resembling human systemic lupus erythematosus. | ||
| 000726 | RBF/DnJ | Level 4 |
| The RBF inbred strain arose from crosses with wild mice, originally known as "tobacco mouse", captured in Valle di Poschiavo in S.E. Switzerland. The wild mice originally known as 'tobacco mouse' because of the coat colour. The strain was transferred to Dr. M. Davisson (Dn) in 1981 and subsequently to the production colony of The Jackson Laborotory (J). Mice are homozygous for Robertsonian translocation Rb(1.3)1Bnr, Rb(8.12)5Bnr and Rb(9.14)6Bnr. This strain is useful for production of antibody producing hybridomas. | ||
| 000687 | SM/J | Level 4 |
| SM/J mice carry a number of rare polymorphic alleles and are often matched to LG/J (Stock No. 000675), A/J (Stock No. 000646) or NZB/BINJ (Stock No. 000684) for quantitative trait locus analysis. These mice are susceptible to diet-induced obesity and diet-induced atherosclerosis. SM/J mice exhibit a hyperresponsiveness to B cell mitogens (Clark et al. 1981, Engel et al. 1981). A point mutation in Neu1 is responsible for a partial deficiency of lysosomal neuraminadase and may explain the altered immune response (Rottier et al. 1998). Small in size at birth and through weaning, SM/J mice attain a normal body weight as they age. | ||
| 001137 | 129P1/ReJ | Repository- Live |
| For a complete history of the numerous 129 substrains please refer to Simpson, et al., 1997. Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. Most recently 129 mice are widely used strain in the production of targeted mutations due to the availability of several lines of embryonic stem cells. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of substrains into three major groups: parental substrains, steel substrains and "ter" substrains. Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. | ||
| 002065 | 129T2/SvEmsJ | Repository- Live |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997. | ||
| 000645 | A/HeJ | Repository- Live |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to induction of congenital cleft palate by cortisone. It has a high incidence of spontaneous lung adenomas and lung tumors readily develop in response to carcinogens. High percentage of mammary adenocarcinomas (a large proportion acinar type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. A small percent (4%) of nonproductive males are hermaphrodites. An additional 17% of nonproductive males have abnormally small testes containing no sperm. | ||
| 000647 | A/WySnJ | Repository- Live |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to induction of congenital cleft palate by cortisone. It has a high incidence of spontaneous lung adenomas and lung tumors readily develop in response to carcinogens. High percentage of mammary adenocarcinomas (a large proportion acinar type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. Unlike A/J mice, A/WySnJ mice carry a spontaneous mutation in Tnfrsf13c and exhibit a significant loss of mature B cells (Miller, et al., 1991, Lentz et al., 1996, Shulga-Morskaya et al., 2004). | ||
| 000199 | AEJ/GnLeJ | Repository- Live |
| 003070 | ALR/LtJ | Repository- Live |
| ALS/LtJ (Stock No. 003072) and ALR/LtJ inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. ALR/LtJ mice are of particular interest to investigators studying the immunogenetics of NOD/ShiLtJ mice in that the ALR/LtJ MHC haplotype (H2gx) is a variant of the diabetogenic NOD H2g7 haplotype. The (H2gx) haplotype is identical to the H2g7 haplotype from the H2-K end of the complex through the class II and class III region distal to Hsp70. However, at the distal H2-D end of the complex, ALR/LtJ mice have a rare H2-Dgx allele. Despite the
..... For more information please see the full phenotype on the strain data sheet | ||
| 003072 | ALS/LtJ | Repository- Live |
| ALS/LtJ and ALR/LtJ (Stock No. 003070) inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. By 34 weeks of age, both untreated ALS/Lt and ALR/Lt males fed a 6% fat-containing chow diet attain a mean body weight of around 50 grams. Genome wide scan comparison shows that ALS/LtJ mice are more closely related to NON/ShiLtJ mice (they share the H2nb1 haplotype) than to NOD/ShiLtJ. Like two other ICR-derived inbred strains selected in Japan (NON and NSY), alloxan-untreated ALS/Lt males exhibit impaired glucose tolerance when tested by intraperitoneal administration of glucose. However, unlike NON/ShiLt males
..... For more information please see the full phenotype on the strain data sheet | ||
| 003005 | BPH/2J | Repository- Live |
| The hypertensive BPH/2 mice have elevated systolic blood pressures at five weeks and by 150 days differ from the BPL/1 by 60 mmHg. The BPH/2 strain has a higher heart rate, larger hearts and kidneys, and higher hematocrits than the BPL/1. It also has lower renin, aldosterone and angiotensin I levels compared to the BPL/1 and BPN/3. The original HBP (high blood pressure) and LBP (low blood pressure) selected lines showed a number of biochemical and physiological differences which have not been reexamined in the inbred strains. These include differences in brain catecholamines, calmodulin concentrations, heat sensitivity, alcohol preference, and longevity. The differences in longevity were striking. The hypotensive selected lines lived two to three hundred days longer, on average, than the hypertensive selected line. Biometrical genetic analysis suggested that three to five genes are responsible for the difference in blood pressure between the BPH/2 and BPL/1. A recent genome scan of an
..... For more information please see the full phenotype on the strain data sheet | ||
| 003006 | BPL/1J | Repository- Live |
| The hypertensive BPH/2 mice (Stock No. 003005) have elevated systolic blood pressures at five weeks and by 150 days differ from the BPL/1 by 60 mmHg. The BPH/2 strain has a higher heart rate, larger hearts and kidneys, and higher hematocrits than the BPL/1. It also has lower renin, aldosterone and angiotensin I levels compared to the BPL/1 and BPN/3 (Stock No. 003004). The original HBP (high blood pressures) and LBP (low blood pressure) selected lines showed a number of biochemical and physiological differences which have not been reexamined in the inbred strains. These include differences in brain catecholamines, calmodulin concentrations, heat sensitivity, alcohol preference, and longevity. The differences in longevity were striking. The hypotensive selected lines lived two to three hundred days longer, on average, than the hypertensive selected line. Biometrical genetic analysis suggested that three to five genes are responsible for the difference in blood pressure between the BPH/2
..... For more information please see the full phenotype on the strain data sheet | ||
| 003004 | BPN/3J | Repository- Live |
| The normotensive BPN/3 inbred strain serves as a control for the high blood pressure (BPH/2, Stock No. 003005) and low blood pressure (BPL/1, Stock No. 003006) inbred strains BPH/2 mice have elevated systolic blood pressures at five weeks and by 150 days differ from the BPL/1 by 60 mmHg. The BPH/2 strain has a higher heart rate, larger hearts and kidneys, and higher hematocrits than the BPL/1. It also has lower renin, aldosterone and angiotensin I levels compared to the BPL/1 and BPN/3. The original HBP (high blood pressure) and LBP (low blood pressure) selected lines showed a number of biochemical and physiological differences which have not been reexamined in the inbred strains. These include differences in brain catecholamines, calmodulin concentrations, heat sensitivity, alcohol preference, and longevity. The differences in longevity were striking. The hypotensive selected lines lived two to three hundred days longer, on average, than the hypertensive selected line. Biometrical ge
..... For more information please see the full phenotype on the strain data sheet | ||
| 000653 | BUB/BnJ | Repository- Live |
| BUB/BnJ mice carry a specific T cell receptor V beta mutation, making this strain highly susceptible to collagen-induced arthritis. This T cell receptor V beta restriction works in concert with other uncharacterized modifying genes present in BUB/BnJ mice. BUB/BnJ mice carry no detectable endogenous ecotropic MuLV DNA sequences. Mice are also reported to have high serum complement activity. In response to challenge, BUB/BnJ mice develop immune-mediated nephritis characterized by proteinuria, glomerulonephritis and tubulointerstitial disease (Xie et al., 2004). BUB/BnJ mice are homozygous for the Mass1frings allele (monogenic, audiogenic seizure susceptibility 1) and are susceptible to audiogenic seizures prior to 25 days of age (Skradski, et al 2001). In addition, the Mass1frings allele acounts for early onset hearing impairment by 3-4 weeks of age (Johnson KR, et al 2005). | ||
| 000661 | C3H/HeSnJ | Repository- Live |
| 003752 | C57BL/10ScNJ | Repository- Live |
| The breeder pair of C57BL/10ScN mice, obtained from NIH, that were the progenitors of all mice of this strain at The Jackson Laboratory were tested by PCR analysis for the spontaneous Il12rb2 mutation described by Poltorak et al. (J. Immunol. 167:2106-2111, 2001) and found to carry only the wild type Il12rb2 allele. C57BL/10ScN mice have a deletion of the Tlr4 gene that results in absence of both mRNA and protein and thus in defective response to LPS stimulation. Tlr4lps-del differs from the Tlr4Lps-d mutation of C3H/HeJ mice, a point mutation that causes an amino acid substitution. The allele for normal LPS response, Tlr4lps-n, occurs in most other C3H and C57BL/10 substrains and most other mouse strains. | ||
| 000476 | C57BL/10ScSnJ | Repository- Live |
| C57BL/10ScSn is a substrain of C57BL, which is one of the most widely used inbred strains. Coat color is black (non-agouti) a/a. The C57BL/10ScSn substrain was separated from the C57BL/10J substrain at F26, when it was transferred to J.P. Scott. At F35-36, it was transferred to George Snell, thus acquiring the informal designation "Scotty Snell" or "Scott Snells". C57BL/10ScSn mice have low brain glutamic acid decarboxylase. Except for this and some minor behavioral differences, they are similar to the C57BL/10J substrain. | ||
| 001139 | C57BL/6ByJ | Repository- Live |
| 5 SNP differences have been identified that distinguish C57BL/6J from C57BL/6ByJ and C57BL/6NJ. Both C57BL/6ByJ and C57BL/6NJ type as follows: 08-015199792-M is C; 11-004367508-M is A; 13-041017317-M is C; 15-057561875-M is G; 19-049914266-M is T. C57BL/6J types as follows: 08-015199792-M is T; 11-004367508-M is G; 13-041017317-M is T; 15-057561875-M is A; 19-049914266-M is G (Petkov and Wiles, 2005.) | ||
| 000924 | C57BL/6JEiJ | Repository- Live |
| 005304 | C57BL/6NJ | Repository- Live |
| This is an NIH subline of C57BL/6. It was separated from C57BL/6J in 1951. 5 SNP differences have been identified that distinguish C57BL/6J from C57BL/6ByJ and C57BL/6NJ. Both C57BL/6ByJ and C57BL/6NJ type as follows: 08-015199792-M is C; 11-004367508-M is A; 13-041017317-M is C; 15-057561875-M is G; 19-049914266-M is T. C57BL/6J types as follows: 08-015199792-M is T; 11-004367508-M is G; 13-041017317-M is T; 15-057561875-M is A; 19-049914266-M is G (Petkov and Wiles 2005.) This strain does not have the deletion in the Nnt gene that has been found in the C57BL/6J strain (Stock No. 000664). | ||
| 000667 | C57BR/cdJ | Repository- Live |
| C57BR/cdJ mice develop early-onset hearing loss that is moderate at seven weeks of age, is severe by 20 weeks and progresses with increasing age (Henry 1982; Zheng et al. 1999). The loss is greatest in the higher frequency range; at seven weeks, Henry reported 50% of the mice showed no 64 kHz auditory brainstem response (ABR), and by 100 days both the 2 kHz and 32 kHz responses were absent. Both labs found this strain to be least vulnerable to loss of the16 kHz response, which persisted through 200 days but was lost before 300 days of age (Henry 1982). C57BR/cdJ did not exhibit aberrant ABR wave patterns, suggesting that the hearing loss results from defects of the peripheral, rather than central auditory system (Zheng et al. 1999). F1 hybrid progeny from matings with the good-hearing strain CAST/Ei exhibited good hearing even at advanced ages, indicating that the allele(s) responsible for hearing loss in C57BR/cdJ are recessive. An allelism test between C57BR/cdJ and NOD
..... For more information please see the full phenotype on the strain data sheet | ||
| 000669 | C58/J | Repository- Live |
| This strain was developed by MacDowell in 1921 from litter mates 58 and 52 of Miss Lathrop's stock. A mating of the same male but a different female gave rise to the commonly used C57BL group of strains. C58/J mice exhibit a high incidence of leukemia (>90% by one year of age). C58/J mice also exhibit an intermediate susceptibility to developing atherosclerotic aortic lesions (1670 to 1690 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). | ||
| 001489 | CALB/RkJ | Repository- Live |
| 000926 | CAROLI/EiJ | Repository- Live |
| 001143 | CBA/CaGnLeJ | Repository- Live |
| 006177 | CD3/JlsJ | Repository- Live |
| Swiss derived CD-1 mice are less responsive to exogenous estradiol than most inbred strains as measured by resistance to decreases in testes weight, spermatogenesis, and spermatid development. Derived from CD-1, the inbred strains CD3/JlsJ, CD7/JlsJ, and CD9/JlsJ mice exhibit a moderate sensitivity to endocrine disruption by estradiol, while CD10/JlsJ mice are highly resistant to endocrine disruption by estradiol. All lines generated in the selection program are significantly less responsive to estradiol than C57BL/6 mice. The selectively bred strains CD3/JlsJ (006177), CD7/JlsJ (006178), CD9/JlsJ (006179) and CD10/Jls (006180) may serve as tools for mapping and characterizing genes responsible for estradiol sensitivity.
SNP data is available for this stra
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| 006178 | CD7/JlsJ | Repository- Live |
| Swiss derived CD-1 mice are less responsive to exogenous estradiol than most inbred strains as measured by resistance to decreases in testes weight, spermatogenesis, and spermatid development. Derived from CD-1, the inbred strains CD3/JlsJ, CD7/JlsJ, and CD9/JlsJ mice exhibit a moderate sensitivity to endocrine disruption by estradiol, while CD10/JlsJ mice are highly resistant to endocrine disruption by estradiol (personal communication). All lines generated in the selection program are significantly less responsive to estradiol than C57BL/6 mice.
The selectively bred strains CD3/JlsJ (Stock No. 006177), CD7/JlsJ (Stock No. 006178), CD9/JlsJ (Stock No. 006179) and CD10/Jls (Stock No. 006180) may serve as tools for mapping and characterizing genes responsible for
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| 006179 | CD9/JlsJ | Repository- Live |
| Swiss derived CD-1 mice are less responsive to exogenous estradiol than most inbred strains as measured by resistance to decreases in testes weight, spermatogenesis, and spermatid development. Derived from CD-1, the inbred strains CD3/JlsJ, CD7/JlsJ, and CD9/JlsJ mice exhibit a moderate sensitivity to endocrine disruption by estradiol, while CD10/JlsJ mice are highly resistant to endocrine disruption by estradiol (personal communication). All lines generated in the selection program are significantly less responsive to estradiol than C57BL/6 mice.
The selectively bred strains CD3/JlsJ (Stock No. 006177), CD7/JlsJ (Stock No. 006178), CD9/JlsJ (Stock No. 006179) and CD10/Jls (Stock No. 006180) may serve as tools for mapping and characterizing genes responsible fo
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| 000657 | CE/J | Repository- Live |
| CE/J mice are resistant to amyloid induction and development of amyloidosis. Amyloidosis is the extracellular deposition of the acute phase protein 'serum amyloid A' (SAA), which is induced in response to inflammation. CE/J mice express a single isoform of SAA designated SAA2.2, which is structurally unable to form amyloid fibrils. Viral expression of amyloidogenic proteins in CE/J mice does result in amyloid depostion, making this a useful model to examine the amyloid deposition potential of altered SAA proteins. Early studies by Dr. Margaret Dickie reported that approximately 1/3 of CE females and of reciprocal DBA x CE F1 hybrids were found to have ovarian tumors at 20 months of age. Virgin reciprocal DBA x CE F1 hybrids were found to develop hyperplasia of the uterus and an increased uterine sensitivity to estrogen that increases with age. This pathology results from a hormonal imbalance characteristic of this F1 cross and breeding the female can ameliorate this trait.<
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| 002799 | CZECHI/EiJ | Repository- Live |
| This strain has a coat color mutation which results in heightened agouti yellow pigment. This mutation has not yet been characterized in detail. | ||
| 001144 | CZECHII/EiJ | Repository- Live |
| 002243 | DDY/JclSidSeyFrkJ | Repository- Live |
| 000804 | HPG/BmJ | Repository- Live |
| Mice homozygous for the hypogonadal mutation (Gnrh1hpg) are characterized by an overall underdevelopment of the reproductive tract. Male mice have a small penis and scrotum and a short ano-genital distance. All male reproductive organs are present but are immature. The testes are small and undescended. Spermatogenesis is arrested, usually by the diplotene stage. The vagina of female mice does not open fully, the uterus is thread-like, and the ovaries are very small. Homozygous mutant mice are deficient in LH, FSH, and gonadal steroids. They also exhibit aberrant PRL secretion patterns. Both sexes are sterile although fertility can be restored with hormone replacement. | ||
| 000674 | I/LnJ | Repository- Live |
| I/LnJ mice were originally derived by Dr. LC Strong in 1926 from an unpedigreed stock of mice. A high proportion of mice from this strain lack a corpus callosum. This absence is associated with slow growth of the medial septum subadjacent to the cavum septi. The reproductive performance of I/LnJ mice is very poor. Further analysis indicates that oocytes from I/LnJ mice display retarded kinetics of meiotic maturation and a high frequency of metaphase I arrest. Some oocytes fail to resume meiosis. Oocytes have many very small centrosomes with an absence of microtubules. I/LnJ mice, in addition to carrying several other coat color alleles, are homozygous for the piebald mutation (Ednrbs). The piebald spontaneous mutation is the result of a mutation in the endothelin receptor type B gene, Ednrb. Mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. They also have dark eyes. The white areas of the coat are complet
..... For more information please see the full phenotype on the strain data sheet | ||
| 003720 | JF1/Ms | Repository- Live |
| 002106 | KK/HlJ | Repository- Live |
| KK/HlJ male mice exhibit diabetic symptoms that includes hyperglycemia, hyperinsulinemia, and insulin resistance. This strains serves as a model of noninsulin dependent diabetes mellitus, type 2. | ||
| 002798 | LEWES/EiJ | Repository- Live |
| 000675 | LG/J | Repository- Live |
| LG/J mice develop antinuclear antibodies and rheumatoid factor as well as renal disease characterized by glomerulonephritis, interstitial nephritis, and perivasculitis (Peng et al., 1996). LG/J was the predominant strain used to develop the MRL/LpJ (Stock No. 000486) inbred strain, a model for autoimmunity. LG/J mice are often compared to SM/J (Stock No. 000687) for quantitative trait locus analysis in the areas of atherosclerosis, obesity, and mandible size . These mice are susceptible to diet-induced obesity and diet-induced atherosclerosis. | ||
| 000677 | MA/MyJ | Repository- Live |
| A characteristic of MA/MyJ is the spontaneous mutation hf (hepatic fusion), which results in varying degrees of fusion in the hepatic lobes. | ||
| 000734 | MOLD/RkJ | Repository- Live |
| A 7 base pair deletion was reported in the Cd4 5' untranslated region of Stock No. 000550, MOLF/EiJ (Wade et al. 1993, Capparelli et al, 2004). Subsequent testing at The Jackson Laboratory indicated that MOLC/EiJ, MOLD/EiJ and MOLG/EiJ also carry the variant sequence. The deletion is not believed to affect expression. | ||
| 000550 | MOLF/EiJ | Repository- Live |
| A 7 base pair deletion was reported in the Cd4 5' untranslated region of MOLF/EiJ (Wade et al. 1993, Capparelli et al. 2004). Subsequent testing at The Jackson Laboratory indicated that MOLC/EiJ, MOLD/EiJ and MOLG/EiJ also carry the variant sequence. The deletion is not believed to affect gene expression. | ||
| 000555 | MOLG/DnJ | Repository- Live |
| A 7 base pair deletion was reported in the Cd4 5' untranslated region of Stock No. 000550, MOLF/EiJ (Wade et al., 1993, Capparelli et al., 2004). Subsequent testing at The Jackson Laboratory indicated that MOLC/EiJ, MOLD/EiJ and MOLG/EiJ also carry the variant sequence. The deletion is not believed to affect expression. | ||
| 003719 | MSM/Ms | Repository- Live |
| This strain has been reported to be resistant to the development of lymphoma, due to at least two loci in crosses involving strain SL/Kh (Pataer et. al., 1996). C3HxMSM F1 hybrids treated with N-methyl-N-nitrosourea (MNU) develop squamous cell carcinomas of the forestomach with about 20% and 15% having mutations in H-ras and p53, respectively (Masui et. al., 1997). | ||
| 005067 | NZL/LtJ | Repository- Live |
| Male NZL/LtJ mice develop juvenile-onset obesity and maturity-onset hyperglycemia (McInerney MF, et al., 2004). Over 90% of males exhibit hyperglycemia of >250 mg/dl by 20 weeks of age. Body weight in males increases to 55 gm by 16 weeks of age. The diabetic phenotype is very similar to that of NZO/HlLt J (Stock No. 002105) mice. An advantage of NZL/LtJ over NZO/HlLtJ as a diabetes model, in addition to the higher disease incidence, is that mice of this strain breed well, whereas NZO/HlLt mice breed very poorly. This strain carries the wildtype Igh-6 allele from the NZO/HlLtJ strain. | ||
| 002676 | NZM2410/J | Repository- Live |
| Of the original 26 NZM strains, many resemble NZBxNZWF1 in lifespan and pathology, some strains show an acceleration of disease onset while others have delayed onset or are symptom free. NZM2410 mice are unusual in that both males and females show early onset of severe lupus nephritis. The NZM2410 strain has been useful in identifying numerous susceptibility genes. All NZM strains are homozygous for the NZW haplotype H2z (Ku, Au, Sz, Dz ). | ||
| 000679 | P/J | Repository- Live |
| P/J mice exhibit a high incidence of lymphatic leukaemia. They also show a high susceptibility to audiogenic and electroconvulsive seizures. P/J mice are also homozygous for a number of other mutations including nonagouti (a), brown (Tyrp1b), pink-eyed dilution (Oca2p), short ear (Bmp5se), dilute Myo5ad), and retinal degeneration 1 (Pdeb1rd1). | ||
| 001384 | PANCEVO/EiJ | Repository- Live |
| 000930 | PERA/EiJ | Repository- Live |
| 001307 | PERC/EiJ | Repository- Live |
| 004660 | PWD/PhJ | Repository- Live |
| PWD/PhJ is an inbred mouse strain of the subspecies Mus musculus musculus. M. m. musculus is estimated to have diverged approximately 1 million years ago from M. m. domesticus, the subspecies from which derives most of the genome of practically every laboratory mouse strain. However, the extent of polymorphism for randomly selected microsatellite markers between the two subspecies (70-80%) is nearly as great as between M. m. domesticus and Mus spretus (84%), which diverged about 3 million years ago (Montagutelli et al. 1991; Gergorova and Forejt 2000). PWD/Ph mice exhibit differences from mice of common laboratory strains for a number of complex phenotypic characteristics, including body mass, distribution of adipose tissue, serum concentrations of intermediary metabolites, susceptibility to type I diabetes and various behavioral traits (Gregorova and Forejt 2000). Male, but not female, F1 hybrid offspring of crosses between mice of most lab
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| 003715 | PWK/PhJ | Repository- Live |
| 000874 | RBA/DnJ | Repository- Live |
| 000682 | RF/J | Repository- Live |
| Derived from an unknown stock at the Rockefeller Institute, RF/J are commonly used in research in genetics, immunology, oncology and virology. This strain displays a high cancer incidence including leukemia (reportedly between 40 and 66%) and reticulum cell sarcomas (approximately 50%). Mice also have a high incidence of spontaneous glomerular hyalinisation and glomerulosclerosis developing between eight and twenty months. | ||
| 005221 | RIII/ImrNhsJ | Repository- Live |
| The original RIII strain was known for its high incidence of hormone-dependent mammary tumors transmissible by milk-born MMTV. The RIII/ImrNhsJ substrain is reported to show a pattern of virus expression and tumor incidence similar to the RIII strain (Sarkar, et al. 2004). RIII/ImrNhsJ mice carry the following endogenous MMTV loci: Mtv-6, 8, 14, 17 and possibly 21 (Popken-Harris, et al. 2001). Exogenous MMTV infection leads to the deletion of CD4+ Vbeta-2 and Vbeta-8 peripheral and central T cells (Uz-Zaman, et al. 2003). It is possible to modulate mammary tumor incidence using high and low calorie diets (Li, et al. 1994). RIII/ImrNhsJ mice infected with exogenous MMTV may be useful for studies of human breast cancer activated by insertional mutagenesis. NOTE: Mice distributed by The Jackson Laboratory are not infected with MMTV. Regrettably, we do not have a source for the virus. | ||
| 000683 | RIIIS/J | Repository- Live |
| RIIIS/J mice have prolonged bleeding times with normal platelet activity and low levels of factor VIII:C and plasma von Willebrand factor antigen, making it a good animal model for human von Willebrand disease. This bleeding tendency is an incomplete dominant, autosomal trait. RIIIS/J mice also produce a low antibody response to several bacterial polysaccharide antigens and are reported to be resistant to collagen induced arthritis. Despite a B cell immunodeficiency, RIIS/J mice develop severe experimental autoimmune myasthenia gravis (EAMG) (Tuzun et al., 2004). RIII/J have a high incidence of mammary tumors and ovarian tumors. RIIIS/J mice carry Mtv8, and Mtv14, but high incidence of tumors has not been reported in these mice. In fact, some studies indicate a resistance to chemically induced tumors. RIIIS/J mice have been reported to develop far fewer lung tumors than A/J or SWR/J mice subsequent to Urethan treatment. BALB/c x RIII F1 males are also highly resistant to
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| 000268 | RSV/LeJ | Repository- Live |
| Mice heterozygous for the varitint-waddler spontaneous mutation (Mcoln3Va) are deaf and show circling behavior, head-tossing, and hyperactivity. Heterozygotes circle somewhat less than some of the other circling mutants. Their coats are variegated with patches of normal-colored, diluted, and white fur. Homozygotes show more intense behavioral abnormalities than heterozygotes, and their coats are white, except for small patches of unaltered color near the ears and base of the tail. The pathological changes in heterozygotes include degeneration of the organ of Corti, stria vascularis, spiral ganglion, saccular macula, cristae ampullares, and vestibular ganglion. In homozygotes the degenerative changes are more severe and also include the utricular macula. Viability of heterozygotes is nearly normal, but fertility is reduced. Mortality is very high in homozygotes, and very few of the survivors are fertile. Compound heterozygotes for the two alleles (Mcoln3Va-J
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..... For more information please see the full phenotype on the strain data sheet | ||
| 000644 | SEA/GnJ | Repository- Live |
| 000280 | SF/CamEiJ | Repository- Live |
| 001393 | SKIVE/EiJ | Repository- Live |
| 001224 | SOD1/EiJ | Repository- Live |
| SOD1/EiJ carries a spontaneous mutation in the Sod1 gene (Luche et al., 1997). The mutation differs from the C57BL/6J sequence at position 231 and changes a glutamate to a lysine in a positively charged amino acid domain within the Zn-subloop. This strain is fertile and exhibits no obvious phenotype. | ||
| 001146 | SPRET/EiJ | Repository- Live |
| The wild-derived inbred strain SPRET/Ei is often used in crosses with common inbred strains to create highly polymorphic panels for genetic mapping. SPRET/Ei mice are resistant to high doses of tumor necrosis factor alpha (TNFa) (Staelens et al 2002). Mice from a C57BL/6 x SPRET/Ei F1 cross were protected from TNFa-induced arthritis and partially protected against induced allergic asthma (Staelens et al 2004). SPRET/Ei may be useful in understanding certain inflammatory diseases. | ||
| 000929 | TIRANO/EiJ | Repository- Live |
| This wild-derived inbred strain is homozygous for 8 Robertsonian translocations: Rb(1.3)1Bnr, Rb(4.6)2Bnr, Rb(5.15)3Bnr, Rb(11.13)4Bnr, Rb(9.14)6Bnr, Rb(16.17)7Bnr, Rb(2.8)2Lub and Rb(10.12)5Lub (abbreviated Rb1Bnr - Rb7Bnr, Rb2Lub and Rb5Lub, respectively)(LL Washburn, pers. comm.). | ||
| 000274 | TSJ/LeJ | Repository- Live |
| 001145 | WSB/EiJ | Repository- Live |
| 001392 | ZALENDE/EiJ | Repository- Live |
| This wild-derived inbred strain is homozygous for 7 Robertsonian translocations: Rb(1.3)1Bnr, Rb(4.6)2Bnr, Rb(5.15)3Bnr, Rb(11.13)4Bnr, Rb(8.12)5Bnr, Rb(9.14)6Bnr, and Rb(16.17)7Bnr (abbreviated Rb1Bnr - Rb7Bnr, respectively)(LL Washburn, pers. comm.). | ||
| 002357 | 129P3/JEmsJ | Repository-Cryopreserved |
| 001198 | 129P4/RrRkJ | Repository-Cryopreserved |
| For a complete history of the numerous 129 substrains please refer to Simpson, et al., 1997. Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. Most recently 129 mice are widely used strain in the production of targeted mutations due to the availability of several lines of embryonic stem cells. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of substrains into three major groups: parental substrains, steel substrains and "ter" substrains. Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. | ||
| 002064 | 129T2/SvEms | Repository-Cryopreserved |
| 000004 | ABP/LeJ | Repository-Cryopreserved |
| Mice homozygous for the Tgfawa1 spontaneous mutation are recognizable at 2 or 3 days of age by their curly whiskers. The first coat is strongly waved and straight in later coats. Most of the whiskers also become straight, but the guard hairs are curved and shorter than normal. Some homozygotes have eyelids open at birth.
Mice homozygous for the recessive Adamts20bt mutation have a dorsal and a ventral unpigmented patch posterior to the midline of the trunk with the dorsal patch usually being larger than the ventral patch. These patches run in a more transverse orientation across the mouse than lengthwise and often extend around the sides of the mouse to form a white belt. The size of the patches can vary from approximately 1 to 20 percent of the surface. Unlike other spotting mutations, no variability in phenotype was identified when belted was transferred onto the C57BL/6J or JU/CtLm backgrounds (Lamoreaux 1999). Murray and Snell reported findin
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| 002720 | AKR/CumJ | Repository-Cryopreserved |
| 000277 | ATEB/LeJ | Repository-Cryopreserved |
| Mice homozygous for the atrichosis spontaneous mutation (at) are characterized by sparsely distributed hair, especially on the trunk. The amount of hair varies, but affected mice can be easily recognized at 8 to 10 days old. Both sexes are sterile and have very small gonads with few germ cells. There is a great deficiency of primary spermatogonia in the testes. A quantitative study of maturation of ovarian oocytes showed that the proportion of resident oocytes recruited into the first wave of growth was much higher than in phenotypically normal heterozygous controls (J.J. Eppig, personal communication). This strain is also segregating for the eye blebs spontaneous mutation (Grip1eb). | ||
| 000649 | AU/SsJ | Repository-Cryopreserved |
| 000650 | BALB/cBy | Repository-Cryopreserved |
| 001905 | BALB/cGaJ | Repository-Cryopreserved |
| 000921 | BALB/cGrRkJ | Repository-Cryopreserved |
| 001311 | BALB/cWtEiJ | Repository-Cryopreserved |
| Experimental allergic encephalitis (EAE) is an autoimmune disease of the nervous system induced by sensitization of experimental animals with homogenates of whole brain and/or spinal cord tissue, myelin, or myelin components. Many of the clinical and histologic aspects of EAE are similar to those of multiple sclerosis (MS), making EAE a useful MS model (Alvord et al., 1984). Mice of different sublines of the BALB/c inbred strain exhibit marked differences in the incidence and severity of EAE induced by immunization with spinal cord homogenate (Hickey et al., 1986) or with myelin proteolipid protein (PLP) (Tuohy et al., 1988). The most severe response to PLP was development in nine of ten BALB/cPt mice of rapid onset, severe clinical disease with limb paralysis accompanied histologically by meningeal and perivascular infiltration by mononuclear and polymorphonuclear lymphocytes, particularly of the spinal cord. At the opposite end of the spectrum, none of ten BALB/
..... For more information please see the full phenotype on the strain data sheet | ||
| 000652 | BDP/J | Repository-Cryopreserved |
| 000250 | BNT/LeJ | Repository-Cryopreserved |
| In the early 1950s, a wild type female from the Namru strain was crossed with a bald hrba/hrba male and one of the pups produced was a male with a bent tail. Pedigree tests revealed the underlying mutation to be semidominant and carried on the X chromosome. The predominant phenotypic trait of kinked, shortened tails results from mis-formed, smaller, and absent tail vertebrae. Heterozygous females have varied expressivity spanning a broad phenotypic range including mice with no apparent phenotype and mice with multiply kinked and shortened tails. Hemizygous males have the highest expressivity; the tail is shortened in some cases to half the normal length and in the most severe cases the kinks in the tail will cause the tail to bend sharply. In males the tail kinks are more common in the distal than the proximal half of the tail. Heterozygous females are fertile, but hemizygous males and homozyous females have decreased viability and fertility. T
..... For more information please see the full phenotype on the strain data sheet | ||
| 001891 | BRVR/WrDvJ | Repository-Cryopreserved |
| 005972 | C3H/HeJBirLtJ | Repository-Cryopreserved |
| Under conventional housing conditions, C3H/HeJBirLtJ mice develop spontaneous colitis. It should be noted that the phenotype of cecocolitis in this strain requires an interaction with an as yet undefined component of the enteric flora. Inflammation is present mainly in the cecum and right colon. Colitis develops early in life and resolves by three months of age. The colitis is characterized by acute and chronic inflammation, ulcerations, crypt abscesses, regenerative hyperplasia and submucosal scarring. A mild recurrence of the disease can occur after one year. Small lesions at the anorectal junction are common throughout life. | ||
| 001824 | C3H/HeJSxJ | Repository-Cryopreserved |
| 000474 | C3H/HeSn | Repository-Cryopreserved |
| 001908 | C3HfB/BiJ | Repository-Cryopreserved |
| 001822 | C57BL/10SxJ | Repository-Cryopreserved |
| 001197 | C57BL/10WtRkJ | Repository-Cryopreserved |
| 000663 | C57BL/6By | Repository-Cryopreserved |
| 006180 | CD10/JlsJ | Repository-Cryopreserved |
| Swiss derived CD-1 mice are less responsive to exogenous estradiol than most inbred strains as measured by resistance to decreases in testes weight, spermatogenesis, and spermatid development. Derived from CD-1, the inbred strains CD3/JlsJ, CD7/JlsJ, and CD9/JlsJ mice exhibit a moderate sensitivity to endocrine disruption by estradiol, while CD10/JlsJ mice are highly resistant to endocrine disruption by estradiol. All lines generated in the selection program are significantly less responsive to estradiol than C57BL/6 mice. The selectively bred strains CD3/JlsJ (Stock No. 006177), CD7/JlsJ (Stock No. 006178), CD9/JlsJ (Stock No. 006179) and CD10/Jls (Stock No. 006180) may serve as tools for mapping and characterizing genes responsible for estradiol sensitivity. ..... For more information please see the full phenotype on the strain data sheet | ||
| 000293 | CHMU/LeJ | Repository-Cryopreserved |
| Mice homozygous for the congenital hydrocephalus (Foxc1ch) spontaneous mutation die at birth, probably from inability to breathe. Homozygous mutant mice have bulging hemorrhagic cerebral hemispheres and open eyelids, urogenital abnormalities, and severely abnormal skull, cervical vertebrae, sternum, laryngeal cartilages, and hyoid bone. The hydrocephalus may trace to lack of formation of subarachnoid space, which is first detectable in 11-day embryos. Most of the defects in the head region are probably secondary to the severe displacements created by the hydrocephalus. Mice homozygous for the muted spontaneous mutation (Mutedmu), maintained in repulsion with congenital hydrocephalus, have light eyes at birth and their fur is a muted brown shade, often with white underfur. Some have a balance defect, similar to that of pallid (Pldnpa). Homozygous mutant mice show head-tilting and loss of postural reflexes, due to absence of otoliths
..... For more information please see the full phenotype on the strain data sheet | ||
| 000284 | CWD/LeJ | Repository-Cryopreserved |
| 000660 | DA/HuSnJ | Repository-Cryopreserved |
| 001907 | DBA/2BiJ | Repository-Cryopreserved |
| 000052 | DBA/2DeJ | Repository-Cryopreserved |
| 000973 | DBA/2HaSmnJ | Repository-Cryopreserved |
| 002860 | DBA/8BiDsmJ | Repository-Cryopreserved |
| 000252 | DC/LeJ | Repository-Cryopreserved |
| Mice heterozygous for the semidominant dancer mutation exhibit head tossing and circling behavior. Heterozygotes are not deaf, but have defects in the vestibular region (Wenngren et al., 1989). Homozygotes die at birth with cleft lip and cleft palate (Deol et al., 1966). Strain background influences cleft lip/palate expression in heterozygotes (Trasler et al., 1982). Positional cloning of Dc revealed a 3.3 kb insertion of the Tebp gene into the first intron of Tbx10. The insertion causes ectopic expression of a Tebp-Tbx10 chimeric transcript (Bush et al., 2004). | ||
| 002814 | DDY/EFrkJ | Repository-Cryopreserved |
| 000253 | DLS/LeJ | Repository-Cryopreserved |
| Mice homozygous for the dilute-lethal spontaneous mutation (Myo5ad-l) display a severe neuromuscular disorder characterized by convulsions and opisthotonus. Homozygous mutant mice usually die by approximately 3 weeks of age. Dilute lethal homozygotes lack smooth endoplasmic reticulum in the dendritic spine of Purkinje cells causing an absence of intracellular calcium. Loss of this intracellular calcium may be the cause of dilute-lethal neurological symptoms. Homozygous dilute-neurological mutant mice (Myo5ad-n, Stock No. 001013) display a neuromuscular disorder, but the condition is less severe than in dilute-lethal homozygotes. In this DLS/Le inbred strain the dilute-lethal mutation is maintained in repulsion with short ear (Bmpse), closely linked mutations on Chromosome 9. | ||
| 002813 | EL/EFrkJ | Repository-Cryopreserved |
| 001956 | EL/SuzSeyFrkJ | Repository-Cryopreserved |
| The EL/Suz inbred strain provides a polygenic model for the study of epilepsy. EL/Suz mice experience recurrent seizures that resemble a common partial complex epilepsy seen in humans. Seizures occur spontaneously beginning around 90-100 days of age, but can be induced in younger mice and analyzed as a semi-quantitative trait after gentle rhythmic stimulation. Quantitative trait analysis has revealed multiple loci (e.g. El1, El2, and El3) that contribute to this phenotype whose effects vary depending on the genetic background. The inbred strain DDY/Jcl (Stock No. 002243) may serve as a control strain for EL/Suz as they are is less susceptible to seizures under similar conditions. | ||
| 000023 | FL/1ReJ | Repository-Cryopreserved |
| 000025 | FL/4ReJ | Repository-Cryopreserved |
| 000619 | FS/EiJ | Repository-Cryopreserved |
| The FS/Ei strain was originally used as a linkage testing stock for gene mapping. It is homozygous for several visible recessive mutations including brown (Tyrp1b), pink-eyed dilution (Oca2p), chinchilla (Tyrc-ch), frizzy (fr), and the neurological mutation shaker 1 (Myo7ash1). It is also homozygous for a couple allelic variants that can be easily typed (Mod2b and Hbbd). Mice homozygous for the shaker 1 show circling, head-tossing, deafness, and hyperactivity characteristic of this type of mutant mice. Viability is normal, and breeding ability is high for a circling mutant. Homozygous mutant mice are most often deaf and swim well on the surface of water up to 4 weeks of age and more but lose the ability later. The degenerative changes of the labyrinth may occur a little later than in some of the other waltzing mutants. By light microscopy, the changes are seen to consist
..... For more information please see the full phenotype on the strain data sheet | ||
| 001491 | FVB/NMob | Repository-Cryopreserved |
| 006131 | GR/J | Repository-Cryopreserved |
| The inbred strain, GR carries the Mtv2a allele. This allele controls expression of endogenous MMTV and the early development of hormone-induced mammary tumors. Nearly all breeding females develop mammary tumors prior to one year of age (van Nie et al. 1977). Most females will exhibit small tumors by the day of first parturition (van Nie et al. 1971). These tumors are most often of the Dunn classification type B adenocarcinoma. MMTV is transmitted through both the milk and the germinal cells of both males and females. Foster nursing does not eliminate endogenous mammary tumor virus (Muhlbock 1965). MTV-antigens are detectable by immunodiffusion assay in the milk of the first lactation period. (van Nie et al. 1977). GR is used extensively to study endocrine regulation of mammary gland development and tumorigenesis. | ||
| 001057 | HPT/LeJ | Repository-Cryopreserved |
| 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 phenotype on the strain data sheet | ||
| 000556 | HTG/GoSfSnJ | Repository-Cryopreserved |
| 000573 | IS/CamRkJ | Repository-Cryopreserved |
| 000259 | JE/LeJ | Repository-Cryopreserved |
| Mice homozygous for the jerker spontaneous mutation (Espnje) show behavior typical of the circling mutants - head-tossing, circling, and hyperactivity. Homozygous mutant mice are deaf from birth and have no detectable stimulus-related cochlear potential at any stage. The abnormal behavior and deafness are associated with postnatal degeneration of the sensory cells of the cochlea and the sacculus and utriculus in homozygotes. The primary influence of the jerker gene appears to be on the apical hair cells, not development of neural structures. Heterozygous jerker mice undergo a similar type of degeneration, but the onset is delayed. Auditory brainstem response is totally absent in homozygotes while heterozygous mice undergo a progressive impairment with age. JE/Le mice are also homozygous for the nonagouti (a), flexed tail (f), and ruby-eye (Hps6ru) mutations. | ||
| 000260 | JGBF/LeJ | Repository-Cryopreserved |
| Mice homozygous for the recessive buff (Vps33abf) mutation on a non-agouti (a/a) background have a lightened coat color that has been described as khaki. On an agouti background, Vps33abf homozygotes have dark ears, opaque eyes, and the belly is lighter in color than is the rest of the coat. Although no change in eye color is outwardly evident, electron microscopy shows fewer and smaller melanosomes than normal in the retinal pigment epithelium and choroid. These mutants have a platelet-storage pool defect evidenced by an increased bleeding time of 9.7 minutes on average, a reduction in the number of platelet dense granules, and slightly decreased collagen-mediated platelet aggregation, secretion of dense-granule ATP and secretion of seratonin. Hakansson and Lundin found increased activity of the lysosomal glycosidases beta- galactosidase, beta-glucuronidase, and N-acetyl-beta-hexosaminidase in kidney cell lysates. Suzuki et al.
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..... For more information please see the full phenotype on the strain data sheet | ||
| 000072 | JGBF/LeTyJ | Repository-Cryopreserved |
| Mice homozygous for the recessive buff (Vps33abf) mutation on a non-agouti (a/a) background have a lightened coat color that has been described as khaki. On an agouti background, Vps33abf homozygotes have dark ears, opaque eyes, and the belly is lighter in color than is the rest of the coat. Although no change in eye color is outwardly evident, electron microscopy shows fewer and smaller melanosomes than normal in the retinal pigment epithelium and choroid. These mutants have a platelet-storage pool defect evidenced by an increased bleeding time of 9.7 minutes on average, a reduction in the number of platelet dense granules, and slightly decreased collagen-mediated platelet aggregation, secretion of dense-granule ATP and secretion of seratonin. Hakansson and Lundin found increased activity of the lysosomal glycosidases beta- galactosidase, beta-glucuronidase, and N-acetyl-beta-hexosaminidase in kidney cell lysates. Suzuki et al.
..... For more information please see the full phenotype on the strain data sheet | ||
| 000572 | JIGR/DnJ | Repository-Cryopreserved |
| JIGR/Dn is maintained with jittery (Atcayji) and grizzled (gr) in repulsion.
Atcayji homozygotes can first be identified at approximately 12 days of age by a leaning, zig-zag gait when they attempt to run and by the difficulty they have righting themselves when placed on their backs. Disease progression is rapid such that within two more days mutants are found to crouch on their heels in a squatting position and can not run without falling. Within three to four days of the first symptoms, tetany is seen during exertion or excitement. This is initially most pronounced in the forelegs, which the mice beat up and down during these two- to three-second spasms. Failure to gain weight is seen by the third week of life and it is unclear whether this results from an inability to take in food. The severity and frequency of tetany increases, and during the fourth week weight loss and increased weakness precede death. The mean age of death is approxi
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| 001266 | LDH2/EiJ | Repository-Cryopreserved |
| 000289 | LDJ/LeJ | Repository-Cryopreserved |
| Attractin (ATRN) deficiencies cause darkened pigmentation, increased locomotor activity, decreased body weight, and vacuolization and myelination defects in the central nervous system.
Agouti protein competes with alpha-melanocyte stimulating hormone (a-MSH) for binding of melanocortin 1 receptor (MC1R), and this in turn signals pigment type switching from eumelanin production to pheomelanin production. ATRN interacts with agouti possibly to facilitate the interaction with MC1R. In mice, ATRN deficiencies result in decreased pheomelanin production causing darkened ears, tail, feet, and coat color which becomes dark reddish brown as these mice age. Thus, the initial Atrn mutation reported by Lane and Green was called mahogany (Atrnmg). ATRN deficiencies darken the coloring caused by nonagouti such that these mice are coal black with no white hairs behind the ears or around the perineum and have blacker ears, tail, and feet. ATRN deficiency can suppress the i
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| 000220 | LPT/LeJ | Repository-Cryopreserved |
| 000262 | LS/LeJ | Repository-Cryopreserved |
| Mice homozygous for the lethal spotting mutation (Edn3ls) resemble piebald mice (Ednrbs/Ednrbs) mice. Homozygous mutant mice exhibit considerable white spotting and like homozygotes for the piebald-lethal allele (Ednrbs-l) usually develop megacolon. Lethal spotting mutant mice usually die in the third week of life from the megacolon abnormality, which is associated with deficiency of intrinsic ganglion cells in the lower colon. A few homozygotes may survive and breed. This strain is also homozygous for the black and tan coat color mutation (at). | ||
| 001850 | MEV-Q/TyJ | Repository-Cryopreserved |
| In 1989 Taylor and Rowe described generating a linkage testing stock homozygous for 11 ecotropic MuLV proviruses on 10 distinct chromosomes. The strain was named MEV/1Ty for Multiple Ecotropic proVirus. These proviral insertions can be identified via Southern blot analysis of PvuII or HindIII digests using the MuLV-specific pEcB4 probe. The first progenitor strain C58/J contributed the following proviruses identified by the PvuII junction fragments indicated in parenthesis: Emv20 (8.2kb), Emv21 (6.6 kb), Emv23 (3.7 kb), Emv24 (3.5 kb), Emv25 (3.4 kb), Emv26 (2.9 kb), and Emv27 (9.4 kb). The second progenitor strain AKXD-14/Ty contributed Emv11 (4.3 kb), Emv13 (3.4 kb), and Emv14 (8.6 kb) from AKR/J and Emv3 (5.2 kb) from DBA/2J. Emv3 is the proviral insertion causing the dilute allele of Myo5a. This strain is also homozygous for nonagouti (a). Further analysis of MEV/1Ty progeny identified subsequent MuLV provirus re-insertions that were used to
..... For more information please see the full phenotype on the strain data sheet | ||
| 001856 | MEV-W/TyJ | Repository-Cryopreserved |
| 001297 | MOR/RkJ | Repository-Cryopreserved |
| 000265 | MY/HuLeJ | Repository-Cryopreserved |
| 003091 | NH/KiPtJ | Repository-Cryopreserved |
| 001289 | NOD/ShiLt | Repository-Cryopreserved |
| 003108 | NZM391/J | Repository-Cryopreserved |
| Of the original 26 NZM strains, many resemble NZBxNZWF1 in lifespan and pathology, some strains show an accelearation of disease onset while others have delayed onset or are symptom free. All strains are homozygous for the NZW haplotype H2z (Ku, Au, Sz, Dz ). | ||
| 003560 | NZW/Osu | Repository-Cryopreserved |
| 005052 | PN/nBSwUmabJ | Repository-Cryopreserved |
| PN/nBSwUmabJ mice develop a predominantly female lupus-like syndrome with age (Walker et al., 1978). Characteristics of the systemic lupus erythemoatosus syndrome include: abnormalities in B and T cell function, hypergammaglobulinemia, antibody production against multiple autoantigens, severe systemic perivasculitis and vasculitis, and immune complex-mediated glomerulonephritis (Walker et al.,1978, Luzina et al., 1999, Davidson et al., 1982, Handwerger et al.,1999). Perivascular and vascular infiltrates are composed of unusual phenotypic markers characteristic of both T and B cells (Luzina et al, 1999). By three months of age 88-100% of mice have IgG autoantibodies (Handwerger et al., 1999). Death usually occurs earlier in females as a result of glomerulonephritis and arteritis. The disease progression is accelerated in the female offspring of NZB and PN F1 crosses (Walker et al., 1986). PN/nBSwUmabJ mice develop hearing loss and otic capsule sclerosis demonstrating some paralle
..... For more information please see the full phenotype on the strain data sheet | ||
| 000173 | PRO/1AReJ | Repository-Cryopreserved |
| 000059 | PRO/ReJ | Repository-Cryopreserved |
| Mice exhibit hyperprolinemia and hyperprolinuria. Proline levels in the blood are increased by seven-fold in comparison to the two parental strains, C57BL/6J and 129P1/ReJ. Proline is detected in the urine of all PRO/ReJ mice, however, it is undetectable in the parental strains. This strain may be useful in studies of human hyperprolinemia. | ||
| 002040 | RB126Bnr/EiJ | Repository-Cryopreserved |
| 002041 | RB16Bnr/EiJ | Repository-Cryopreserved |
| 000609 | RBB/DnJ | Repository-Cryopreserved |
| 000889 | RBC/DnJ | Repository-Cryopreserved |
| 001000 | RBD/DnJ | Repository-Cryopreserved |
| 000807 | RBJ/DnJ | Repository-Cryopreserved |
| 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. | ||
| 001088 | RIII/DmMobJ | Repository-Cryopreserved |
| 000267 | ROP/GnLeJ | Repository-Cryopreserved |
| The Sox18Ra and Sox18Ra-J alleles cause a less severe phenotype than the Sox18Ra-Op allele. The Sox18Ra and Sox18Ra-J alleles are similar mutations and give a very similar phenotype. The Sox18Ra allele has been more broadly described in the literature and will be covered here. Heterozygotes are viable and fertile. Heterozygotes have developmentally retarded sinus hair growth apparent at embryonic day 16.5 and retarded development of pelage follicles apparent by embryonic day 17.5. Thus, heterozygotes have slightly shorter vibrissae evident at birth, and can be distinguished at three days of age by their pink skin which, due to the abnormally sparse development of the coat, fails to darken like that of wildtype siblings. A paucity of fur is apparent by nine days of age and persists throughout life. Compared with the wild type pelage, Sox18Ra/+ coats have l
..... For more information please see the full phenotype on the strain data sheet | ||
| 000269 | SB/LeJ | Repository-Cryopreserved |
| The SB/Le inbred strain is homozygous for both the satin (Foxq1sa) and beige (Lystbg) mutations. Most of the immunological phenotype is due to the beige mutation. Homozygous mutant beige mice are characterized by a condition that 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 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. They have a severe deficiency of natural killer (NK) cells. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibo
..... For more information please see the full phenotype on the strain data sheet | ||
| 000270 | SEC/1GnLeJ | Repository-Cryopreserved |
| 002746 | SENCARA/PtJ | Repository-Cryopreserved |
| The acronym SENCAR is derived from SENsitivity to CARcinogenesis. SENCAR mice are commonly used for studies of susceptibility and resistance to the induction of skin tumors. Dr. Michael Potter of the National Cancer Institute developed three inbred lines, designated A, B, and C, from random breeding of outbred SENCAR mice. Characterization of these mice for sensitivity to skin tumor development indicated that mice of all three inbred strains displayed increased sensitivity to initiation by 7,12-dimethylbenz[a]anthracene (DMBA), urethane, or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). Promotion by mezerein as well as carcinogenesis by repeated treatment with DMBA or MNNG produced papillomas with a high frequency of conversion to squamous cell carcinomas (SCCs). Compared with outbred SENCAR mice, development of both squamous papillomas and carcinomas was increased at least two-fold by all protocols tested. | ||
| 002747 | SENCARB/PtJ | Repository-Cryopreserved |
| The acronym SENCAR is derived from SENsitivity to CARcinogenesis. SENCAR mice are commonly used for studies of susceptibility and resistance to the induction of skin tumors. Dr. Michael Potter of the National Cancer Institute developed three inbred lines, designated A, B, and C, from random breeding of outbred SENCAR mice. Characterization of these mice for sensitivity to skin tumor development indicated that mice of all three inbred strains displayed increased sensitivity to initiation by 7,12-dimethylbenz[a]anthracene (DMBA), urethane, or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). Promotion by mezerein as well as carcinogenesis by repeated treatment with DMBA or MNNG produced papillomas with a high frequency of conversion to squamous cell carcinomas (SCCs). Compared with outbred SENCAR mice, development of both squamous papillomas and carcinomas was increased at least two-fold by all protocols tested. | ||
| 002748 | SENCARC/PtJ | Repository-Cryopreserved |
| The acronym SENCAR is derived from SENsitivity to CARcinogenesis. SENCAR mice are commonly used for studies of susceptibility and resistance to the induction of skin tumors. Dr. Michael Potter of the National Cancer Institute developed three inbred lines, designated A, B, and C, from random breeding of outbred SENCAR mice. Characterization of these mice for sensitivity to skin tumor development indicated that mice of all three inbred strains displayed increased sensitivity to initiation by 7,12-dimethylbenz[a]anthracene (DMBA), urethane, or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). | ||