Search Criteria: Research Area is "Dermatology Research"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 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 descriiption on the strain data sheet | ||
| 000058 | B6(Cg)-Tyrc-2J/J | Level 2 |
| Mice homozygous for Tyrc-2J are phenotypically identical to homozygotes for the classic albino allele. Pigment is completely absent from skin, hair and eyes. While Tyr mRNA levels of Tyrc-2J homozygotes are similar to those of wild-type mice, there is virtually no tyrosinase protein present (Le Fur et al. 1996). Both homozygote and heterozygote mice are highly resistant to light damage and exhibit retinal degeneration (increased photoreceptor death) into young adulthood. Degeneration does not continue in adult mice (Bravo-Nuevo et al. 2004). | ||
| 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 | ||
| 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). | ||
| 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 | ||
| 100410 | WBB6F1/J-KitW/KitW-v/J | Level 2 |
| Kit mutant 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. KitW/KitW-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. KitW/KitW-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment. | ||
| 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 | ||
| 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. | ||
| 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 descriiption on the strain data sheet | ||
| 000819 | B6.Cg-Foxn1nu/J | Level 4 |
| The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when
..... For more information please see the full descriiption on the strain data sheet | ||
| 002282 | BTBR T+ tf/J | Level 4 |
| BTBR mice exhibit a 100% absence of the corpus callosum and a severly reduced hippocampal commissure (Wahlsten D, 2003 Brain Res). This strain exhibits several symptoms of autism including: reduced social interactions, impaired play, low exploratory behavior, unusual vocalizations and high anxiety as compared to other inbred strains (McFarlane HG, 2008, Gen, Brain Behav; Moy SS, 2007, Behav Br Res, Scattoni ML, 2008, PLos). | ||
| 000051 | C57BL/6J-Aw-J/J | Level 4 |
| Mice are agouti (hairs are black with a subapical yellow band) with a cream or white belly. Females may be used as foster mothers for ovary transplantation of mutations maintained in a/a strains because Aw-J is dominant to the nonagouti a. Since a to Aw is a common mutation, strains possessing this mutation in laboratory stock may not be of a common origin. | ||
| 000049 | C57BL/6J-KitW-v/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 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 | ||
| 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. | ||
| 000711 | CByJ.Cg-Foxn1nu/J | Level 4 |
| The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when d
..... For more information please see the full descriiption on the strain data sheet | ||
| 000692 | WB/ReJ KitW/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. The lack of germ cells in homozygous mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 004293 | 129-Shhtm2Amc/J | Repository- Live |
| Mice that are homozygous for the Shhtm2Amc targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This conditional mutant contains two loxP sites flanking exon 2 of the targeted allele. Cre-mediated recombination excises exon 2 and some surrounding intronic sequence, generating a null allele. When the conditional mutant is crossed with a ubiquitously-expressing Cre recombinase carrier to remove Shh activity in the early embryo, the resulting phenotype resembles the Shh null mutation. These conditional mutant mice may be mated to strains expressing Cre recombinase to study the effects of temporal and tissue-specific ablation of the targeted allele. This mutant mouse strain represents a model that may be useful in studies of developmental defects resulting from disruption of Shh-dependent pathways.
When bred to a strain expressing Cre recombinase under the control of a tet
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| 006661 | 129S.B6-Tg(KRT14-RAF1/ESR1)1Pkha/J | Repository- Live |
| Mice hemizygous for this "K14-Raf:ER" transgene are viable and fertile. Inducible expression of the human Raf1(Raf-1 [DD]):estrogen receptor (ER) fusion protein is observed in the epidermis following topical application of 4-hydroxytamoxifen (4OHT). Prolonged (4 weeks) induction of human Raf-1[DD] activity promotes the undifferentiated, proliferative phenotypic characteristics observed in epidermal cancer; including hyperplasia, increased mitotic index, decreased expression of differentiation markers and increased expression of beta-1 and beta-4 integrin subunits. Raf-1[DD]-induced skin abnormalities are entirely reversed within one month after 4OHT cessation. These mice have a similar 4OHT-inducible skin phenotype as the transgenic mice expressing human H-RasG12V (Stock No. 006403) or human Mek1R4F (Stock No. 006822), and may be useful in studies of the
..... For more information please see the full descriiption on the strain data sheet | ||
| 002655 | Mus pahari/EiJ | Repository- Live |
| 002565 | A.B6-Tyr+/J | Repository- Live |
| 000199 | AEJ/GnLeJ | Repository- Live |
| 000578 | B6 x STOCK Tyrc-ch Bmp5se +/+ Myo6sv/J | Repository- Live |
| Mice homozygous for the Snell's waltzer spontaneous mutation (Myo6sv) show to a marked degree the typical circling, head-tossing, deafness, and hyperactivity of other mutant mice of this type. Homozygous mutant mice are recognizable by the age of 1 week. The abnormalities of the inner ear consist of degeneration of the entire neuroepithelium comprising the organ of Corti, the saccular and utricular maculae, and the cristae of all three semicircular canals. Although viability of homozygotes is nearly normal, breeding ability is reduced and males are more reliable breeders than females.
Specific cytoskeletal components are critical for specific cellular structures. The microvilli of intestinal brush border cells in Myo6sv homozygotes are shorter than normal. While myosin 6 is not critical for the development of hair cell stereocilia, it is essential for their maintenance. At birth the stereocilia appear nearly normal with only occasional stereocil
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| 004684 | B6(129P2) Nos2tm1Lau-chtl/J | Repository- Live |
| This mutant has an overall lighter coat, tail and ears than a black +/+ control. Both males and females breed and it is maintained as a homozygous stock. | ||
| 005071 | B6(Cg)-DctSlt-lt3J/J | Repository- Live |
| DctSlt-lt3J heterozygous mice are diluted to a dark brown and homozygous mice are diluted to a light brown. | ||
| 003046 | B6(FVB)-MitfMi-Mee/J | Repository- Live |
| On the C57BL/6 background, homozygotes have a white coat color while heterozygotes have a black coat. Clinically, heterozygotes have variable amounts of pigment in the retina with a normal optic cup and retinal vessels. Homozygotes have an iris coloboma, a large optic cup and poor or no retinal vessels. Homozygotes show some pigment in the iris, which does not dilate. | ||
| 008129 | B6(V)-Bhrd/J | Repository- Live |
| 001809 | B6-Aw-J.Cg-EdaTa-6J +/+ ArTfm/J | Repository- Live |
| Testicular feminization (ArTfm) is a dominant spontaneous mutation on the X chromosome. Hemizygous male mice are outwardly female in appearance except that the vagina does not open until 3 months of age if at all. Male reproductive development is abnormal leading to very small testes, and the absense of vas deferens, the epididymis, and male accessory glands. Spermatogonia and Sertoli cells are present in the testes, but spermatogenesis does not proceed past meiotic prophase. Leydig cells, which normally produce androgen in males, fail to develop normally. This strain is also segregating for the tabby 6J mutation (EdaTa-6J) that affects both the coat color and hair pattern growth. The tabby mutation is maintained in repulsion with the testicular feminization mutation and is used as a coat color marker to assist in identifying resulting genotypes obtained from matings. | ||
| 006201 | B6.129-Scd1tm1Ntam/J | Repository- Live |
| Homozygous mice are viable and fertile. Transcripts from the targeted gene are absent in homozygous liver, eyelid, skin, and white adipose tissues. In addition, the endogenous protein and enzyme activity are absent from homozygous liver tissue. Homozygous mice exhibit cutaneous abnormalities and narrow eye fissure with atrophic sebaceous and meibomian glands. Mutant mice also have reduced body adiposity, increased insulin sensitivity, increased basal and insulin-mediated glucose uptake, and are resistant to diet-induced weight gain. Homozygotes have altered hepatic glycerophospholipid profiles. Homozygous mice are not recommended for breeding as skin lesion severity may prohibit colony success. These mutant mice may be useful in studies of monounsaturated fatty acid synthesis, cholesterol homeostasis, skin disease, obesity, and diabetes. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background differ
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| 006879 | B6.129-Scd2tm1Myz/J | Repository- Live |
| While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die within 24 hours of birth. Brain tissues from homozygous mice show no expression from the targeted gene. Homozygotes exhibit neonatal lethality with 100% penetrance on this genetic background (less penetrant on 129SvEv genetic background) likely due to severe skin permeability barrier abnormalities. Null mice also have abnormal epidermal morphology and abnormal lipid homeostasis in the skin and liver. These mutant mice may be useful in studying monounsaturated fatty acid synthesis, lipid biosynthesis and metabolism, cholesterol homeostasis, and skin disease, as well as obesity and diabetes. | ||
| 006133 | B6.129S4-Vdrtm1Mbd/J | Repository- Live |
| Heterozygous mice are phenotypically indistinguishable from wildtype siblings. Homozygous mice are viable and fertile with normal survival until approximately 14 months. RNA isolated from the intestine and kidney show a truncated deletion of the second zinc finger coding region followed by a premature termination codon, resulting in the absence of receptor protein. Homozygous mice exhibit an identical phenotype as the human disease hereditary vitamin D-dependent rickets type II (HVDDR). As early as 21 days of age, mutant mice demonstrate hypocalcemia, hypophosphatemia, hyperparathyroidism, increased serum parathyroid hormone, abnormal blood mineral levels, and growth retardation. In addition, renin and plasma angiotensin II levels are increased. Homozygous mice are hypertensive and exhibit cardiachypertrophy. At 4 weeks of age, homozygous mice exhibit perioral and periorbital alopecia that progresses over the entire body by 4 months of age. Rickets and osteomalacia develop by 35 days.
..... For more information please see the full descriiption on the strain data sheet | ||
| 007621 | B6.129S6-Hrtm1Cct/J | Repository- Live |
| Homozygotes are viable and fertile, but optimal breeding is done with heterozygotes. The mice appear normal at birth and for about two weeks postnatally. Once the animals begin to shed, the hair is lost and does not grow back. They remain bald and over time, the skin becomes thicker and progressively more wrinkled. The degree of wrinkling is variable but can be severe; frequently the skin protrudes over the eyes and off the sides of the animals. Wrinkling is more severe than in the hairless rhino allele. Northern analysis of mRNA from back skin confirmed the absence of expression. This strain maybe be useful in studies of skin and hair. | ||
| 002128 | B6.129S7-Itgb2tm1Bay/J | Repository- Live |
| Mice homozygous for the Itgb2tm1Bay mutation are viable and fertile. Homozygous mutant mice show an increased neutrophil count, and a decreased inflammatory response to peritonitis. Responses to delayed-type hypersensitivity and rejection of transplanted tissue are impaired. PLEASE NOTE: The Itgb2tm1Bay allele is not a null mutation; it is a hypomorphic mutation which results in the expression of very low levels of Itgb2 protein. This strain serves as a model for the moderate form of human CD18 deficiency. | ||
| 003568 | B6.129S7-Trp63tm2Brd/J | Repository- Live |
| Mills 1999 Nature 398:708 describes the homozygous phenotype on a mixed B6-Tyrc-Brd;129S7(129S5) background. Further, they not distinguish between the two targeted alleles (pTV6H(90)-generated p63Brdm1 [Trp63tm1Brd] or pTV12E(60)-generated p63Brdm2 [Trp63tm2Brd]) as both "produced an identical phenotype." Homozygous mice are born alive, but die several hours after birth. No transcripts have been detected in homozygotes. They have striking developmental defects, exhibiting truncated forelimbs, absent hindlimbs, and transparent skin with a complete lack of hair follicles. Both the gross and histological appearance of internal organs is normal. Functional permeability of the skin is dramatically increased; homozygous mice lose thirty times more water than normal littermates. It is presumed that death occurs from dehydration. Heterozygous mice are viable, fertile, and do not exhibit any overt developm
..... For more information please see the full descriiption on the strain data sheet | ||
| 008115 | B6.129X1-Pomctm2Ute/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. 60 to 75% of homozygotes die perinatally. Surviving homozygotes have decreased fertility and homozygous females produce milk that does not allow pups to survive past 14 days of age. No serum adrenocorticotropic hormone (ACTH) or corticosterone was detected by radioimmunoassay (RIA) of homozygotes. Serum epinephrine and aldosterone levels are reduced. Although homozygotes are born with adrenal glands or normal size, adrenal glands fail to grow postnatally and become almost undetectable with age. By 3 months of age, mice homozygous for the mutation are twice the weight of wildtype controls and increased serum leptin levels. Heterozygotes exhibit elevated serum leptin levels, but not increased weight and reduced levels of serum adrenocorticotropic hormone (ACTH), corticosterone, and aldosterone levels. Both heterozygotes and homozygote
..... For more information please see the full descriiption on the strain data sheet | ||
| 003625 | B6.C-H2-Ab1bm12/KhEg-Mc1re-J/J | Repository- Live |
| 000002 | B6.C3-Pde6brd1 Hps4le/J | Repository- Live |
| 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 | ||
| 000305 | B6.Cg-Fbn1Tsk +/+ Pldnpa/J | Repository- Live |
| Mice homozygous for the pallid spontaneous mutation Pldnpa and nonagouti (a) have pink eyes and a light, yellow-brown coat. The Pldnpa/Pldnpa mice have a slightly lighter coat than strains that are homozygous for the pink-eyed dilution allele (Oca2p/Oca2p). Viability of homozygous mutant mice is slightly reduced. Some homozygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manganese, L-dopa, and L-tryptophane in the brain. Homozygotes have elevated basal and testosterone-induced levels of the kidney lysosomal enzymes b-glucuronidase, b-galactosi
..... For more information please see the full descriiption on the strain data sheet | ||
| 004088 | B6.Cg-Foxp3sf/J | Repository- Live |
| Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. Phenotypes associated with these mice include runting, scaly, crusty skin on the eyelids, ears and tails, dermal thickening, squinted eyes, cachexia, reddening and swelling of the genital papilla, and small testicles that are retained in the abdominal cavity. This disorder, which parallels X-linked autoimmunity-allergic disregulation syndrome (XLAAD) in humans, results in Coombs' test-positive anemia, hypergammaglobulinemia, a small, thin thymus, and lymphohistiocytic proliferation in the skin and lymphoid organs, with splenomegaly, lymphadenomegaly, and hepatomegaly. Foxp3sf/Y males generally die by 16-25 days of age. Transgenic expression of Foxp3 prevents scurfy disease in Foxp3sf/Y mice. Neonatal thymectomy of scurfy males ameliorates disease and increases lifespan; athymic nude Foxp3sf/Y mice do not develop scurfy
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| 005051 | B6.Cg-KitW-sh/HNihrJaeBsmJ | Repository- Live |
| Kit mutations affect melanogenesis, hematopoiesis and gametogenesis. The sash mutation affects melanoblast survival. Melanoblast density is severely reduced in homozygotes by E12 (Cable et al., 1995). Homozygote are white with black eyes and some pigment around the ears. Heterozygotes are black with a white sash at the midline. The KitW-sh mutation affects Kit expression in a tissue specific manner. Kit expression is abolished in mast cells and mutant mice have a mast cell deficit (Tono et al., 1992, Berrozpe et al., 1999). However, young animals (<4 weeks) have been reported to have mast cells in skin (Yamakazi et al., 1994). KitW-sh mRNA is expressed normally in the cerebellum and is weakly expressed in testis and spleen (Tono et al., 1992). In contrast to the KitW and KitW-v mutations, KitW-sh germ cells and erythrocytes are not affected. Homozygtes have some
..... For more information please see the full descriiption on the strain data sheet | ||
| 007484 | B6.Cg-Tyrc-2J Tg(Tyr)3412ARpw Tg(Sry-EGFP)92Ei/EiJ | Repository- Live |
| On an albino background Tg(Tyr)3412ARpw permits the identification of gender as early as embryonic day 10.5. This strain is segregating for Tg(Tyr)3412ARpw and homozygous for Tyrc-2J so the individuals not carrying Tg(Tyr3412)ARpw are albino. Because Tg(Tyr)3412ARpw inserted into the X Chromosome, breeding a carrier male with a noncarrier (wild-type) female results in embryos in which all XX individuals develop eye pigment, due to the Tg(Tyr)3412ARpw inherited from their father, while all XY individuals have non-pigmented eyes, having inherited a wild-type X Chromosome from their mother.
This strain is also homozygous for Tg(SryEGFP)92Ei. This reporter transgene consists of a 5 prime regulatory segment of the Sry gene driving EGFP. This transgene is expressed in the pre-support cell lineage (pre-sertoli and pre-granulosa cells) of the fetal genital ridge (Albrecht and Eicher, 2001) and in discrete areas the adult male but not female brain (Dewing et al., 20
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| 005244 | B6.Cg-Tg(Krt1-15-EGFP)2Cot/J | Repository- Live |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Enhanced Green Fluorescent Protein (EGFP) under the direction of the mouse keratin complex 1, acidic, gene 15 promoter. The high levels of specific transgene expression observed in 'bulge cells' (hair follicle stem cells) allow these cells to be isolated with FACS techniques. This mutant mouse strain may be useful in studies of epithelial stem cells. | ||
| 000160 | B6.D2-KitlSl-d/J | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (KitlSl-d/KitlSl-d) and compounds of steel and steel Dickie (KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu
..... For more information please see the full descriiption on the strain data sheet | ||
| 006238 | B6;129S4-Thbs2tm1Bst/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile. Multiple analyses has confirmed the absence of protein in embryonic and adult tissue of homozygous mice. Homozygotes exhibit skin disorders (abnormal collagen fiber patterns, reduced tensile strength, increased fragility) and skin fibroblasts have attachment defects. Mice also exhibit an increase in total density/cortical thickness of the long bones, abnormally long bleeding times, and a significant increase in blood vessel density. Homozygous mice exhibit accelerated wound healing after biopsy and accelerated/increased tumor formation following chemically-induced skin carcinogenesis. Mutant mice may be useful in studies of collagen fibrillogenesis in skin and tendons, angiogenesis and vascular pathophysiology, wound healing, chemically-induced tumor progression, and as a potential model for Ehlers Danlos syndrome. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are fre
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| 005956 | B6;D1Lac-Scd1ab-2J/J | Repository- Live |
| The overall appearance of mice homozygous for either the Scd1ab-J allele or the Scd1ab-2J allele (Stock No. 002304 or 005956) includes slightly hunched posture, dry, scaly skin, thin fur sometimes detectable by 7 days of age, and small eyes with encrusted eyelids stuck shut. They have hypoplasia of the sebaceous glands and other hair follicle abnormalities that result in scarring alopecia. These mice have a paucity of adipose tissue, thin subcutis, and a distinctive odor. Hepatic cholesterol ester and triglyceride synthesis has been shown to be deficient in Scd1ab-J homozygotes and could not be restored through diet. Early studies of skin lipids in the original asebia mutant (Scd1ab) revealed a deficiency in wax esters, wax diesters, and sterols esterified with very long-chain fatty acids along with an in
..... For more information please see the full descriiption on the strain data sheet | ||
| 007622 | B6;SJL-Tg(KRT14-Hr)551Cct/J | Repository- Live |
| Hemizygous mice are viable and fertile. When young, these mice look similar to wildtype mice, but as they age, their coats become shorter and more sparse. Molecular analysis shows delayed development of sebaceous glands, accelerated hair cycle and less-differentiated epidermis. RNA and protein expressed from the transgene are detected in skin as determined by Western and Northern analysis. This strain may be useful as a model for skin and hair development studies. | ||
| 007678 | B6;SJL-Tg(KRT14-rtTA)208Jek/J | Repository- Live |
| Homozygous females and hemizygous males carrying this X-linked K14-rtTA transgene (K14-rtTetA(X) or rtTAX) are viable and fertile. These mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the human keratin 14 promoter. As the transgene is located on the X chromosome, random inactivation of the X chromosome may result in mosaic rtTA expression patterns in female mice. When mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE or tetO), expression of the target gene in the basal cells of the squamous epithelia and in the outer root sheath of the hair follicles is induced with administration of the tetracycline analog, doxycycline (dox). These K14-rtTA mice provide a Tet-On tool that allows the inducible expression of genes in skin cells. | ||
| 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. | ||
| 000314 | B6CBACa Aw-J/A-EdaTa/J-XO | Repository- Live |
| XO or monsomy X mice lack a second sex chromosome. The condition is inherited as an X-linked dominant trait with male lethality. XO mice exhibit some degree of growth retardation, high frequency hearing loss, reduced thyroid activity, reduced body temperature and some behavioral abnormalities. Unlike Turner Syndrome in humans, XO females are fertile. The two-step mating system for this strain (described under Mating System) incorporates the X-linked coat color marker tabby so that mice can be identified by a combination of coat color and sex. This strain may be useful for studies of Turner Syndrome or X-linked recessive alleles. | ||
| 000501 | B6CBACa Aw-J/A-Aifm1Hq/J | Repository- Live |
| Harlequin mice exhibit paucity of fur resulting in near baldness in hemizygous males and homozygous females. Heterozygous females have a patchy absence of hair that is not always obvious, since the degree of hair loss is notably less than 50%. Homozygotes and hemizygous males weigh less than heterozygous or wild type controls. Ataxia is noticeable by 5 months and progresses as the mice age. Initially the ataxia manifests itself as a side-to-side, unsteady gait with a lateral tremor visible at rest. A delayed cerebellar cortical atrophy has been characterized in these mutants, with an apoptotic loss of granule cells beginning at 4 months of age and a necrotic loss of Purkinje cells occurring subsequently. The granule cells re-enter the cell cycle, but the Purkinje cells do not, supporting the postulate that inappropriate cell cycle re-entry of terminally differentiated neurons can induce apoptosis. Cell loss is greater in the caudal lobules of the cerebellum and is extensive by 9 to 11
..... For more information please see the full descriiption on the strain data sheet | ||
| 002044 | B6Ei.Cg-Atp7aMo-blo/J | Repository- Live |
| Female mice heterozygous for the blotchy alleles (Atp7aMo-blo) are viable and fertile. They have irregular patches of light-colored fur. Hemizygous males and homozygous females have reduced viability and many are infertile. Hemizygotes and homozygotes are light all over with no blotching, are usually small, and occasionally have deformed hindlegs.. Most hemizygotes and homozygotes have defective elastin in the aorta and usually die with aortic aneurysm. Hemizygous males have enlarged air spaces in the lung (emphysema), probably because of defective elastin and collagen. Skin collagen and aortic elastin have defective crosslinking at the step at which lysine residues are converted to aldehydes. Hemizygous males have a deficiency of noradrenalin in the brain, probably because a deficiency of copper shown to exist in the brain causes defective activity of the enzyme dopamine-beta-hydroxylase. Copper absorption from the gut and hepatic copper concentration are reduced to
..... For more information please see the full descriiption on the strain data sheet | ||
| 003215 | B6Pin.C3-Ap3b1pe/J | Repository- Live |
| The homozygous pearl phenotype includes hypopigmentation of hair and eyes, prolonged bleeding times associated with platelet storage pool deficiency (SDP) and lysosomal accumulation of ceroid pigment. This combination of abnormalities is characteristic of a human hereditary disease, Hermansky-Pudlak syndrome. Pearl mice also exhibit reduced sensitivity in the dark-adapted state, altered somatostatin binding to the retina, and an increased rate of renal apoptosis, making them a potential model for human congenital stationary night blindness. | ||
| 002167 | BALB/cJ-Cst6ichq/J | Repository- Live |
| 000036 | BXD1/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity.The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000013 | BXD16/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. A mutation has been identified in the BXD16 strain in the amylase 1 gene from the parental Amy1a allele to an allele that has an electrophoretic mobility closer to that of Amy1b. This allele is distinct from all others identified and no evidence of genetic contamination was found. Thus, this is believed to have resulted from a spontaneous mutation. (Hjorth, 1982.) | ||
| 000015 | BXD18/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000010 | BXD19/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000077 | BXD21/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000043 | BXD22/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000029 | BXD29/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000037 | BXD5/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000007 | BXD6/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000084 | BXD8/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity.The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000105 | BXD9/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 005440 | C.129S4-Ccr3tm1Cge/J | Repository- Live |
| Mice homozygous for this CCR3 (chemokine (C-C motif) receptor 3) 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 RNA protection assay analysis of thymus, spleen and lung tissues. Mice homozygous for the mutation have impaired trafficking of eosinophils. A 7-fold decrease in the number of eosinophils in the small intestine and a 6-fold increase in the spleen is observed. Aerosol allergen challenge does not cause the expected infiltration of eosinophils to the lung tissue and airway lumens (50-70% reduction), although abundant eosinophils are found in the airway blood vessels. Concurrent increases in eosinophils in the spleen and intraepithelial mast cells in the spleen occur after allergen challenge. Homozygotes exhibit increased bronchoconstriction with allergen-induced airway hyperresponsiveness. There is no increase in eosinophils or eosinophil product major basic protein (M
..... For more information please see the full descriiption on the strain data sheet | ||
| 000899 | C.B6-Tyr+ Hbbs/J | Repository- Live |
| 000198 | C3FeLe.B6-a/J | Repository- Live |
| 004806 | C3H/HeJ-Mfs/J | Repository- Live |
| 002441 | C3H/HeJ-jal/J | Repository- Live |
| 006926 | C57BL/6J-EgfrVel/J | Repository- Live |
| Mice homozygous for this mutation have an embryonic lethal phenotype, failing to develop past embryonic days 13.5. Heterozygous mice are viable, fertile, do not display any behavioral abnormalities and are born with open eyelids and curly vibrissae. Adult heterozygotes often have small eyes and corneal opacity with excessive secretions at the eyelid edges. MEFs (mouse embryonic fibroblasts) exhibit reduced migratory ability, approximately 53% of wildtype controls. Histological analysis of homozygous E12.5 embryos reveals placental defects. This mutant mouse strain may be useful in studies of development and as a visible dominant marker for the Egfr allelic series. | ||
| 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. | ||
| 000565 | C57BL/6J-Pax3Sp-d/J | Repository- Live |
| Mice homozygous for the splotch-delayed spontaneous mutation (Pax3Sp-d) have a phenotype that is generally less severe than mice homozygous for the splotch mutation (Pax3Sp, Stock No. 002469). Splotch-delayed homozygous embryos survive to birth, compared to splotch mutant embryos that die at E13 due to neural tube defects. Homozygous splotch-delayed mutant embryos display caudal rachischisis only. Heterozygous splotch-delayed have a white belly spot. Delayed splotch is a point mutation within the paired domain of Pax3. This impairs DNA binding of this domain and also, suprisingly, of the homeodomain, not directly affected in the mutant gene. | ||
| 002469 | C57BL/6J-Pax3Sp/J | Repository- Live |
| Mice homozygous for the splotch spontaneous mutation (Pax3Sp) die at E13 due to neural tube defects. Malformations of homozygous mutant embryos include rachischisis in the lumbosacral region and frequently in the region of the hindbrain. Heterozygous splotch mice show white spotting on the belly and occasionally on the back, feet, and tail. Splotch is a point mutation within intron 3 of the paired homeobox 3 (Pax3) gene on mouse Chromosome 1. The mutation interferes with normal splicing of intron 3 and leads to at least 4 aberrantly spliced mRNAs with exon 4 deleted. The Pax3Sp mutation also impairs homodimerization of the protein, a function associated with the octapeptide-encoding central segment of the gene. There are multiple alleles at this locus including splotch-delayed (Pax3Sp-d, Stock No. 000565), which is similar to splotch but displays caudal rachischisis only. | ||
| 000811 | C57BL/6J-Ptpn6me-v/J | Repository- Live |
| Mice homozygous for the viable motheaten spontaneous mutation (Ptpn6me-v) develop severe autoimmune disease. Characteristics include by granulocytic skin lesions, pneumonitis, impaired humoral and cell-mediated immune responses, decreased responses to T cell and B cell mitogens and deficient cytotoxic T cell and NK cell activity. B cells are LY-1+. Homozygous mutant mice also exhibit hyperimmunoglobulinemia, and express multiple autoantibodies. Macrophages show increased proliferative capacity. In addition to defects in the immune system, viable motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The osteoporosis phenotype includes significantly lower bone mineral density and mineral content in the femurs of viable motheaten mice compared to normal littermate controls. In addition, these mice show reduced amounts of trabecular bone and decreased cortical thickness. The lifespan of homozygo
..... For more information please see the full descriiption on the strain data sheet | ||
| 005135 | C57BL/6J-Sls/J | Repository- Live |
| 007599 | C57BL/KaLawRij-Sharpincpdm/RijSunJ | Repository- Live |
| Mice homozygous for this spontaneous mutation develop a severe, chronic, inflammatory skin disease beginning at 3-5 weeks of age. Mice appear runted and life span is shortened. In addition to dermatitis, homozygotes exhibit multi-organ inflammation with eosinophilia, defective TH1 cytokine production, splenomegaly, absent Peyer's patches (adult), diminished serum immunoglobulins, and an absence of B cell follicles, follicular dendritic cells, and germinal centers in secondary lymph organs. This mutant mouse strain may be useful in studies related to eosinophilic dermatitis, inflammation, and secondary lymphoid organ deveopment. | ||
| 000516 | C57BLKS-Rpl24Bst/J | Repository- Live |
| Belly spot and tail (Rpl24Bst) is a semidominant, homozygous in utero lethal mutation. Adult heterozygotes are viable and fertile although a reduced birth rate for heterozygotes has been reported. This may reflect incomplete penetrance, or, more likely, prenatal mortality. The Rpl24Bst mutation has variable expressivity and the heterozygous phenotypic traits include shortened and kinked tail, white feet and belly spot, malocclusion, smaller body size, exencephaly, abnormalities of the spine, ocular defects, and polydactyly. Polydactyly is found predominantly in the right rear paw, occasionally in the left front paw and rarely in the left rear or right front paws. Approximately 50-60% of the heterozygotes have a reduction in pupillary light reflex in one or both eyes due to an underlying optic nerve atrophy. Ontological studies showed a delay in the developmental fusion of the optic fissure, a disruption of the retinal layers by embryonic day 1
..... For more information please see the full descriiption on the strain data sheet | ||
| 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. | ||
| 004828 | FVB.129P2-Pde6b+ Tyrc-ch/AntJ | Repository- Live |
| These mice are homozygous for the 129P2/OlaHsd wildtype Pde6b allele and do not suffer from blindness due to retinal degeneration. Mice from the colony of FVB.129P2-Fmr1tm1Cgr/J, Stock No. 004624, that no longer carried the mutant allele for Fmr1 were used to establish this line. Mice are pigmented as a result of the homozygosity of the Tyrc-ch allele. This mutant mouse strain may be useful in studies where a sighted mouse on the FVB background is an appropriate control, such as behavioral studies. This strain serves as the control for the FVB.129P2-Fmr1tm1Cgr/J strain, Stock No. 004624 . | ||
| 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 descriiption on the strain data sheet | ||
| 006956 | NOD.Cg-Vdrtm1Ska/CmatJ | Repository- Live |
| Heterozygous mice are viable, fertile, and phenotypically indistinguishable from wildtype siblings. Homozygous mutant mice are viable but infertile. No VDR mRNA is detected by RT-PCR in samples from the intestine or kidney or from homozygous mutant embryo. Increased expression of CTP27B1 and reduced expression of CYP24A1 and calbindin-D9k is detected by RT-PCR in samples from VDR-deficient kidneys. Although mice homozygous for this targeted mutation are viable, shortly after weaning they exhibit dysmorphic features including a flat face and short nose, alopecia, growth retardation, and skeletal defects including hypocalcaemia, decreased bone mineral density, widened growth plates with hypomineralization, less trabeculae and thicker osteo seams. Homozygous mutant mice exhibit metabolic imbalances including abnormally high and low levels of 1,25(OH),2D3 and 25(OH)D3, respectively and abnormal cytokine and chemokine profiles.
Homozygous mice exhibit normal pancreatic islet archite
..... | ||
| 004774 | NOD/ShiLtJ-wly/J | Repository- Live |
| Mice develop curly hair by 4 weeks of age; whiskers are normal (straight). Giant hair follicles in anagen and a paucity of subdermal fat were found in histology of the skin at 5 weeks of age. | ||
| 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). | ||
| 005354 | RB156Bnr/Ei rul-Gulosfx-2J/J | Repository- Live |
| The phenotype of the sfx2J remutation is identifiable at 4-5 weeks of age when the mutants appear smaller than their control littermates and begin to hobble about their cage. Between 5 and 8 weeks of age the mutants develop rear limb paralysis and many die by 8 weeks of age. The phenotypic characteristics of this mutation are similar to the original mutation spontaneous fracture (Gulosfx ) except for the eye phenotype described below that is inherent in the background strain on which the sfx2J mutation arose. Mice homozygous for the sfx2J remutation also had cataracts and rosettes and wavy outer nuclear layer of retinas. The eyes of a female mutant were checked using an opthalmascope and it was found to have cataracts on both eyes (as the strain background has characteristically). It has not yet been determined if the rosettes and wavy outer nuclear layer of the retinas is also characteristic of the background s
..... For more information please see the full descriiption on the strain data sheet | ||
| 005362 | RB156Bnr/Ei-rul/J | Repository- Live |
| The phenotype of this mutation can be identified at about 10 days of age by a ruffled looking coat, which is different than the smooth coat of control littermates. The hair of mutant mice is sparse and has some curling. The ruffled looking coat is maintained throughout the animal's lifespan, unlike the caracul and caracul-like mutants who lose some of their curly coat with age. Mice homozygous for the ruffled mutation have a normal lifespan and both sexes breed normally. | ||
| 005415 | RHJ/LeJ-stpm/J | Repository- Live |
| The phenotype of this mutation can be identified by a curly coat, which is different from the smooth coat of control littermates. At 3 weeks of age, mice homozygous for this new mutation have very curly coats and slightly curved vibrissae. In several weeks time the curly coat disappears but the hair retains a rough texture, and the vibrissae then appear normal. Heterozygous mice have normal smooth coats and straight whiskers. | ||
| 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
>
..... For more information please see the full descriiption on the strain data sheet | ||
| 000644 | SEA/GnJ | Repository- Live |
| 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. | ||
| 001743 | STOCK dwg/J | Repository- Live |
| Mice homozgyous for the dwarf grey spontaneous mutation (dwg) are viable but do not breed. Homozygous mutant mice have grey coats, are smaller than littermates, and develop cataracts by 3-4 weeks of age. Additional characteristics include increased numbers of osteoclasts, reduced bone mass, reduced red pulp area of the spleen, and slightly reduced thyroxin levels. | ||
| 003100 | STOCK dwgBayer/J | Repository- Live |
| The dwarf-Bayer mutation (dwgBayer) occurred spontaneously in an embryonic stem cell line during genetic targeting of the insulin receptor gene. The phenotype of the mice resemble drawf grey (dwg, Stock No. 001743) and subsequent characterization determined that the two mutations are allelic. Homozygous mutant mice are grey and smaller in size than wildtype littermates. | ||
| 004623 | STOCK Tg(Fos-lacZ)34Efu/J | Repository- Live |
| These TOPGAL transgenic mice are a reporter strain that express Beta-galactosidase in the presence of the lymphoid enhancer binding factor 1/transcription factor 3 (LEF/TCF) mediated signaling pathway and activated Beta-catenin. The transgene contains the lacZ gene under the control of a regulatory sequence consisting of three consensus LEF/TCF-binding motifs upstream of a minimal c-fos promoter. Transgenic mice display TOPGAL activity (Beta-galactosidase activity) during early embryonic development in a subset of pluripotent embryonic basal cells of the epithelium and dermis of developing hair follicles, but not during the next stage of hair follicle development; formation of hair germs. TOPGAL transgene activity reappears in hair follicles at E16.5 and TOPGAL expression is strongly upregulated in the postnatal hair shaft precursor cells in both whisker and body hair anagen follicles (active periods of hair growth). TOPGAL expression ceases during catagen (regression and
..... For more information please see the full descriiption on the strain data sheet | ||
| 005107 | STOCK Tg(KRT14-cre/Esr1)20Efu/J | Repository- Live |
| These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the human keratin 14 (KRT14) promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain. The mutant mouse estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen (tamoxifen). Restricted to the cytoplasm, the cre/Esr1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted keratinocyte-specific deletions. Oral tamoxifen administration induces Cre recombination in toe, back skin and tongue. Topically administered tamoxifen induces Cre-mediated recombination in a specific localized area of the skin, occuring in 50 to 60% of the
..... For more information please see the full descriiption on the strain data sheet | ||
| 000274 | TSJ/LeJ | Repository- Live |
| 000693 | WC/ReJ KitlSl/J | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing
..... For more information please see the full descriiption on the strain data sheet | ||
| 100401 | WCB6F1/J KitlSl KitlSl-d | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Many steel alleles cause severe anemia resulting in death in utero of homozygous mutant mice. However, mice homozygous for some steel mutations and compound heterozygotes for two steel alleles (e.g., KitlSl/KitlSl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtuall
..... For more information please see the full descriiption on the strain data sheet | ||
| 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.). | ||
| 002516 | 129-Edn3tm1Ywa/J | Repository-Cryopreserved |
| This mutation is alleleic with the lethal spotting spontaneous mutation. Homozygous mice are viable at birth, but most die within about a month. They show a disruption in neural crest lineage development. They die from peritonitis subsequent to aganglionic megacolon. They may serve as a model for human Hirschsprung's disease. | ||
| 006403 | 129S.B6-Tg(KRT14-Esr1/HRAS)1Pkha/J | Repository-Cryopreserved |
| Mice hemizygous for this "K14-ER:Ras" transgene are viable and fertile. Inducible expression of the ER:Ras fusion protein is observed in the epidermis following topical application of 4-hydroxytamoxifen (4OHT). Prolonged (4 weeks) induction of human H-RasG12V activity promotes the undifferentiated, proliferative phenotypic characteristics observed in epidermal cancer; including hyperplasia, increased mitotic index, decreased expression of differentiation markers and increased expression of beta-1 and beta-4 integrin subunits. H-RasG12V-induced skin abnormalities were entirely reversed within one month after 4OHT cessation. These mice have a similar 4OHT-inducible skin phenotype as the transgenic mice expressing human Raf-1[DD] (Stock No. 006661) or human Mek1R4F (Stock No. 006822), and may be useful in studies of the Ras/Raf/MEK/ERK cell proli
..... For more information please see the full descriiption on the strain data sheet | ||
| 000090 | 129S1/Sv-Oca2+ Tyr+ KitlSl-J/J | Repository-Cryopreserved |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing a
..... For more information please see the full descriiption on the strain data sheet | ||
| 000091 | 129T1/Sv-Oca2+ Tyrc-ch Dnd1Ter/J | Repository-Cryopreserved |
| 001279 | 129T1/Sv-Oca2+ Tyrc-ch-Aft/J | Repository-Cryopreserved |
| Aft is a dominant mutation that causes increased postnatal lethality in heterozygotes and nearly 100% embryonic or perinatal lethality in homozygotes. Aft/+ mice can be identified by tail kinks near the tail tip and syndactyly of the third and fourth digits of the hind feet, a trait which is often unilateral. This syndactyly does not result from bone fusion, but rather from the persistence of the skin web that normally is removed via apoptosis during development. The tail kinks appear to result from cartilage overgrowth and fusion. Alopecia is found at six to eight months of age and can progress into bleeding ulcerations. Histology of Aft/+ skin shows fewer follicles, fibrosis, and an increase in the number of mast cells. The penetrance of this mutation is only approximately 65% on the 129/Sv and C57BL/6J backgrounds and the expressivity is variable. The most prevalent trait in Aft/+ mice is tail kinks, followed by syndactyly then skin lesions. The
..... For more information please see the full descriiption on the strain data sheet | ||
| 005445 | A.B6 Tyr+-Cybanmf333/J | Repository-Cryopreserved |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf333 entry. | ||
| 005012 | A.B6 Tyr+-Myo5ad-l31J/J | Repository-Cryopreserved |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page. | ||
| 001498 | A/J-lgh/J | 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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| 000251 | AEJ.Cg-ae +/a Gdf5bp-H/J | Repository-Cryopreserved |
| 000202 | AEJ/Gn-bd/J | Repository-Cryopreserved |
| 000820 | AKR/J-Foxn1nu-str/J | Repository-Cryopreserved |
| Mice homozygous for the streaker spontaneous have a phenotype that is very similar to nude mice. Homozygosity prevents the development of T cell lymphomas seen in AKR mice. | ||
| 003656 | AKR/J-we4J/J | Repository-Cryopreserved |
| 001005 | AKXD1/TyJ | Repository-Cryopreserved |
| 001017 | AKXD10/TyJ | Repository-Cryopreserved |
| 001003 | AKXD11/TyJ | Repository-Cryopreserved |
| 000765 | AKXD13/TyJ | Repository-Cryopreserved |
| 000779 | AKXD14/TyJ | Repository-Cryopreserved |
| 000954 | AKXD15/TyJ | Repository-Cryopreserved |
| 000958 | AKXD16/TyJ | Repository-Cryopreserved |
| 001093 | AKXD18/TyJ | Repository-Cryopreserved |
| 000776 | AKXD2/TyJ | Repository-Cryopreserved |
| 001062 | AKXD21/TyJ | Repository-Cryopreserved |
| 000947 | AKXD22/TyJ | Repository-Cryopreserved |
| 000969 | AKXD24/TyJ | Repository-Cryopreserved |
| 000949 | AKXD25/TyJ | Repository-Cryopreserved |
| 000764 | AKXD27/TyJ | Repository-Cryopreserved |
| 000959 | AKXD3/TyJ | Repository-Cryopreserved |
| 000777 | AKXD6/TyJ | Repository-Cryopreserved |
| 000763 | AKXD9/TyJ | 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). | ||
| 000475 | B10.129-weBkr/CyJ | Repository-Cryopreserved |
| 000409 | B10.129P-H1b Hbbd Tyrc Ea7a/(5M)oSnJ | Repository-Cryopreserved |
| 000418 | B10.129P-H1b Tyrc Hbbd/(5M)nSnJ | Repository-Cryopreserved |
| 002472 | B10.A/SgSnJ-Hps3coa-5J/J | Repository-Cryopreserved |
| 000432 | B10.C-H1b Hbbd Tyrc/(41N)SnJ | Repository-Cryopreserved |
| 000427 | B10.CE-H13b Aw/(30NX)SnJ | Repository-Cryopreserved |
| 000580 | B10.D2/nSn-Tyrc-4J/J | Repository-Cryopreserved |
| 001013 | B10.D2/nSnJ-Myo5ad-n/J | Repository-Cryopreserved |
| Mice homozygous for the dilute-neurological spontaneous mutation (Myo5ad-n) display a neuromuscular disorder, but the condition is less severe than in dilute-lethal mutant mice (Myo5ad-l, Stock No. 000253). | ||
| 000420 | B10.LP-H13b Aw/Sn | Repository-Cryopreserved |
| 000422 | B10.LP-H3b H13b/(36NS)Sn | Repository-Cryopreserved |
| 000477 | B10.PA-Pldnpa H3e at/SnJ | Repository-Cryopreserved |
| This minor histocompatibility 3 (H3e) congenic strain is also carrying the closely linked pallid mutation (Pldnpa) as well as the black and tan allele of nonagouti also residing on Chromosome 2. Histocompatibility 3 is one of several loci isolated and identified by Dr. George Snell and co-workers. Histocompatibility gene differences were identified by generating congenic resistant strains and testing for resistance to transplantable tumors. Homozygous pallid mice have pink eyes, a diluted coat color and their viability is slightly reduced. Some homozygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manga
..... For more information please see the full descriiption on the strain data sheet | ||
| 000456 | B10.SM H2v H2-T18b/(70NS)Sn-cw/J | Repository-Cryopreserved |
| 000419 | B10.UW-H3b we Pax1un at/SnJ | Repository-Cryopreserved |
| 003879 | B10;TFLe-a/a T tf/+ tf/J | Repository-Cryopreserved |
| 000234 | B10Gn.Cg-Rn/J | Repository-Cryopreserved |
| 000822 | B6 x 129S1/SvEi Oca2+ Tyr+-Vsx2or-J/J | Repository-Cryopreserved |
| 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. | ||
| 000599 | B6 x B6CBCa Aw-J/A-T(5;13)264Ca KitW-v/J | Repository-Cryopreserved |
| 000507 | B6 x B6EiC3 a/A-Otcspf/J | Repository-Cryopreserved |
| 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. | ||
| 002542 | B6 x CByJ.Cg-Crm/J | Repository-Cryopreserved |
| 000618 | B6 x FSB/GnEi a/a Ctslfs/J | Repository-Cryopreserved |
| 003602 | B6 x STOCK Cln6nclf-Edardl-3J/J | Repository-Cryopreserved |
| 001518 | B6 x STOCK T tf/th45 tf/J | Repository-Cryopreserved |
| 000577 | B6 x STOCK a Oca2p Hps5ru2 Ednrbs/J | Repository-Cryopreserved |
| 006564 | B6(C)-KitW-41J Gusbmps/BrkJ | Repository-Cryopreserved |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. In appearance, homozygous KitW-41J mice are mostly white with black eyes and brown or grey spots. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage disease
..... For more information please see the full descriiption on the strain data sheet | ||
| 002016 | B6(Cg)-Aw-J EdaTa-6J Chr YB6-Sxr/EiJ | Repository-Cryopreserved |
| 005565 | B6(V)-chtl2J/J | Repository-Cryopreserved |
| Mice homozygous for this spontaneous recessive mutation are recognized by a diluted coat color that appears chocolate brown. This color dilution also lightens the eyes, feet, ears, and tail of affected animals. | ||
| 000552 | B6-Aw-J-EdaTa-6J.Cg-Sxr | Repository-Cryopreserved |
| 001730 | B6-Aw-J-EdaTa-6J.Cg-Sxrb Hya-/J | Repository-Cryopreserved |
| 000841 | B6-Aw-J.CBy-EdaTa-By/J | Repository-Cryopreserved |
| 000311 | B6-Pax3Sp.Cg-N/J | Repository-Cryopreserved |
| Mice homozygous for the splotch spontaneous mutation (Pax3Sp) die at E13 due to neural tube defects. Malformations of homozygous mutant embryos include rachischisis in the lumbosacral region and frequently in the region of the hindbrain. Heterozygous splotch mice show white spotting on the belly and occasionally on the back, feet, and tail. There are multiple alleles at this locus including splotch-delayed (Pax3Sp-d, Stock No. 000565), which is similar to splotch but displays caudal rachischisis only. This C57BL/6 congenic strain is also carrying the semidominant naked spontaneous mutation (N). | ||
| 003509 | B6.129-Blmhtm1Geh/J | Repository-Cryopreserved |
| Bleomycin (BLM) is a clinically used glycopeptide anticancer agent. It is deaminated in vitro by BLMH. Blmh null mice have decreased viability and fertitility. Only about 65% of the expected number survive the neonatal period. Mice lacking Blmh exhibit variably penetrant tail dermatitis that resembles rodent ringtail. This resembles skin lesions in humans with pellagra, necrolytic migratory erythema, and acrodermatitis enteropathica. Null mice also are more sensitive to acute BLM lethality and develop pulmonary fibrosis following BLM treatment. | ||
| 005951 | B6.129-Dgat2tm1Rvf/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation have a perinatal lethal phenotype, most fail to survive past 6 hours after birth due to dehydration, skin barrier abnormalities, hypothermia and energy deficiencies. Reduced levels of gene product (mRNA) are detected by RT-PCR analysis of brown adipose tissue and livers of neonate homozygous mutants. Growth retardation is observed in homozygous embryos after embryonic day 12.5. Newborn homozygotes are hypoglycemic and lipopenic, exhibiting reduced plasma triglyceride, free fatty acid and glucose levels and have almost no white fat tissue. Within a few hours of birth, the skin of homozygotes becomes dry and cracked. Homozygous mutants rapidly lose weight due to dehydration caused by impaired permeability barrier function. Histological analysis of skin tissue from homozygotes reveals abnormally thin epidermis and compact orthohyperkeratosis of the stratum corneum. Homozygotes surviving between 8 and 24 hours develop tail necrosis. Hetero
..... For more information please see the full descriiption on the strain data sheet | ||
| 003360 | B6.129-Juptm1Kem/J | Repository-Cryopreserved |
| Plakoglobin Jup null-mutant embryos die from embryonic day 10.5 onward due to severe heart defects. Some mutant embryos develop further, especially on a C57BL/6 background. These mice die around birth, presumably due to cardiac dysfunction, and with skin blistering and subcorneal acantholysis. The skin phenotype in plakoglobin-deficient mice is reminiscent of the human blistering disease, epidermolytic hyperkeratosis. | ||
| 006156 | B6.129-Sceltm1Hba/J | Repository-Cryopreserved |
| Homozygous mice are viable and have no overt morphological or developmental abnormalities. The donating investigator reports that fertility may be impaired in homozygous mice (limited number of litters possible). No endogenous gene expression is observed in skin or stratified squamous epithelia. These mutant mice may be useful in dermatological studies, such as cornified envelope formation, organization of the intima, as well as structural distinctions between arteries and veins, and respiratory structure and function. | ||
| 003533 | B6.129P-B2mtm1Unc-rs2J/J | Repository-Cryopreserved |
| 002037 | B6.129P-cpy/J | Repository-Cryopreserved |
| 002219 | B6.129P2-Tgfatm1Ard/J | Repository-Cryopreserved |
| Mice homozygous for the Tgfatm1Ard mutation develop normally, are of normal size, weight, and health, and are fertile. They display a pronounced waviness in the coat and whiskers, and dramatic derangement of the hair follicles. Older homozygous mice occasionally show some corneal inflammation that may be the result of a defect in wound healing. | ||
| 007015 | B6.129S1-Gadd45gtm1Flv/J | Repository-Cryopreserved |
| Homozygotes are viable and fertile, but are poor breeders. TH1 helper T cells from homozygotes are severely compromised in their abilities to activate p38 (MAPK14)and JNK (MAPK8) in response to T cell receptor (TCR) signaling, produce much less interferon gamma (IFNG) upon restimulation, and are deficient in activation-induced cell death (AICD). Deficiencies in this gene also cause reduced contact hypersensitivity in the animals. | ||
| 004042 | B6.129S2-Alox12tm1Fun/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Alox12 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Alox12 protein product or enzyme activity is detected in platelets derived from homozygous null animals. Platelets exhibit a hyperresponsiveness to ADP-induced aggregation. Studies examining basal transepidermal water loss indicate that null animals exhibit greater water loss through the skin when compared to control animals. | ||
| 002612 | B6.129S2-Bmp4tm1Blh/J | Repository-Cryopreserved |
| Mice homozygous for the Bmp4tm1Blh targeted mutation mutation die early in embryogenesis. Fifteen to twenty percent of heterozygous mice show developmental defects including polydactyly, craniofacial defects, and cystic kidneys. Heterozygotes have also been reported to show eye abnormalities. | ||
| 003321 | B6.129S6-Gbatm1Nsb/J | Repository-Cryopreserved |
| Mice homozygous for this mutation die neonatally due to a defect in the skin vapor barrier. Homozygous mice are small at birth and display an abnormal respiration that progresses to cyanosis and death. This phenotype is similar to a severe infantile form of Gaucher's disease in humans. | ||
| 003329 | B6.129S7-Itgb2tm2Bay/J | Repository-Cryopreserved |
| Mice homozygous for the Itgb2tm2Bay targeted mutation are viable and fertile, though not good breeders. This mutation differs from the Itgb2tm1Bay mutation (Stock No. 2128) in that it is a null mutation for the Itgb2 subunit of leukocyte integrins. Mutant mice develop chronic dermatitis with extensive facial and submandibular erosions. They also exhibit elevated neutrophil counts, increased immunoglobulin levels, lymphadenopathy, splenomegaly, and abundant plasma cells in skin, lymph nodes, gut and kidney. A severe defect in T cell proliferation can be found in mutant mice when T cell receptors are stimulated either by staphylococcal enterotoxin A or by major histocompatibility complex alloantigens. The phenotype of the mutant mice resembles the phenotype for the human disorder Leukocyte Adhesion Deficiency Type I (LADI). | ||
| 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 homozygou | ||