JAX Mice Database - Endocrine Deficiency Research

Search Criteria: Research Area is "Endocrine Deficiency Research"

Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
000648	AKR/J	Level 2
	Originally inbred at the Rockefeller Institute, AKR mice are widely used in cancer research for their high leukemia incidence (60-90%) and in immunology as a source of the Thy1.1 (theta AKR) antigen. AKR/J mice are viremic from birth, and express the ecotropic retrovirus AKV in all tissues. The hair interior defect (hid) mutation, a strain characteristic of AKR mice, causes alterations in hair development that is only evident microscopically. Adrenocortical lipid depletion (ald) in AKR mice is caused by a mutation in sterol O-acyltransferase 1 (Soat1), and leads to a truncated SOAT1 protein. AKR/J mice are relatively resistant to aortic lesion formation on a semi-synthetic high fat diet and are hyporesponsive to diets containing high levels of fat and cholesterol.
000632	B6.V-Lep^ob/J	Level 2
	Mice homozygous for the obese spontaneous mutation, (Lep^ob; commonly referred to as ob or ob/ob), are first recognizable at about four weeks of age. Homozygous mutant mice gain weight rapidly and may reach three times the normal weight of wild-type controls. In addition to obesity, mutant mice exhibit hyperphagia, a diabetes-like syndrome of hyperglycemia, glucose intolerance, elevated plasma insulin, subfertility, impaired wound healing, and an increase in hormone production from both pituitary and adrenal glands. They are also hypometabolic and hypothermic. The obesity is characterized by an increase in both adipocyte number and size. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase in body weight, and probably results from it. Homozygotes have an ab ..... For more information please see the full descriiption on the strain data sheet
000642	BKS.Cg-m +/+ Lepr^db/J	Level 2
	Mice homozygous for the diabetes spontaneous mutation (Lepr^db) 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-Lepr^db homozygotes. Wound healing is delayed, and metabolic efficiency is increased. Female homozygotes exhibit decreased uterine and ovarian weights, decreased ovarian hormone production and hypercytolipidemia in fol ..... For more information please see the full descriiption on the strain data sheet
002468	KK.Cg-A^y/J	Level 2
	A^y 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 A^y 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 (A^y) 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-Kit^W/Kit^W-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. Kit^W-v homozygotes resemble Kit^W 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. Kit^W/Kit^W-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. Kit^W/Kit^W-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 +/+ Lepr^db/J	Level 3
	Mice homozygous for the diabetes spontaneous mutation (Lepr^db) 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 (Lepr^db/+) 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 Lepr^db 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
002019	NU/J	Level 3
	The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1^nu, formerly Hfh11^nu) 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-Foxn1^nu/J	Level 4
	The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1^nu, formerly Hfh11^nu) 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
003008	B6;129S-Tnf^tm1Gkl/J	Level 4
	Mice homozygous for the Tnf^tm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does ..... For more information please see the full descriiption on the strain data sheet
000049	C57BL/6J-Kit^W-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. Kit^W-v homozygotes resemble Kit^W 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-Foxn1^nu/J	Level 4
	The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1^nu, formerly Hfh11^nu) 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
004104	FVB.Cg-Mmp9^tm1Tvu/J	Level 4
	Mice that are homozygous null for the Mmp9 gene are viable and fertile. No Mmp9 activity is detected in spleen cell lysates. Long bones (tibia, femur) are 10% shorter in homozygous null mice. Histological examination of 3-week-old mice reveals a dramatically lengthened zone of hypertrophic cartilage (6 to 8 times larger vs. wildtype) due to delayed apoptosis, vascularization, and ossification. Subsequent remodeling resolves the condition, resulting in normal appearing bones by 8 weeks of age. Null mice show altered responses to repair of injury in skin, cornea, central nervous system and bone marrow reconstitution, and altered inflammatory responses.
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.
003658	STOCK Tg(TIE2GFP)287Sato/J	Level 4
	This strain expresses Green Fluorescent Protein (GFP) under the direction of the endothelial-specific receptor tyrosine kinase (Tek, formerly, Tie2) promoter. Endothelial cells expressing GFP can be visualized via fluorescent microscopy or purified by FACS.
000692	WB/ReJ Kit^W/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.
006365	129-Cckar^tm1Kpn Cckbr^tm1Kpn/J	Repository- Live
	Mice that are homozygous for both of the targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The donating investigator reports that the double mutants have a combined phenotype. No CCKBR receptor function was detected in competition binding assay of brain (cerebral plasma) membranes. When compared to wildtype, gastric pH in homozygotes is higher, pH 5.2, after overnight fast. Histological analysis reveals diminished parietal cell, enterochromaffin-like cell and antral comatostatin-producing D cell densities. An increase in the number of gastrin-producing G cells is observed. There is an increased number of H+, K+ -ATPase immunoreactive negative cells and abnormal distribution of parietal cells in oxyntic glands. Circulating gastrin levels are 10-fold higher in homozygotes. No CCKAR receptor function was detected in competition binding assay of pancreatic membranes. Homozygotes do not exhibit decreased ..... For more information please see the full descriiption on the strain data sheet
006367	129-Cckar^tm1Kpn/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No receptor function was detected in competition binding assay of pancreatic membranes. Mice homozygous for the targeted mutation do not exhibit decreased food intake due to peritoneal injection of cholecystokinin. Baseline food and water intake and body weight is normal in mutant mice. These mutant mice have larger gallbladder volumes and are more likely to develop spontaneous gallstones than wildtype controls. Gastric function is impaired due to diminished intestinal lipid feedback response. Small-intestine transit time is increased in mutant mice. When fed a lithogenic diet, mutant mice have an increase in biliary cholesterol secretion rates, when compared to the wildtype. Although the total number of olfactory-gonadotropin-releasing hormone-1 neuroendocrine (GnRH-1)neurons is the same in embryonic day 14.5 aged mutant and wildtype ..... For more information please see the full descriiption on the strain data sheet
006369	129-Cckbr^tm1Kpn/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No receptor function was detected in competition binding assay of brain (cerebral plasma) membranes. When compared to wildtype, gastric pH in homozygotes is higher, pH 5.2, after overnight fast. Histological analysis reveals diminished parietal cell, enterochromaffin-like cell (ECL) and antral comatostatin-producing D cell densities. An increase in the number of gastrin-producing G cells is observed. There is an increased number of H+, K+ -ATPase immunoreactive negative cells and abnormal distribution of parietal cells in oxyntic glands. Circulating gastrin levels are 10-fold higher in homozygotes. Gastric mucosal histamine levels are greatly reduced and histamine-immunoreactive ECL cells are absent. This mutant mouse strain may be useful in studies of hypochlorhydria, hypergastinemia, gastric antral endocrine regulation, and ..... For more information please see the full descriiption on the strain data sheet
007175	129S-Cyp4a14^tm1Jhc/J	Repository- Live
	Mice homozygous for this "Cyp 4a14" mutant allele are viable and fertile. Homozygous deficiency of the targeted gene leads to spontaneous hypertension (more severe in males) that is androgen-sensitive. Homozygotes also exhibit other interrelated metabolic and regulatory effects; increased renal vascular resistance, impaired renal hemodynamics, elevated plasma androgens (5a-dihydrotestosterone (DHT) and testosterone), upregulated Cyp4a12 gene expression, and increased formation of prohypertensive 20-HETE. These "Cyp 4a14" mutant mice may be useful studying kidney function and metabolism, cardiovascular physiology, hypertension, and the relationships between blood pressure, sex hormones, and p450 ω-hydroxylases.
007005	129S-Scg5^tm1Led/J	Repository- Live
	The following text reflects the phenotype reported by the donating investigator on a "129Sv" genetic background (probably "Taconic Sv129" (129S6/SvEvJ)). While heterozygotes are viable and fertile, mice homozygous for this mutation (7B2-null) die in prepubertal or pubertal ages (5 weeks) with severe cardio-respiratory failure, convulsions, and hypothermia. No transcripts are detected in brain tissue from the targeted gene. 7B2 null mice are unable to make an active form of prohormone convertase 2 (PC2) and have high circulating corticosterone. Homozygotes on the 129S genetic background exhibit Cushing's-like disease pathologies of liver, pancreas, and pituitary; including pituitary-dependent hyperadrenocorticosteronism, severe hypoglycemia, hyperproinsulinemia, adrenal hypertrophy, pituitary hypotrophy, and altered islet cell morphology. 7B2-null mice develop the disease from intermediate lobe ACTH hypersecretion (rather than from pituitary adenomas). Other abnormalities include thinni ..... For more information please see the full descriiption on the strain data sheet
001809	B6-A^w-J.Cg-Eda^Ta-6J +/+ Ar^Tfm/J	Repository- Live
	Testicular feminization (Ar^Tfm) 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 (Eda^Ta-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.
008104	B6.129(FVB)-Ptgs2^{tm2.1(Ptgs1)Fun}/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Female homozygotes have a longer period between successive pregnancies and reduced litter sizes. Ptgs1 gene product (protein), COX1, is increased approximately 5 fold in LPS-stimulated macrophages from homozygotes. Prostacyclin metabolite level in urine is reduced by 55% when compared to wildtype controls. No increase in prostaglandin-glycerol in mutant macrophages after LPS challenge is observed. Homozygotes exhibit reduced bradykinin-induced vasculature permeability and at 6 months of age have enlarged glomeruli due to increased inflammatory infiltrate. By 5 months of age, mutant mice develop chronic peritonitis and progressive renal cortex deterioration. This mutant mouse strain may be useful in studies of prostaglandin synthesis and inflammation.
006411	B6.129-Gast^tm1(INS)Ez/J	Repository- Live
	Mice heterozygous for this "G-InsKi" allele are viable and fertile. Human insulin expressed from this mutant allele retains full biological activity. Expression of human insulin is specific to gastrin-expressing cells (G cells of the antral stomach and some duodenum cells), and is released into portal circulation in response to the same meal-associated stimuli that control gastrin release. Heterozygous mice exhibit normal blood glucose levels, and toxic hypoglycemia is not observed. The donating investigators report that human insulin levels are sufficient to activate insulin signaling cascades in the liver but not in skeletal muscle. These mutant mice may be useful for diabetes and obesity research, specifically for studying the molecular and physiological mechanisms by which the hepatic action of transgenic insulin prolongs the survival of diabetic mice (e.g. Ins2^Akita mutant mice).
006860	B6.129-Ins2^Akita Bdkrb2^tm1Jfh/SmiJ	Repository- Live
	Mice homozygous for the targeted mutation and heterozygous for the Ins2^Akita spontaneous mutation are viable and fertile. Similar to mice only heterozygous for the Ins2^Akita mutation, the double mutant mice are severely diabetic: their body weights are 70% of wildtype, they consume over 3-fold the normal amount of food, and their urinary output is approximately 20-fold more than that of wildtype mice. Double mutant mice have markedly enlarged kidneys. Urinary albumin excretion in double mutants is almost 4-fold that of either single mutant, and double mutants experience more severe nephropathy than mice that are heterozygous for the Akita mutation alone. Megsin and nephrin expression is markedly increased in double mutant mice when compared to wildtype or to mice with either single mutation alone. By 12 months of age, double mutant mice experience hair loss due to a reduction in hair follicle numbers and thinning of the dermis. Double mutants ..... For more information please see the full descriiption on the strain data sheet
006201	B6.129-Scd1^tm1Ntam/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 ..... For more information please see the full descriiption on the strain data sheet
006879	B6.129-Scd2^tm1Myz/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.
004745	B6.129P2-Esr2^tm1Unc/J	Repository- Live
	Mice that are homozygous for this targeted allele are viable, normal in size and do not display any gross physical abnormalities. Stop codons inserted into exon 3 result in the production of truncated transcripts that are unlikely to be translated into a functional protein. Immunostaining of ovary tissue derived from homozygous females fails to detect protein product. Homozygous females are subfertile, producing fewer and smaller litters than wildtype controls. Decreased numbers of oocytes are also produced in response to superovulation (6 compared to 33.7 in wildtype controls). Male homozygotes are fertile and present no marked abnormalities other than epithelial hyperplasia in the bladder wall and prostatic collecting ducts. This mutant mouse strain may be useful in studies related to discerning the physiological roles of the estrogen signaling system.
005540	B6.129S-Tnf^tm1Gkl/J	Repository- Live
	Mice homozygous for the targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does not affect the degree of obe ..... For more information please see the full descriiption on the strain data sheet
005897	B6.129S4-Ppard^tm1Rev/J	Repository- Live
	These mice possess loxP sites on either side of exon 4 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice with a cre recombinase gene under the control of a promoter of interest, exon 4 of the targeted gene is deleted in the tissue of interest, leading to premature termination of the translation product upstream of the DNA binding domain. This strain may be useful in generating tissue-specific mutants of the floxed allele for use in studies including embryo development, adipocyte physiology, fat metabolism and storage, inflammation, and cancer.
006133	B6.129S4-Vdr^tm1Mbd/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-B4galt1^tm1Shur/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
006943	B6.129S7-B4galt1^tm2Shur/J	Repository- Live
	These mice carry a mutant allele that has a point mutation in the first translation initiation codon in exon 1, which initiates translation of the long isoform of beta 1,4-galactosyltransferase. The second translation initiation codon in exon 1 is not affected. These mice express only the shorter isoform of beta 1,4-galactosyltransferase. No long isoform protein is detected in mammary tissue by Western blot analysis. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Total Beta 1,4-galactosyltransferase activity is reduced to 72% of wildtype levels in mammary gland epithelial cells while activity on mammary epithelial cell surfaces is diminished by over 60%. Sperm and testis exhibit near wildtype levels of enzyme activity and glycoprotein galactosylation. The short isoform is expressed ectopically in sperm. Although able to undergo normal acrosomal exocytosis induced by calcium ionoph ..... For more information please see the full descriiption on the strain data sheet
003819	B6.129S7-Per2^tm1Brd/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display gross physical or behavioral abnormalities. A mutant transcript, if translated, would generate a protein with an 87 amino acid deletion. When maintained in constant darkness, two phenotypic components are exhibited: a shortened circadian period and a loss of persistent circadian rhythmicity. When housed under constant light, homozygotes exhibit normal activity rhythm but a period length of less than 24 hours. Female homozygotes, 9-12 months of age, exhibit low reproductive success and produce small litters when compared to wildtype. This mutant mouse strain may be useful in studies related to the regulation of the sleep-wake cycle.
008115	B6.129X1-Pomc^tm2Ute/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-Ab1^bm12/KhEg-Mc1r^e-J/J	Repository- Live

000021	B6.Cg-A^y/J	Repository- Live
	Mice homozygous for the yellow spontaneous mutation (A^y) 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
006183	B6.Cg-Col4a5^tm1Yseg/J	Repository- Live
	Heterozygous females and hemizygous males for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Immunofluorescence analysis of kidney tissue from mutant male mice does not detect gene product (protein), but in kidney from mutant female mice a mosaic pattern of gene product (protein) is detected (due to X-inactivation). RNase protection assay analysis of kidney tissue from mutant male mice detects a significantly lower level than wildtype. Hemizygous male and heterozygous female mice develop progressive kidney disease. By 7 weeks of age, 97% of mutant male mice and 78% of heterozygous female mice exhibit proteinuria. Histological analysis of kidneys from mutant male mice at 4 weeks of age reveals thickened capillary walls and mesangial hypercellularity. The pathology progresses to interstitial inflammation, glomerular abnormalities, and focal sclerosis. Electron microscopic examination of glomerular basement memb ..... For more information please see the full descriiption on the strain data sheet
004088	B6.Cg-Foxp3^sf/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. Foxp3^sf/Y males generally die by 16-25 days of age. Transgenic expression of Foxp3 prevents scurfy disease in Foxp3^sf/Y mice. Neonatal thymectomy of scurfy males ameliorates disease and increases lifespan; athymic nude Foxp3^sf/Y mice do not develop scurfy ..... For more information please see the full descriiption on the strain data sheet
006580	B6.Cg-Ins2^Akita Ldlr^tm1Her/J	Repository- Live
	Mice homozygous for the Akita spontaneous mutation die postnatally, typically by 12 weeks of age. Independently, heterozygous Akita mutant mice are a model of insulin dependent diabetes mellitus (IDDM) with severe hyperglycemia (see the datasheet for Stock No. 003548 for additional information). LDLR-null homozygotes have elevated serum cholesterol levels (200-400 mg/dl) which can escalate to very high levels (> 2000 mg/dl) when the mice are fed a high fat diet. LDLR-deficient mice also are predisposed to develop atherosclerosis. These double mutant mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, hypercholesterolemia, and diabetes-related macrovascular complications.
006906	B6.Cg-Lep^ob Ldlr^tm1Her/J	Repository- Live
	Independently, the C57BL/6-Lep^ob homozygotes (Stock No. 000632) model the increasingly prevalent metabolic disorder seen in humans (hyperglycemia, hyperinsulinemia, and hyperlipidemia), while LDLR-deficient mice (Stock No. 002207) are predisposed to atherosclerosis. When mutant mice are homozygous for both mutant alleles, they exhibit exacerbated hyperlipidemia and extensive atherosclerotic lesions in the aorta. The mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, and hypercholesterolemia.
000528	B6.Cg-Phex^Hyp/J	Repository- Live
	Hypophosphatemia (Phex^Hyp) is an X-linked semidominant mutation that causes defects in phospate metabolism. It is allelic with the gyro mutation (Phex^Gy) but hypophosphatemia mutant mice do not circle. Hemizygous males and heterozygous females can be recognized at 20 to 30 days of age by their shortened hindlimbs and tail. They have reduced body size which persists throughout life, and skeletal changes resembling rickets. Hemizygous males are more affected than heterozygous females. Viability is normal in both sexes, but heterozygous females show better fertility than hemizygous males.
004369	B6.Cg-Rag1^tm1Mom Ins2^Akita/J	Repository- Live
	Mice homozygous for the Rag1 targeted mutation and heterozygous for the Akita spontaneous display the diabetes phenotype in the absence of B and T cells and unlike single Akita mice, double mutants do not reject allografts. Mice heterozygous for only the Akita spontaneous mutation are viable and fertile. (Homozygotes typically die by 12 weeks of age from extreme hyperglycemia.) Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. The diabetic phenotype is more severe and progressive in heterozygous males than in females. Obesity and insulitis do not accompany diabetes. This double mutant strain is ideally suited for use in allogeneic or xenogeneic islet or stem cell transplantation protocols because the mice are severely immunocompromised and spontaneously develop diabetes at a young age.
006200	B6.Cg-Tnks2^tm1.1Yjc/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of activated spleen lymphocytes. While neither telomere shortening nor chromosomal abnormalities (even across multiple generations) are observed, homozygous mice have significantly decreased body weight. These mutant mice may be useful in studies of both telomerase function and telomerase-independent pathways which affect development and metabolism.
004659	B6.Cg-Tg(TIE2GFP)287Sato/1J	Repository- Live
	This strain expresses Green Fluorescent Protein (GFP) under the direction of the endothelial-specific receptor tyrosine kinase (Tek, formerly, Tie2) promoter. Endothelial cells expressing GFP can be visualized via fluorescent microscopy or purified by FACS. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
000160	B6.D2-Kitl^Sl-d/J	Repository- Live
	The multiple steel mutations (Kitl^Sl) 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 (Kitl^Sl-d/Kitl^Sl-d) and compounds of steel and steel Dickie (Kitl^Sl/Kitl^Sl-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
006451	B6.FVB(129X1)-Tg(Sim1-cre)1Lowl/J	Repository- Live
	Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgene expression is observed in all areas that endogenously express Sim1, including paraventricular hypothalamus and other parts of the brain. When these Sim1-Cre mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the flanked sequences in Sim1-expressing tissues (including hypothalamus). As such, Sim1-Cre transgenic mice may be useful in studying body weight homeostasis, obesity, leptin metabolism, or as a reporter strain for Sim1-transcription factor activity. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the st ..... For more information please see the full descriiption on the strain data sheet
007084	B6.FVB(Cg)-Mmp9^tm1Tvu/J	Repository- Live
	Mice that are homozygous null for the Mmp9 gene are viable and fertile. No Mmp9 activity is detected in spleen cell lysates. Long bones (tibia, femur) are 10% shorter in homozygous null mice. Histological examination of three-week-old mice reveals a dramatically lengthened zone of hypertrophic cartilage (six to eight times larger vs. wild-type) due to delayed apoptosis, vascularization, and ossification. Subsequent remodeling resolves the condition, resulting in normal appearing bones by eight weeks of age. Null mice show altered responses to repair of injury in skin, cornea, central nervous system and bone marrow reconstitution, and altered inflammatory responses. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain de ..... For more information please see the full descriiption on the strain data sheet
006333	B6.FVB(Cg)-Tg(Neurog3-cre)C1Able/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. Expression of the transgene is directed by a neurogenin 3 promoter. Tissues where Cre recombinase expression is detected include the small intestine (base of intestinal crypts) and fetal pancreatic epithelial cells. Cre activity has been shown in islets of the adult pancreas, small intestine enteroendocrine cells, endocrine portions of the stomach, all pancreatic endocrine cells, and in some non-endocrine intestinal cells. When bred with a mouse containing a loxP site-flanked sequence of interest, Cre-mediated recombination results in deletion of the flanked gene in the tissues that normally express neurogenin 3. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be not ..... For more information please see the full descriiption on the strain data sheet
003923	B6.HRS(BKS)-Cpe^fat/J	Repository- Live
	Mice homozygous for the fat spontaneous mutation (Cpe^fat) on a C57BL/6J genetic background (N10) become noticeably obese by 14-15 weeks of age. There is also some sexual dimorphism; female homozygous mutant mice develop obesity at a later age than males. Cpe^fat mice actually weigh less than wildtype controls prior to weaning age. Homozygous mutant mice develop a diabetic phenotype characterized by hyperglycemia and insulin resistance. Cpe^fat mice appear healthier on the C57BL/6J genetic background, avoiding the hereditary hydronephrosis present in C57BLKS/J and a lower incidence of malocclusion.
008041	B6;129-Sirt1^tm1Ygu/J	Repository- Live
	Mice homozygous for this targeted allele (SirT1^co/co) are viable and fertile. A loxP-flanked neomycin cassette just upstream of exon 4 and a third loxP site downstream of exon 4 were inserted to create this targeted mutant Sirt1 allele. The floxed mutation does not affect SIRT1 protein expression in MEFs or mammary gland tissue in homozygotes. When bred to mice that express Cre recombinase, the resulting offspring have exon 4 (encoding an evolutionarily conserved Sir2 motif) deleted in cre-expressing tissue(s); (the donating investigator reports only one recombination event: complete removal of the neomycin cassette and exon 4, leaving a single loxp). These SirT1^co/co mice may be useful in generating conditional mutants for studying transcriptional regulation and the role of estrogen, insulin growth factor-1 (IGF-1), and transcription factors (including NF-kappaB) in mammary gland development, mammary cancer, apoptosis, and metabolic di ..... For more information please see the full descriiption on the strain data sheet
007203	B6;129S4-Zfand5^{Gt(ROSA)72Sor}/J	Repository- Live
	Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Histological examination of E18.5 homozygous embryos reveals thin blood vessel walls, hemorrhages and lung edema. There are fewer vascular smooth muscle cells (vSMCs) in blood vessels as indicated by immunohistochemistry for desmin and alpha-smooth muscle actin. Skeletal defects are observed in 20% of animals in the sternum and calvarial bones. Homozygotes die a few hours after birth due to difficulty breathing and bruising is visible beneath the skin. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Zfand5-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation.
006043	B6;SJL-Tg(Oxt/EGFP)AI03Wsy/J	Repository- Live
	Hemizygous mice are viable and fertile with no gross or behavioral abnormalities. This transgene expresses an enhanced green fluorescent protein (EGFP) fused to the end of the neurophysin at the C-terminus of the oxytocin pre-prohormone. The transgene is selectively expressed in oxytocin-magnocellular neurons of the paraventricular and supraoptic nuclei of the hypothalamus. The fusion protein is faithfully trafficked to secretory granules and transported to neurosecretory terminals in the neurohypophysis, where the EGFP fluorescence undergoes depolarization-induced calcium-dependent secretion. Immunohistochemical detection of EGFP in individual oxytocin-magnocellular neurons is suggested as intrinsic fluorescence is low. However, the endogenous fluorescence in the neural lobes is sufficiently intense to image secretory events in individual oxytocin nerve terminals (neurosecretosomes) isolated from the posterior pituitary. These mice may be useful in studies of hormone biology, pharmaco ..... For more information please see the full descriiption on the strain data sheet
000231	B6C3Fe a/a-Csf1^op/J	Repository- Live
	Mice homozygous for the osteopetrosis spontaneous mutation (Csf1^op) are viable and exhibit osteopetrosis. The osteoclasts are the primary cell type affected in homozygous mutant mice. This results in a generalized macrophage deficiency, monocytopenia, and defective bone remodeling. Homozygous mutant mice also have abnormal calcium regulation, impaired dental growth and female mice fail to lactate. Total leukocyte counts are reduced and marrow cells are decreased to one-tenth of normal control mice. Homozygous mutant mice have a deficient microglia and macrophage response, and therefore may be useful tools to study the role of glia in neurological disease if mated to transgenic models of neurodegenerative disease.
001573	B6C3Fe a/a-Mitf^Mi/J	Repository- Live
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice heterozygous for the Mitf^Mi mutation have less iris pigment than wildtype and often have white spotting on the belly, head, and tail. Homozygous mutant mice have small eyes and are devoid of pigment in the eyes, inner ear, and skin. Homozygotes are deaf at an early age. There is a decrease of mast cells in the spleen and gut. Most homozygotes die around weaning but some may live for several months. There is a deficiency of secondary bone resorption (osteopetrosis) and the incisors fail to erupt. Immunological defects include decreased macrophage chemotactic responses, impaired proliferative responses to B cell and T cell mitogens, diminished responses in vitro to T-dependent and T-independent antigens and reduced NK cell activity.
004824	BTBR.V(B6)-Lep^ob/WiscJ	Repository- Live
	Mice homozygous for the obese spontaneous mutation, (Lep^ob commonly referred to as ob or ob/ob) exhibit obesity hyperphagia, a diabetes-like syndrome of hyperglycemia, glucose intolerance, elevated plasma insulin, subfertility, impaired wound healing, and an increase in hormone production from both pituitary and adrenal glands. They are also hypometabolic and hypothermic. The obesity is characterized by an increase in both number and size of adipocytes. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase body weight and is probably the result of it. Homozygotes do have an abnormally low threshold for stimulation of pancreatic islet insulin secretion even in very young preobese animals. As is the case with mice carrying the diabetes mutation (Lepr^db ..... For more information please see the full descriiption on the strain data sheet
007810	C.129-Stat5b^tm1Hwd/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. No gene product (mRNA or protein) is detected by Northern and immunoblot analysis of liver, spleen, mammary gland, thymus, kidney or skeletal muscle from homozygous animals. Levels of the closely related Stat5a gene products (mRNA and protein) are unaffected in thymus and spleen. At 4 - 5 weeks of age, male homozygotes are smaller in size and have a reduced body weight (27% lighter than wildtype controls) when compared to wildtype. Female homozygotes exhibit spontaneous abortion between day 8 and 17 of pregnancy and have impaired lactation. Pups (independent of genotype) born to heterozygous females have higher perinatal death than pups born to wildtype females. Some homozygotes have pale and enlarged livers. Homozygotes have less adipose tissue than wildtype controls, exhibit abnormal gene expression in liver, reduced insuli ..... For more information please see the full descriiption on the strain data sheet
003548	C57BL/6-Ins2^Akita/J	Repository- Live
	Mice heterozygous for the Akita spontaneous mutation (Ins2^Akita) are viable and fertile. Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning around 3-4 weeks of age. The diabetic phenotype is more severe and progressive in the male than in the female. Obesity or insulitis does not accompany diabetes. Aged mice exhibit gait disturbance and decreased sensory nerve conduction velocity, but do not exhibit learning or memory deficits (Choeiri C et al., 2005). Progressive retinal abnormalities begin as early as 12 weeks after the onset of hyperglycemia. Retinal complications include increased vascular permeability, alterations in the morphology of astrocytes and microglia, increased apoptosis and thining of the inner layers of the retina. (Barber AJ, et al., 2005) The mean lifespan of diabetic male mice on the C57BL/NJcl background (305 days) was significantly shorter than that of nondiabetic males in anothe ..... For more information please see the full descriiption on the strain data sheet
000533	C57BL/6J-Ghrhr^lit/J	Repository- Live
	Mice homozygous for the little spontaneous mutation (Ghrhr^lit) are characterized by a deficiency in pituitary growth hormone and prolactin and growth retardation. Male mice have reduced fertility and female mice show a delay in lactation.
002134	C57BL/6J-Mitf^mi-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 Mitf^mi-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.
006699	C57BL/6J-Pcsk1^N222D/J	Repository- Live
	Mice homozygous for this ENU-induced "Pc1^N222D" mutation are viable and fertile, although the donating investigator reports that homozygous breeders have diminished reproductive performance. Unlike mice homozygous for the traditional knockout allele, Pc1^N222D homozygotes are not runted. Homozygous mice exhibit obesity, abnormal proinsulin processing and multiple endocrinological defects. Increased energy intake and a more efficient metabolism contribute to the obesity. Defective proinsulin processing leads to glucose intolerance, but neither insulin resistance nor diabetes develop despite obesity. Obesity is associated with impaired autocatalytic and neuropeptide processing. These mutant mice are a model of human PC1 deficiency, and may be useful in studying obesity, fat metabolism, propeptide processing, and neuroendocrinology.
000811	C57BL/6J-Ptpn6^me-v/J	Repository- Live
	Mice homozygous for the viable motheaten spontaneous mutation (Ptpn6^me-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
000805	CBy.RF-Tshr^hyt/J	Repository- Live
	Mice homozygous for the hypothyroid spontaneous mutation (Tshr^hyt) are characterized by growth retardation, low thyroid hormone levels, elevated thyroid stimulating hormone (TSH) and hypoplastic thyroid glands. Homozygous mice of both sexes are infertile but fertility as well as growth can be restored by treatment with thyroid hormone. The mice do not respond to exogenous TSH. Homozygous mutant mice also display audiotory defects characterized by morphologic abnormalities of the stereocilia on both inner and outer hair cell systems
007562	D2.B6-Ins2^Akita/MatbJ	Repository- Live
	DBA/2J mice heterozygous for the Akita spontaneous mutation are viable and fertile. The donating investigator reports that the symptoms in heterozygous mutant mice are more severe and progressive in the males than in the females and include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. Obesity and insulitis do not accompany diabetes. Litter sizes range from 2-8 pups. Heterozygous Akita males develop albuminuria at two months of age. The albuminuria is progressive such that by 6 months of age albumin/creatine levels are approximately 600ug/mg. Additionally, it has been reported that DBA/2J heterozygous mutant mice develop diabetic nephropathy. Although not studied in the DBA/2J heterozygotes, C57BL/6 heterozygous mutant mice exhibit gait disturbance and decreased sensory nerve conduction velocity, but do not exhibit learning or memory deficits (Choeiri C et al., 2005). Progressive retinal abnormalities begin as early as ..... For more information please see the full descriiption on the strain data sheet
000643	DW/J Mlph^ln Pou1f1^dw/J	Repository- Live
	Mice homozygous mice for the dwarf spontaneous mutation (Pou1f1^dw) 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.
006364	FVB-Tg(Nr5a1-cre)2Lowl/J	Repository- Live
	Mice hemizygous for the "Sf1-Cre" transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgene expression mimics the mRNA pattern of Nr5a1; with Cre activity observed in steroidogenic factor-1 (SF1)-positive neurons in the ventromedial hypothalamic nucleus (VMH) as well as pituitary, gonad, and adrenal tissue. Expression is also noted in the cerebral cortex and in a few scattered cells in the caudal brainstem of mice derived from line 2 (but not line 7). If bred with mice containing a loxP-flanked sequence of interest, tissue-specific deletion of that genome results in the offspring. Specifically, these cre-expressing mice may be useful in studies involving the hypothalamus, such as body weight homeostasis, obesity, leptin metabolism, or as a reporter strain for SF1-transcription factor activity.
005710	FVB.129S-Mmp13^tm1Werb/J	Repository- Live
	Mice that are homozygous for this loxP-flanked ("floxed") allele are viable and fertile with normal endogenous gene function. Cre-mediated recombination results in replacement of exons 3-5 of targeted gene with a single loxP site. When bred to cre-expressing transgenic strains, these floxed mutant mice may be used to generate whole mouse or tissue-specific targeted mutants that may be useful in examining extracellular matrix remodeling and bone development. Of note: when these floxed mice are bred to mice containing a beta-actin promoter-driven cre transgene the resulting cre-positive, homozygous-null mice show robust accumulation of cartilage matrix caused by a transient expansion of the hypertrophic zone and increased trabecular bone mass that persists for months.
006867	FVB.B6-Ins2^Akita/MlnJ	Repository- Live
	FVB/NJ mice heterozygous for the Akita spontaneous mutation are viable and fertile. The donating investigator reports that the symptoms in heterozygous mutant mice are more severe than those observed in C57BL/6-Ins2^Akita mice (Stock No. 003548). These symptoms include hyperglycemia (females > 600mg/dl, males ~560 mg/dl), hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. In contrast to Akita heterozygotes on a C57BL/6 background, FVB/NJ adult heterozygous females are more hyperglycemic than heterozygous males. Obesity and insulitis do not accompany diabetes. Ins2 is expressed in the fetal yolk sac and is maternally imprinted. Heterozygous mutant females become more hyperglycemic during pregnancy, and are susceptible to embryo malformations leading to reabsorption, even with insulin therapy. Heterozygous mutant males do not produce mutant and wild-type offs > ..... For more information please see the full descriiption on the strain data sheet
006654	FVB.BKS(D)-Lepr^db/ChuaJ	Repository- Live
	The phenotype of this congenic "FVB-db" strain varies from that previously published on other genetic backgrounds. Specifically, obese FVB-db mice show long-term hyperglycemia that is primarily due to severe insulin resistance. The hyperglycemia in the fed state persists despite escalating insulin secretion and a massive increase in pancreatic beta-cell mass. Obese FVB-db mice show evidence of mesangial matrix expansion, a hallmark of diabetic nephropathy. Whereas the original C57BLKS/J-db mice are hyperglycemic due to the development of hypoinsulinemia and loss of beta-cell mass, the hyperglycemia of FVB-db appears to be due to severe insulin resistance with continual increases in insulin secretory capacity from beta-cell mass expansion. As the phenotype varies by genetic background, these mutant mice, along with db mutants on other genetic backgrounds (see Stock No. 000642, For more information please see the full descriiption on the strain data sheet
000804	HPG/BmJ	Repository- Live
	Mice homozygous for the hypogonadal mutation (Gnrh1^hpg) are characterized by an overall underdevelopment of the reproductive tract. Male mice have a small penis and scrotum and a short ano-genital distance. All male reproductive organs are present but are immature. The testes are small and undescended. Spermatogenesis is arrested, usually by the diplotene stage. The vagina of female mice does not open fully, the uterus is thread-like, and the ovaries are very small. Homozygous mutant mice are deficient in LH, FSH, and gonadal steroids. They also exhibit aberrant PRL secretion patterns. Both sexes are sterile although fertility can be restored with hormone replacement.
006956	NOD.Cg-Vdr^tm1Ska/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 ..... For more information please see the full descriiption on the strain data sheet
006873	STOCK Cebpb^tm1Vpo/J	Repository- Live
	Significant numbers of mice homozygous for this C/EBP-beta mutationon this mixed genetic background die perinatally due to hypoglycemia and a failure to mobilize glycogen. Homozygous males that survive to adulthood are fertile, but females are sterile, and display altered mammary duct formation. Macrophages isolated from homozygous mutant mice have impaired bactericidal activity. Surviving homozygotes exhibit fasting hypoglycemia, with reduced plasma insulin, plasma lipids, and free fatty acids (FFAs), and impaired hepatic glucose production. Further, they have a blunted response to glucagon and adrenaline primarily due to altered levels of hepatic cAMP production and reduced protein kinase A activity. Homozygous mice are resistant to obesity and have increased carbon dioxide production from increased metabolism in the brown adipose tissue and muscle. On a high-fat diet, homozygotes are protected from obesity and fatty liver due to reduced hepatic expression of lipogenic genes. Homozyg ..... For more information please see the full descriiption on the strain data sheet
001618	STOCK Oca2^p/Oca2^p Prop1^df/J	Repository- Live
	Mice homozygous for the Ames dwarf spontaneous mutation (Prop1^df) resemble mice homozygous for the Snell's dwarf mutation (Pit1^dw). 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.
006327	STOCK Pcsk1^tm1Dfs/J	Repository- Live
	Mice that are heterozygous for the targeted mutation are viable and fertile. No gene product (mRNA or protein) is detected in the homozygotes by Northern blot analysis of hypothalamic tissue or Western blot analysis of pituitary and brain tissue. Homozygote mice experience perinatal lethality, as the number of homozygotes born is less than the expected Mendelian ratio, and high postnatal lethality. By postnatal day 3, homozygotes are smaller in size than littermates. By 6 weeks of age, the surviving homozygotes are approximately 60% of wildtype body weight. Homozygotes have chronic mild diarrhea with bulky moist stools. Pituitary growth hormone transcript levels are only 25-20% of normal levels. Somatotroph cells in the anterior pituitary are reduced in size and inactive. Insulin-like growth factor 1 serum levels are significantly reduced. Transcript (mRNA) levels are greatly increased for growth hormone-releasing hormone in the hypothalamus and proopiomelanocortin in the pituitary. Ma ..... For more information please see the full descriiption on the strain data sheet
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 dwg^Bayer/J	Repository- Live
	The dwarf-Bayer mutation (dwg^Bayer) 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.
006395	STOCK Tg(Sim1-cre)1Lowl/J	Repository- Live
	Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgene expression is observed in all areas that endogenously express Sim1, including paraventricular hypothalamus and other parts of the brain. When these Sim1-Cre mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the flanked sequences in Sim1-expressing tissues (including hypothalamus). As such, Sim1-Cre transgenic mice may be useful in studying body weight homeostasis, obesity, leptin metabolism, or as a reporter strain for Sim1-transcription factor activity. Of note, Sim1-Cre mice may also available on a C57BL/6J congenic background (see Stock No. 006451).
000693	WC/ReJ Kitl^Sl/J	Repository- Live
	The multiple steel mutations (Kitl^Sl) 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. Kitl^Sl/Kitl^Sl-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 Kitl^Sl Kitl^Sl-d	Repository- Live
	The multiple steel mutations (Kitl^Sl) 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., Kitl^Sl/Kitl^Sl-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
004166	129-Itgb5^tm1Des/J	Repository-Cryopreserved
	Mice that are homozygous for the Itgb5^tm1Des targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No Itgb5 gene product (mRNA or protein) is detected. Homozygotes display defects in VEGF-mediated vascular permeability. Cultured keratinocytes derived from homozygous mutant animals display impaired adhesion and migration on vitronectin-coated surfaces.
005989	129;FVB-Tg(PTH-cre)4167Slib/J	Repository-Cryopreserved
	Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre activity is observed only in parathyroid tissue; no activity is seen in thyroid, muscle, lymph node, trachea, thymus, salivary tissues, lung, heart, liver, brain, stomach, spleen, kidney, large intestine, small intestine, and pancreas. When bred with any mouse containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in parathyroid-specific deletion of the flanked genome. These transgenic mice may be useful in generating mouse models of parathyroid-specific deletion of genes of interest, such as multiple endocrine neoplasia type 1, extracellular calcium-sensing receptor, and vitamin D receptor.
000709	129P3/J-Lepr^db-3J/J	Repository-Cryopreserved
	Mice homozygous for the diabetes 3J spontaneous mutation (Lepr^db-3J) become identifiably obese around 3 to 4 weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at 4 to 8 weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. Homozygous mutant mice on the 129P3/J background exhibit severe obesity but the diabetes phenotype is much reduced.
003117	129S-Sst^tm1Ute/J	Repository-Cryopreserved
	Mutant mice are healthy, fertile and of normal body size despite having three times the plasma growth hormone levels than wildtype littermates. Somatostatin is virtually absent in the adult cerebellum but is expressed during development. There is impaired motor learning and motor coordination as demonstrated in accelerating rotorod testing.
000090	129S1/Sv-Oca2⁺ Tyr⁺ Kitl^Sl-J/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) 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. Kitl^Sl/Kitl^Sl-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 Tgfa^wa1 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 Adamts20^bt 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 ..... For more information please see the full descriiption on the strain data sheet
000593	B6 x B6CBCa A^w-J/A-Grid2^Lc T(2;6)7Ca Mitf^Mi-wh/J	Repository-Cryopreserved
	Mice homozygous for the Mitf^Mi 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 A^w-J/A-T(5;13)264Ca Kit^W-v/J	Repository-Cryopreserved

002048	B6 x C57BLKS-m Lepr^db Myo15^sh2-J/J	Repository-Cryopreserved
	Mice homozygous for the shaker 2 Jackson spontaneous mutation (Myo15^sh2-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 (Myo15^sh2, Stock No. 000109). Homozygous mutant mice of both alleles display a phenotype very similar to the behavior and pathology to shaker-1 (Myo7a^sh1) 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 (Lepr^db) spontaneous mutations.
005543	B6(129)-Duox2^thyd/J	Repository-Cryopreserved

006564	B6(C)-Kit^W-41J Gusb^mps/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 Kit^W-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
000562	B6(Cg)-Tub^tub/J	Repository-Cryopreserved
	Mice homozygous for the tubby spontaneous mutation experience maturity-onset obesity. Homozygous mutant mice are recognizable by increased body weight at 3 to 4 months in males and at 4 to 6 months in females. Both sexes are fertile. The increased weight is composed of excess adipose tissue. Blood glucose is normal, but plasma insulin is increased prior to obvious signs of obesity and may rise to 20 times normal by 6 months. Despite elevated plasma total cholesterol, triglycerides, and high-density lipoprotein cholesterol, homozygous mutant mice do not exhibit atherosclerotic fatty streak blood vessel lesions. Tubby mutant mice also exhibit retinal degeneration, initially believed due to the presence of another mutation which was called rd5, but since demonstrated to be a pleiotropic effect of the Tub^tub mutation (Ohlemiller et al., 1997); the retinal phenotype is moderated by a QTL on Chromosome 11 (Ikeda et al., 2002). Tubby homozygotes additionally exhibit p ..... For more information please see the full descriiption on the strain data sheet
003509	B6.129-Blmh^tm1Geh/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.
002681	B6.129P2-Agt^tm1Unc/J	Repository-Cryopreserved
	Newborn homozygotes for the targeted disruption of Agt have no obvious pathological defects although only a few survive to adulthood. There are pathological changes in adult kidney and blood vessels. The effect of gene copy number was examined using these mice and C57BL/6J-TgH(Agtdup)1Unc (002690). Plasma angiotensinogen levels increase progressively, although not linearly, from zero in zero-copy (Agt^tm1Unc/Agt^tm1Unc) mice to 145% of normal in four-copy (Agt^dup/Agt^dup) mice. Mice of all genotypes are normal at birth, but most zero-copy animals show pathological changes as adults, the kidneys are normal in the other genotypes. The blood pressures of the one-copy through four-copy animals show significant and almost linear increases of approximately 8mmHg per gene copy despite their normal compensatory mechanisms being intact.
002690	B6.129P2-Agt^tm2Unc/J	Repository-Cryopreserved
	The entire agiotensinogen gene (Agt) was duplicated by homologous recombination allowing the examination of the effects of gene copy number on normal AGT function. Homozygous mice (Agtdup/Agtdup) are viable and fertile. They show blood pressure levels ~16 mmHg higher than normal wildtype siblings (two copies of Agt gene). Hemizygous mice (Agtdup/+) show blood pressure levels ~8 mmHg higher than normal wildtype siblings. This transgenic demonstrates the causality between genotypes at the angiotensinogen locus and blood pressures. Blood pressures of one-copy (Agt^tm1Unc/+) through four-copy (Agtdup/Agtdup) animals show significant and almost linear increases of approximately 8mmHg per gene copy despite their normal compensatory mechanisms being intact.
003316	B6.129P2-Gck^tm1Efr/J	Repository-Cryopreserved
	Glucokinase catalyzes a rate-limiting step in glucose metabolism in hepatocytes and pancreatic beta cells and is considered the "glucose sensor" for regulation of insulin secretion. Patients with maturity-onset diabetes of the young (MODY) have heterozygous point mutations in the glucokinase gene that result in reduced enzymatic activity and decreased insulin secretion. Disruption of the glucokinase gene results in a phenotype similar to MODY in heterozygous mice. These mice manifest a decreased insulin secretory response to glucose.
003142	B6.129P2-Prlr^tm1Cnp/J	Repository-Cryopreserved
	There is complete female sterility due to abberant estrous cycles, abnormal preimplantation development of eggs, no implantation of blastocysts, lack of pseudopregnancy. Males show slightly delayed fertility. Mammary development is markedly affected. Homozygotes have no mammary development and do not lactate. Heterozygotes are unable to lactate after the first pregnancies, but attain some degree of lactation as they age or after multiple pregnancies. Serum prolactin levels are increased 60 - 100 fold in both males and females. Maternal behavior is diminished in pimiparous and nulliparous animals. Bone remodelling is decreased in homozygote mutants.
002219	B6.129P2-Tgfa^tm1Ard/J	Repository-Cryopreserved
	Mice homozygous for the Tgfa^tm1Ard 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.
003462	B6.129S1-Thrb^tm1Df/J	Repository-Cryopreserved
	Mice homozygous for the Thrb^tm1Df targeted mutation are viable and fertile displaying normal growth rates. Homozygous mutant mice exhibit goiter and elevated levels of both thyroid hormone and thyroid stimulating hormone. Defects in liver responses to thyroid hormone and subtle behavioral abnormalities are observed. The mice fail to develop normal hearing, as assessed by impaired auditory-evoked brainstem responses, and are susceptible to audiogenic seizures. This strain provides a recessive model for the human syndrome of generalized thyroid hormone resistance (GTHR).
003808	B6.129S2(Cg)-Prl^tm1Hmn/J	Repository-Cryopreserved
	Mice that are homozygous for the null Prl allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null females have an irregular estrous cycle and are completely infertile. Homozygous null males and heterozygous females exhibit no fertility problems. The targeted insertion of a neomycin resistance gene into exon 4 results in a truncated Prl transcript that produces an 11 kDa prolactin protein that lacks any detectable bioactivity. Mammary gland development is marked by an absence of terminal or lateral lobulation. The disruption of the prolactin gene appears to have no effects on the hematopoietic system.
002612	B6.129S2-Bmp4^tm1Blh/J	Repository-Cryopreserved
	Mice homozygous for the Bmp4^tm1Blh 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.
003114	B6.129S2-Crh^tm1Maj/J	Repository-Cryopreserved
	Mice homozygous for the Crh^tm1Maj targeted mutation are viable and fertile. Pups born to homozygous mothers must be supplemented with corticosterone in the drinking water from day 12 of gestation until weaning. Homozygous mice have reduced adrenocortical secretion following stress. They may be susceptible to complications from hypoglycemia when fasting. Heterozygous mice are phenotypically indistinguishable from normal wildtype siblings.
004802	B6.129S2-Slc34a1^tm1Hten/J	Repository-Cryopreserved
	Mice that are homozygous for the targeted mutation are viable and fertile, and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern blot analysis of bone, kidney, liver or lung, or by Western blot analysis of kidney. Homozygotes are smaller in size and have reduced weight compared to wildtype littermates. Secondary ossification defects revealed at weaning are followed by compensatory bone development. Mutant mice exhibit increased urinary excretion of inorganic phosphate and calcium, diet dependent hypercalciuria and hypercalcemia, as well as decreased serum parathyroid hormone levels, increased serum alkaline phosphatase activity, and elevated serum 1,25-dihyudroxyvitamin D. Homozygous mice do not respond to dietary challenges of low inorganic phosphate or parathyroid hormone content. Calcium and inorganic phosphate containing renal stones, nephrocalcinosis, are found in homozygotes at all ages. This mutant mouse stra ..... For more information please see the full descriiption on the strain data sheet
005517	B6.129S4-Cyb5r4^tm1Hfb/HfbJ	Repository-Cryopreserved
	Mice heterozygous for the targeted mutation are viable and fertile, glucose tolerant, have normal blood sugar levels, serum lipid profiles and white adipose tissue mass. No protein from the targeted gene was detected by Western Blot analysis of mice homozygous for the allele. Homozygous mice consume more food, have decreased adipose tissue mass and are hyperlipidemic compared to wildtype controls post-weaning. At 4 weeks of age glucose levels are normal but insulin levels are 40% of wildtype controls. At 7 weeks of age clinical diabetes is present in both male and female of homozygous mice. Histological evaluation of pancreas from 21 week old homozygote animals revealed a significant reduction in the number of islets and decreased cytoplasmic to nuclear ratio in the islet cells and there was no insulitis nor phagocytosis of necrotic beta cell fragments. While there is a progressive loss of beta cells in aging homozygous mice, there is no loss of alpha, delta or PP cells. Electron m ..... For more information please see the full descriiption on the strain data sheet
002939	B6.129S4-Insr^tm1Dac/J	Repository-Cryopreserved
	Mice homozygous for the Insr^tm1Dac targeted mutation die 48-72 hours after birth due to diabetic keto-acidosis which causes weight loss by dehydration and protein wasting. There are no apparent gross anatomical or morphological changes. Embryonic growth is unaffected. Heterozygotes exhibit a form of mild insulin resistance.
005901	B6.129S4-Ppard^tm2Rev/J	Repository-Cryopreserved
	Heterozygous mice are viable and fertile. All homozygous mice die in utero. Macrophages homozygous for this mutation have no transcriptional response to very low-density lipoprotein treatment. No evaluation of lacZ expression is published. The donating investigator reports homozygous mice on this background have a similar, albeit earlier, embryonic phenotype as the exon 4 deleted mutants described in other publications (Barak PNAS 2002 99:303-8, Chawla PNAS 2003 100:1268-73, and Lee Science 2003 302:453-7). Heterozygous mice or homozygous embryo-derived cells may be useful in studies of embryo development, adipocyte physiology, fat metabolism and storage, inflammation, and cancer.
002188	B6.129S7-Amh^tm1Bhr/J	Repository-Cryopreserved
	Male mice homozygous for the Amh^tm1Bhr mutation have testes that are fully descended and produce functional sperm. They also develop a uterus which interferes with sperm transfer rendering most infertile. The testes develop Leydig cell hyperplasia. Homozygous females are fertile.
003264	B6.129S7-Gck^tm1Ts/J	Repository-Cryopreserved
	Mice homozygous for the Gck^tm1Ts targeted mutation die perinatally with severe hyperglycemia. Heterozygous mutant mice exhibit elevated blood glucose levels and reduced insulin secretion.
004366	B6.129X1-Brs3^tm1Jfb/J	Repository-Cryopreserved
	Mice that are homozygous for the targeted mutation are viable, normal in size at birth and do not display any gross physical or behavioral abnormalities. This targeted mutation is X-linked; males bearing the targeted allele display a mutant phenotype. At 15 to 16 weeks of age male mice heterozygous for the mutant allele display increased body weight as compared to wildtype littermates. This mutant mouse strain represents a model that may be useful in studies related to energy metabolism and obesity.
003126	B6.129X1-Grpr^tm1Jfb/J	Repository-Cryopreserved
	Mice homozygous (females) or hemizygous (males) for the X-linked Grpr^tm1Jfb targeted mutation are viable with no gross phenotypic abnormalities observed. There is a deficiency in bombesin-induced mediation of satiety as measured by glucose intake. A modest increase in body weight is observed in older animals. At 18-20 months of age, hemizygous males (N = 8) are 44.5g ± 5.1 (mean ± std dev) and wildtype littermates (N = 8) are 38.3g ± 5.1 (L. Hampton, unpublished observation). We have recently observed head tilts and bobbing in the hemizygous males in our production colony. The donating investigator of this strain has also observed this phenotype and considers it a mutation not related to the gene. We are working to remove this phenotype, but we will continue to ship from the colony while we finish this process.
000495	B6.C-H38^c/By-Kit^W-56J/J	Repository-Cryopreserved

000560	B6.C-H7^b/By Kit^W-50J/J	Repository-Cryopreserved

000122	B6.C3-Kit^W-44J/J	Repository-Cryopreserved
	Kit^W-44J heterozygotes have white-tipped feet and a white tail tip although the belly spot standardly found in Kit^W* 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 Kit^W-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 Kit^W-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
000017	B6.C3Fe-A^vy/J	Repository-Cryopreserved
	Homozygous (A^vy/A^vy) and heterozygotes (A^vy/A and A^vy/a) show considerable variation in appearance, ranging from clear yellow, to mottling with dark patches, to a completely agouti-like coat. The variation is strongly influenced by the agouti-locus genotype and strain genome of the dam. Homozygotes and heterozygotes tend to become obese, and the degree of obesity is correlated with the amount of yellow in the coat. A^vy resembles A^y in causing greater tumor susceptibility and lower graft vs. host reactivity and higher hepatic malic enzyme activity. Homozygotes have a reduced humoral response to tetanus toxoid and decreased rates of carbon clearance as well as impaired mononuclear phagocyte function. The greater tumor susceptibility as well as several altered immune responses occur in A^vy/a mice of mottled phenotype but not in those of agouti phenotype.
000991	B6.C58-Kit^W-57J/J	Repository-Cryopreserved

002644	B6.Cg-Hmga2^pg-Tg40BCha/BmJ	Repository-Cryopreserved
	A human globin gene transgene caused an insertional mutation in the pygmy locus, which has been identified as the high mobility group protein I, isoform C gene. The phenotype is a "mini-mouse", where homozygous transgenics are about 40 percent of the size of wild-type littermates as adults, and heterozygotes are about 80 percent as large as wild-types. Homozygotes are recognizably smaller at birth. Organ sizes were reduced proportionately to the body size reduction, except that the brain was proportionately larger, the adrenals smaller, and less adipose tissue was produced. Homozygotes are viable but infertile.
000133	B6.Cg-Kit^W-24J/J	Repository-Cryopreserved

000139	B6.Cg-Kit^W-25J/J	Repository-Cryopreserved

000164	B6.Cg-Kit^W/J	Repository-Cryopreserved

000124	B6.Cg-Kitl^Sl Krt71^Ca/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) 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. Kitl^Sl/Kitl^Sl-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 Kit^W-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. Kit^W-v homozygotes resemble Kit^W 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 Kit^W-v/ ..... For more information please see the full descriiption on the strain data sheet
000158	B6.Cg-Mitf^Mi-wh/Mitf^Mi/J	Repository-Cryopreserved
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (Mitf^Mi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes white mutant mice show slight microphthalmia but normal skeleton. Mice heterozygous for the microphthalmia (Mitf^Mi) mutation have less iris pigment than wildtype and often have white spotting on the belly, head, and tail. Homozygous mutant mice have small eyes and are devoid of pigment in the eyes, inner ear, and skin. Homozygotes are deaf at an early age. There is a decrease of mast cells in the spleen and gut. Most homozygotes die around weaning but some may live for several months. There is a deficiency of secondary bone resorption (osteopetrosis) and the incisors fail to erupt. Immunological defects include decreased macrophage chemotac ..... For more information please see the full descriiption on the strain data sheet
000184	B6.Cg-Mitf^Mi-wh/Mitf^mi-rw/J	Repository-Cryopreserved
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the red-eyed white spontaneous mutation Mitf^mi-rw have some pigmentation around the neck and have small red eyes. Compound heterozygotes of white and red-eyed white (Mitf^Mi-wh/Mitf^mi-rw) are mostly white with tan spots and red eyes.
000157	B6.Cg-Mitf^Mi-wh/Mitf^mi-sp/J	Repository-Cryopreserved
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (Mitf^Mi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes white mutant mice show slight microphthalmic but normal skeleton. Both homozygous and heterozygous mice for the microphthalmia-spotted spontaneous mutation (Mitf^mi-sp) are not detectably different form wild-type mice in color but have slightly less tyrosinase activity in the skin. Compound heterozygotes (Mitf^Mi-wh/Mitf^mi-sp) are light yellow with dorsal and ventral white spots and pigemented eyes.
000057	B6.Cg-Mitf^Mi-wh/J	Repository-Cryopreserved
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (Mitf^Mi-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 (Mitf^Mi-wh/+) have a diluted coat color, light ears, a white belly spot, and in rare cases a dorsal spot. In addition, they display abnormalitites of both the cochlear and vestibular portions of the inner ear.
002863	B6.Cg-Tgfa^wa1/J	Repository-Cryopreserved
	Mice homozygous for

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