Search Criteria: Research Area is "Endocrine Deficiency Research: Skin Defects"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 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. | ||
| 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 | ||
| 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. | ||
| 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 | ||
| 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. | ||
| 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. | ||
| 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 | ||
| 006941 | B6.129S7-B4galt1tm1Shur/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. Ninety percent of homozygotes die soon after birth or within two to three weeks of birth. Surviving homozygotes are initially smaller than wild-type or heterozygotes and exhibit abnormal skin and coat, but assume a normal growth rate and appearance at three to four weeks of age. No gene product (mRNA) is detected by RT-PCR analysis of homozygous tissues. Neither the long or short isoform is expressed. Beta 1,4-galactosyltransferase enzyme activity is undetectable except for residual activity in brain and testis. Galactose residues are absent from testis. Heterozygotes have an intermediate enzyme activity level. Surviving homozygotes exhibit puffy faces (hypothyroid myxedema), thin skin, decreased density of hair follicles, reduction in subdermal adipose tissue, delayed spermatogenesis and incomplete lung development. Histological an
..... For more information please see the full descriiption on the strain data sheet | ||
| 003625 | B6.C-H2-Ab1bm12/KhEg-Mc1re-J/J | Repository- Live |
| 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 | ||
| 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
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| 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 | ||
| 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 | ||
| 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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| 000599 | B6 x B6CBCa Aw-J/A-T(5;13)264Ca KitW-v/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 | ||
| 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. | ||
| 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. | ||
| 000495 | B6.C-H38c/By-KitW-56J/J | Repository-Cryopreserved |
| 000560 | B6.C-H7b/By KitW-50J/J | Repository-Cryopreserved |
| 000122 | B6.C3-KitW-44J/J | Repository-Cryopreserved |
| KitW-44J heterozygotes have white-tipped feet and a white tail tip although the belly spot standardly found in KitW* mutations is very small in this mutant, sometimes restricted to only a few hairs. Homozygotes have a flecked pelt that is predominantly white, especially ventrally, with pigmented patches particularly at the lateral borders. The pigmentation fades with age yielding black-eyed white mice by approximately 9 months of age. While many KitW-44J homozygotes are viable, fertility is diminished. Homozygous females have greatly reduced fertility and gonads that are smaller in size with reduced activity. Homozygous males are sterile although spermatogenesis occurs. The KitW-44J allele does not produce anemia in either its heterozygous or homozygous state. The red blood cell count, white blood cell count, hematocrit, and mean cell volume are normal. However, bone marrow transplantation experiments reveal that t
..... For more information please see the full descriiption on the strain data sheet | ||
| 000991 | B6.C58-KitW-57J/J | Repository-Cryopreserved |
| 000133 | B6.Cg-KitW-24J/J | Repository-Cryopreserved |
| 000139 | B6.Cg-KitW-25J/J | Repository-Cryopreserved |
| 000164 | B6.Cg-KitW/J | Repository-Cryopreserved |
| 000124 | B6.Cg-KitlSl Krt71Ca/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 adva
..... For more information please see the full descriiption on the strain data sheet | ||
| 000194 | B6.Cg-Lx KitW-v/J | Repository-Cryopreserved |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Heterozygous lx mice show preaxial polydactyly (including hyperphalangy of the first digit) of the hindfeet. Homozygotes show preaxial polydactyly or oligodactyly of the hindfeet, reduction of the tibia, loss of part of the femur and pubis, decrease in number of presacral vertebrae, and anomalies of the urogenital system including horseshoe kidney, hydronephrosis, and hydroureter.
Although homozygous KitW-v/
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| 002863 | B6.Cg-Tgfawa1/J | 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. Ventricular enlargement and striatal reduction is observed in adult homozygous wa1 mice. The phenotype is more severe in males. In addition, adult males exhibit reduced hippocampal volume and impaired auditory and contextural fear learning. Both sexes demonstrate an abnormal fear response. Peripubertal mice do not exhibit behavioral deficits despite slight forebrain structural abnormalities. (Koshibu K, et al., 2005) | ||
| 000171 | B6.D2-KitW-45J/J | Repository-Cryopreserved |
| 001563 | B6.D2-KitW-73J/J | Repository-Cryopreserved |
| 001177 | B6.LP-KitW-49J/J | Repository-Cryopreserved |
| 006086 | B6.SJL-Tg(HBB-GH1)420King/J | Repository-Cryopreserved |
| Mice hemizygous for this transgene are viable. While males are fertile, transgenic females are unreliable breeders and mothers. Homozygotes are sterile. In both fetal and adult tissues, erythroid-specific expression of the transgene is observed. Transgenic mice have 120-150% greater mature body mass and increased bone mass. The donating investigator also reports transgenic mice have increased dermatological stiffness and toughness. Transgenic mice have a characteristic coat with few guard hairs compared to wildtype littermates. These mice may be useful in studies of bone formation and development, dermatology, and acromegaly. | ||
| 004161 | B6;129-Fgf7tm1Efu/J | Repository-Cryopreserved |
| Mice homozygous for this targeted allele are viable, fertile and normal in size. No Fgf7 transcript is detected. By 2 months of age, the hair coat takes on a matted/greasy appearance that becomes more prominent with age. Homozygote kidneys are markedly smaller and posses structural anomalies. Morphometric analyses indicate a reduction (~30% of wildtype) in the total number of nephrons present. Kidney development appears to be effected as early as embryonic day 16.5. This mutant mouse strain represents a model that may be useful in studies related to kidney disease. | ||
| 000350 | B6By.Cg-KitW-v MitfMi-wh T/J | Repository-Cryopreserved |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a dilut
..... For more information please see the full descriiption on the strain data sheet | ||
| 000553 | B6EiC3Sn a/A-Egfrwa2 Wnt3avt/J | Repository-Cryopreserved |
| Mice homozygous for the spontaneous waved 2 mutation (Egfrwa2) are recognizable at 2 to 3 days by curly whiskers. The first coat is waved but later coats are not; vibrissae usually remain curled and the guard hairs curved. Some homozygotes have eyelids open at birth. Fertile mutant females have impaired lactation. Mice homozygous for the vestigial tail spontaneous mutation (Wnt3avt) have very short tails, few presacral vertebrae, and abnormal formation of the lumbar vertebrae. | ||
| 000291 | C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-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 adva
..... For more information please see the full descriiption on the strain data sheet | ||
| 000627 | C3H/HeJ-KitW-x/J | Repository-Cryopreserved |
| 000847 | C3Sn.B6-KitW-39J/J | Repository-Cryopreserved |
| 001380 | C3Sn.Cg-KitlSl-con/J | Repository-Cryopreserved |
| Both homozygous and heterozygous mice with the contrasted induced mutation (KitlSl-con) are viable. Male homozygous mutant mice are fertile but females are usually sterile. Mice heterozygous for the contrasted mutation are recognizable soon after birth by dark pigmentation of the genital papilla with the adult coat being slightly lighter than normal. Homozygous mutant mice also have dark genitalia and a markedly diluted coat and mild macrocytic anemia. | ||
| 000166 | C57BL/6J-KitW-17J/J | Repository-Cryopreserved |
| 000167 | C57BL/6J-KitW-18J/J | Repository-Cryopreserved |
| 000169 | C57BL/6J-KitW-20J/J | Repository-Cryopreserved |
| 000117 | C57BL/6J-KitW-34J/J | Repository-Cryopreserved |
| 000128 | C57BL/6J-KitW-35J/J | Repository-Cryopreserved |
| 000134 | C57BL/6J-KitW-37J/J | Repository-Cryopreserved |
| 000062 | C57BL/6J-KitW-39J/J | Repository-Cryopreserved |
| 000121 | C57BL/6J-KitW-40J/J | Repository-Cryopreserved |
| 000119 | C57BL/6J-KitW-41J/J | Repository-Cryopreserved |
| 000127 | C57BL/6J-KitW-42J/J | Repository-Cryopreserved |
| 000129 | C57BL/6J-KitW-43J/J | Repository-Cryopreserved |
| 000990 | C57BL/6J-KitW-55J/J | Repository-Cryopreserved |
| 001179 | C57BL/6J-KitW-62J/J | Repository-Cryopreserved |
| 003252 | C57BL/6J-KitlSl-20J/J | Repository-Cryopreserved |
| KitlSl-20J is a dominant allele. On the C57BL/6J background heterozygotes have a light black coat color with lighter tail and feet and a steel colored belly with a belly spot. Heterozygotes of both sexes are viable and fertile. | ||
| 000060 | C57BL/6J-Mc1re/J | Repository-Cryopreserved |
| 000965 | CBACa.C3-KitW-x/J | Repository-Cryopreserved |
| 001723 | CByJ.A-Ttc7fsn/J | Repository-Cryopreserved |
| Homozygous fsn mice suffer from hypochromic and normocytic anemia at birth which becomes more severe with age. The anemia makes the homozygous mice distinguishable as pups because of the pale color of ears and eyes. At 2 weeks of age focal epidermal hyperplasia and inflammation is evident with psoriasiform skin lesions becoming confluent and diffuse in 3-4 week old weanlings. The skin lesions progress to generalized alopecia and shedding of thick white scales. The gross lesions are accompanied by thickening and keratinization of the skin. A progressive paplosquamous disease ensues which is a model for some forms of psoriasis. fsn/fsn mice show hematocrit levels and red blood cell counts that are significantly decreased from birth through adulthood. Consequently the heart, liver and spleen become enlarged but the thymus weight is less than half normal. As the spleen enlarges, the mice also develop a potbellied appearance aiding in homozygous fsn identification. G
..... For more information please see the full descriiption on the strain data sheet | ||
| 001595 | DW/J-Acdacd/J | Repository-Cryopreserved |
| acd/acd homozygotes can be distinguished from their wildtype (?/+) littermates by darkened pigmentation, short, curly vibrissae, smaller overall size, and abnormal pelage. Hair growth is retarded and lacks zigzag and guard hairs producing a sparse coat. There is heavy pigmentation in the nose, ears, body, feet and tail, and foci of melanin are also found in the skin and lymph nodes. Tail kinks or polydactyly of the hind feet are sometimes found and external genitalia are underdeveloped. It is rare for homozygotes to breed. Hydronephrosis is sometimes found in post-wean aged homozygotes resulting from focal hypertrophy of ureteral epithelium which causes ureteral blockage. The adrenals are abnormal in both males and females. Although the size of the medullary cells is normal, the cortical cells and nuclei are much larger than normal with nuclear inclusions and many mitochondria in the cytoplasm. These mitochondria have tubular cristae and cholesterol ester droplets, whic
..... For more information please see the full descriiption on the strain data sheet | ||
| 000092 | FL/1Re-KitW/J | Repository-Cryopreserved |
| 001000 | RBD/DnJ | Repository-Cryopreserved |
| 000807 | RBJ/DnJ | Repository-Cryopreserved |
| 002857 | STOCK Egfrtm1Mag/J | Repository-Cryopreserved |
| Mice homozygous for the Egfrtm1Mag targeted mutation are recognizable at 2 to 3 days by curly whiskers. The first coat is waved but later coats are not; vibrissae usually remain curled and the guard hairs curved. Fertile mutant females have impaired lactation. | ||
| 003118 | STOCK Es1e Foxn1nu/J | Repository-Cryopreserved |
| Mice homozygous for Es1e are viable and fertile and exhibit no apparent defect. Es1e was discovered in a screen of progeny of triethylenemelamine (TEM) treated male mice for mutations at specific loci, but appears to have pre-existed in the male. The screen employed analysis of blood and kidney homogenates by "standard starch gel electrophoresis techniques" and focused on enzymes known to differ in electrophoretic mobility between the parental strains (DBA/2J and C57BL/6J). Es1e was initially thought to be a null allele, but characterization of homozygous F2 mice demonstrated presence of a faint band migrating between those of the parental strains, which was not perceived in the presence of either parental band. Thus, Es1e was shown to be a hypomorphic electrophoretic variant (Soares 1979). The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11<
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| 000979 | STOCK KitlSl-16J/J | Repository-Cryopreserved |
| The steel mutations cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations. Most steel homozygous mice are severely anemic in utero and die usually at 15 to 16 days of gestation. However, compounds of two MgfSl mutants (e.g. MgfSl/MgfSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous 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 MgfSl/ MgfSl homozygotes and deficient in the MgfSl/+ 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 age. | ||
| 000317 | STOCK a/a Egfrwa2/J | Repository-Cryopreserved |
| Mice homozygous mice for the waved 2 spontaneous mutation (Egfrwa2) are recognizable at 2 to 3 days by curly whiskers. The first coat is waved but later coats are not; vibrissae usually remain curled and the guard hairs curved. Some homozygotes have eyelids open at birth. Fertile mutant females have impaired lactation. | ||
| 000161 | WB.D2-KitlSl-d/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, 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 | ||
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