JAX Mice Database - Endocrine Deficiency Research

Search Criteria: Research Area is "Endocrine Deficiency Research"

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JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
000697	B6.BKS(D)-Lepr^db/J	Level 2
	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 four to eight 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 ..... For more information please see the full phenotype on the strain data sheet
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. Adipose tissue transplants in Lep^ob homozygotes protect them from obesity, normalize insulin sensitivity, and restore fertility. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight mainte ..... For more information please see the full phenotype on the strain data sheet
000642	BKS.Cg-Dock7^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 phenotype on the strain data sheet
000648	AKR/J	Level 3
	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.
002468	KK.Cg-A^y/J	Level 3
	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 phenotype 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 phenotype 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 phenotype 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 phenotype 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.
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.
007850	J:NU	Level 4
	Outbred homozygous nude (Foxn1^nu/Foxn1^nu) mice are the standard in vivo model for drug efficacy testing in oncology. Nude mice are athymic and hairless as a result of the recessive nu mutation. T cell precursors exist but development is blocked in the absence of a thymus, resulting in an immunodeficiency that permits transplantation of tumor cell xenografts. Homozygous females are poor breeders and fail to lactate. Heterozygous males and females breed well and have normal immune function. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers.
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.
100410	WBB6F1/J-Kit^W/Kit^W-v	Level 4
	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.
012888	129-Wls^tm1.1Lan/J	Repository- Live
	These Wls floxed mutant mice possess loxP site before the ATG start site in the 5' untranslated region of exon 1 and another upstream of exon 2 of the wntless homolog (Drosophila) (Wls) gene. Mice that are homozygous for this allele are viable, fertile, and normal in size. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 1 deleted in cre-expressing tissues, abolishing gene function. When bred to a strain expressing Cre recombinase in the germline, homozygotes fail to develop mesoderm and are embryonic lethal by E8.5. When bred to a strain expressing Cre recombinase in pancreatic precursors, the mutant mice develop pancreatic hypoplasia. When bred to a strain expressing Cre recombinase in neural crest cells, the mutant mouse strain has severe brain malformations and exhibit postnatal lethality. This mutant mouse strain is useful to study Wnt signaling in any organ or tissue that can be targeted ..... For more information please see the full phenotype on the strain data sheet
007853	129S/SvEv-Tg(Alb1-Ren)2Unc/CofJ	Repository- Live
	Mice heterozygous for the RenTgMK transgene are viable and fertile. The RenTgMK transgene contains a liver-specific albumin promoter/enhancer controlling the expression of a synthetic renin gene (engineered to allow efficient cleavage and secretion of the prorenin transgene product by the liver). This, and because the transgene was targeted to the apolipoprotein locus on Chromosome 9, results in active renin secretion from the liver independently of renal or other homeostatic cardiovascular control mechanisms (i.e. genetically clamped). RenTgMK heterozygotes have high ectopic levels of active mouse renin in the liver and elevated plasma levels of prorenin and active renin. Heterozygous mice display significantly elevated blood pressure, enhanced thirst, high urine output, proteinuria, and kidney damage. Because active renin overexpression results in increased circulating levels of angiotensin II (Ang II), heterozygotes also exhibit cardiac hypertrophy and 50% male mortality between 6-8 ..... For more information please see the full phenotype on the strain data sheet
007688	129S6.B6-Ins2^Akita/CofJ	Repository- Live
	Congenic 129S6/SvEvTac mice heterozygous for the Ins2 ^Akita (Akita) spontaneous mutation are viable and fertile. Mice carrying the Akita mutation exhibit hyperglycemia, polydipsia, polyuria and elevated systolic blood pressure when compared to wild-type controls. The diabetic phenotype is more severe and progressive in the male than in the female. Heterozygous males exhibit significantly increased albuminuria and albumin-to-creatine ratios compared to wild-type controls. The absolute level of 129S6-Akita albumin excretion is intermediate when compared to C57BL/6-Ins2^Akita/J (Stock No. 003548) being the lowest and D2.B6-Ins2^Akita/MatbJ (Stock No. 007562) being the highest. At six months of age, glomerular filtration rates (GFR) are significantly higher in the 129S6-Ins2^Akita mice than either ..... For more information please see the full phenotype on the strain data sheet
009106	B6.129-Cyp27a1^tm1Elt/J	Repository- Live
	These mice harbor a targeted mutation of the Cyp27a1 (cytochrome P450, family 27, subfamily a, polypeptide 1) locus that abolishes endogenous gene expression. Homozygous mice (also called Cyp27a1^-/-, cyp27^-/-, or sterol 27-hydroxylase-deficient mice) are viable and fertile, with no RNA or protein expression from the targeted gene detected in liver tissue. Both formation of bile acids and excretion of fecal bile acids are decreased in homozygous mice. Compensatory up-regulation of hepatic enzymes that convert cholesterol to bile acids (bile acid synthesis) is also observed. Cyp27a1^-/- mice exhibit a dramatic increase in cytochrome P450 3A (Cyp3a11) which catalyzes side-chain hydroxylations of bile acid intermediates subsequently facilitating their excretion in the bile and urine. Homozygous mice also have increased expression of other nuclear xenobiotic receptor PXR (pregnane X receptor) target genes.
003124	B6.129-Ucp1^tm1Kz/J	Repository- Live
	Mice that are homozygous for this knockout allele are viable and fertile, but exhibit sensitivity to cold temperatures. The Donating Investigator notes that homozygous offspring have increased survival rates to weaning age when maintained at 25°C to 28°C. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brown adipose tissue from homozygotes. When maintained at 20°C, homozygotes are resistant to diet induced obesity with reduced white fat depot weights, exhibit a 0.1-0.3°C higher body temperature, and a slightly lowered respiratory quotient compared to controls. Notably, when maintained at 27°C, homozygous mutant mice are no longer resistant to diet induced obesity and gain weight at a rate similar to wildtype controls. An increase in the number of brown adipocytes in the inguinal fat depots is observed in mutant mice maintained at 20°C, on either diet. Homozygotes have reduced levels of plasma fatty acids, circula ..... For more information please see the full phenotype on the strain data sheet
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.
016222	B6.129S(Cg)-Id2^{tm1.1(cre/ERT2)Blh}/ZhuJ	Repository- Live
	The Id2-CreERT2 knockin allele was designed to both abolish inhibitor of DNA binding 2 (Id2) gene function and express CreER^T2 fusion protein from the Id2 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible and can be observed following tamoxifen administration. As such, when Id2-CreERT2 knockin mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Id2-expressing cells of the offspring. No mRNA or protein expression from the Id2-CreERT2 allele is observed. The donating investigator reports that homozygous mice are runted with defective lung alveolarization. Other organ systems have not been evaluated. However, Id2-CreERT2 homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (including postnatal lethality and defects of the immune system, digestive tract, ..... For more information please see the full phenotype on the strain data sheet
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 phenotype on the strain data sheet
016234	B6.129S1(FVB)-Ret^tm2.1Cos/J	Repository- Live
	These Ret^MEN2B mice contain a point mutation (M919T) in codon 919 (exon 16) of the Ret proto-oncogene (Ret) gene. This mutation corresponds to mutations in human codon 918 commonly found in humans with multiple endocrine neoplasia type 2 (MEN2). This construct also contains two silent mutations in codons 920 and 921, which abolish a restriction site and allows for detection. Females homozygotes are fertile while male homozygotes are sterile. Homozygotes, while viable, have a reduced life span. Ret encodes a receptor tyrosine kinase which serves as a receptor for glial cell derived neurotrophic factor (GDNF). RET is expressed in excretory, central, and peripheral nervous systems, neural crest, enteric nervous system (ENS), and neuroendocrine cells such as C cells of the thyroid and chromaffin cells of the adrenal gland. This methionine mutation in the catalytic core accounts for 95% of human MEN2B cases. Heterozygous mice display C cell and chromaffin ..... For more information please see the full phenotype on the strain data sheet
008117	B6.129S4(129S6)-Sst^tm1Ute/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern blot, in situ hybridization or radioimmunoassay analysis of brain tissue. Homozygotes exhibit increased baseline plasma growth hormone, corticosterone and total ghrelin levels compared to wildtype. Mutant mice have impaired motor performance ability. Somatostatin-deficient mice have enlarged stomachs with an increased number of parietal cells and hyperchlorhydria. Hippocampal neprilysin activity is diminished. Compared to wildtype controls, amyloid beta 42 peptides levels are elevated in the hippocampus. This mutant mouse strain may be useful in studies of gastric homeostasis, learning and memory and endocrinology.
008519	B6.129S4-Nos1^tm2Plh/J	Repository- Live
	In this targeted mutation exon 6, which encodes the heme-binding domain, is deleted. Mice that are homozygous for the targeted mutation are viable only when maintained on a liquid diet and are not fertile. Some truncated gene product (mRNA) containing exon 2 but completely lacking exon 6 is detected by RR-PCR of brain. Nitric oxide synthase activity is only 0.3% of wildtype levels in the brain. Homozygotes have smaller total body and gonad weight and develop pyloric stenosis. Female homozygotes have fewer ovarian corpora lutea and increased hypothalmic gonadotropin-releasing hormone and circulating luteinizing hormone. Homozygous males have decreased follicle stimulating hormone levels and do not display mating behavior. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of hypothalamo-pituitary axis and neuroendocrine regulation of ..... For more information please see the full phenotype on the strain data sheet
010672	B6.129S4-Tnfrsf11b^tm1Eac/J	Repository- Live
	Mice homozygous for this osteoprotegerin (OPG)-mutant allele are viable and fertile. While a smaller transcript is made from the disrupted allele, the spliced product is predicted to be out of frame and result in a nonfunctional protein. OPG-deficient mice exhibit dysregulation of osteoclast production leading to drastic changes in the bone architecture; homozygotes develop severe osteoporosis, gross deformations in bone structure, decreased bone density, and altered long bones physical dimension. Hematopoietic, B lymphocyte, and dendritic cell functions are also dysregulated. It has been the experience of The Jackson Laboratory that animals homozygous for the Tnfrsf11b^tm1Eac exhibit significant (~50%) pre-wean mortality. 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 ..... For more information please see the full phenotype on the strain data sheet
006133	B6.129S4-Vdr^tm1Mbd/J	Repository- Live
	Heterozygous mice are phenotypically indistinguishable from wildtype siblings. As originally characterized on a mixed B6;129 genetic background, 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 bod ..... For more information please see the full phenotype on the strain data sheet
012564	B6.129S5-Dhcr24^tm1Fein/SbpaJ	Repository- Live
	Homozygous mice on the C57BL/6 genetic background die within the first postnatal day with features of lethal restrictive dermopathy; including taut, wrinkle-free, shiny skin, severe defects in epidermal maturation/epidermal barrier function (impaired epidermal development), and increased presence of hyperproliferative immature keratinocytes (defective keratinocyte differentiation). The increased transepidermal water loss/increased epidermal water content is associated with increased aquaporin-3 (AQP3) expression throughout the epidermis. Mice heterozygous for this allele are viable and fertile, with no overt phenotype. As the Dhcr24 protein functions to catalyze the last step of cholesterol biosynthesis (the conversion of desmosterol to cholesterol), homozygous disruption of this locus results in desmosterolosis: almost no cholesterol in plasma and tissues with ~99% of total sterols in the form of desmosterol. lacZ expression from the mutant allele is not characterized. <> ..... For more information please see the full phenotype on the strain data sheet
016902	B6.129S5-Irf6^{Gt(OST398253)Lex}/J	Repository- Live
	In this strain a gene construct (VICTR48), containing a neomycin resistance (neo), integrated downstream of the splice donor site of the interferon regulatory factor 6 (Irf6) gene. Mice that are heterozygous for the gene trap mutation are viable and fertile. Homozygotes have a perinatal lethal phenotype. IRF6 is a transcription factor involved in keratinocyte, epidermal, and epithelial cell proliferation as well as craniofacial development. IRF6 is expressed in the skin and oral epithelium from E17.5. Heterozygotes have mild oral adhesions between epithelial layers of the maxilla and mandible. Homozygous embryos have taut, shiny skin, lack external ears and have snouts and jaws shorter and more rounded than their wild-type littermates. They also have short forelimbs that lacked visible digits, a single caudal projection that lacked visible hindlimbs and tail, and a cleft secondary palate. Their skeleton also exhibits a split xiphoid process, shortened sternum, delayed oss ..... For more information please see the full phenotype on the strain data sheet
003568	B6.129S7-Trp63^tm2Brd/J	Repository- Live
	Mills 1999 Nature 398:708 describes the homozygous phenotype on a mixed B6-Tyr^c-Brd;129S7(129S5) background. Further, they not distinguish between the two targeted alleles (pTV6H(90)-generated p63^Brdm1 [Trp63^tm1Brd] or pTV12E(60)-generated p63^Brdm2 [Trp63^tm2Brd]) as both "produced an identical phenotype." Homozygous mice are born alive, but die several hours after birth. No transcripts have been detected in homozygotes. They have striking developmental defects, exhibiting truncated forelimbs, absent hindlimbs, and transparent skin with a complete lack of hair follicles. Both the gross and histological appearance of internal organs is normal. Functional permeability of the skin is dramatically increased; homozygous mice lose thirty times more water than normal littermates. It is presumed that death occurs from dehydration. Heterozygous mice are viable, fertile, and do not exhibit any overt developm ..... For more information please see the full phenotype on the strain data sheet
017292	B6.129X1(Cg)-Pkd2^tm1.1Tjwt/J	Repository- Live
	These Pkd2^cond mutant mice possess loxP sites flanking exons 11-13 of the polycystic kidney disease 2 (Pkd2) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. PKD2 is a calcium-permeable membrane channel expressed in fetal kidneys and in most adult tissues. Along with PKD1, PKD2 regulates cell proliferation, cell migration, and interactions with other cells, and is necessary for normal development and function of the kidneys. Mutations in PKD2 are responsible for 15% of all cases of autosomal dominant polycystic kidney disease (ADPKD). When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exons 11-13 deleted in the cre-expressing tissues. This strain may be useful for studying renal development in ADPKD. For example, when crossed to a strain expressing Cre recombinase in endothelial cells (see Stoc ..... For more information please see the full phenotype on the strain data sheet
001809	B6.Cg-A^w-J 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.
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 phenotype 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 (Foxn1^nu/Foxn1^nu) ..... For more information please see the full phenotype on the strain data sheet
003819	B6.Cg-Per2^tm1Brd Tyr^c-Brd/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. By 9-12 months of age, homozygous females exhibit low reproductive success and produce small litters when compared to wildtype. These mice also carry the recessive Tyr^c-Brd mutation that, when homozygous, results in albino coat color. This mutant mouse strain may be useful in studies related to the regulation of the sleep-wake cycle.
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.
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 phenotype 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 phenotype 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 phenotype 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.
016209	B6;129-Lrrk2^tm2.1Shn/J	Repository- Live
	Mice homozygous for the LRRK2 KO1 mutation are viable and fertile, with the promoter and exon 1 of the Lrrk2 (leucine-rich repeat kinase 2) gene deleted. No mRNA or protein expression from the targeted allele is observed in brain tissues, however and truncated mRNA signal is observed in kidney tissue. Homozygous mice do not exhibit neurodegeneration or neuropathological changes in the brain. In the kidneys, a tissue where LRRK2 is normally expressed at ~6-fold greater levels than brain, homozygous loss of LRRK2 results in renal atrophy by 20 months of age. This is accompanied by significant (~60-fold) age-dependent accumulation of aggregated α-synuclein and ubiquitinated proteins in the kidney. Specifically, homozygous KO kidneys show widely distributed cytosolic α-synuclein-immunoreactive granular aggregates (some amy also contain phospho-Ser-129 α-synuclein) or inclusions in boxy cells of renal tubules in the cortical area by 20 months of age. Other kidney ..... For more information please see the full phenotype on the strain data sheet
016210	B6;129-Lrrk2^tm3.1Shn/J	Repository- Live
	Mice homozygous for the LRRK2 KO2 mutation are viable and fertile, with exons 29-30 (encoding the first half of the Ras-like small GTPase domain) of the Lrrk2 (leucine-rich repeat kinase 2) gene deleted. No mRNA or protein expression from the targeted allele is observed in brain tissue, however some truncated mRNA is observed in kidney tissues. Homozygous mice do not exhibit neurodegeneration or neuropathological changes in the brain. In the kidneys, a tissue where LRRK2 is normally expressed at ~6-fold greater levels than brain, homozygous loss of LRRK2 results in renal atrophy by 20 months of age. This is accompanied by significant (~60-fold) age-dependent accumulation of aggregated α-synuclein and ubiquitinated proteins in the kidney. Specifically, homozygous KO kidneys show widely distributed cytosolic α-synuclein-immunoreactive granular aggregates (some of them may also contain phospho-Ser-129 α-synuclein) or inclusions in boxy cells of renal tubules in ..... For more information please see the full phenotype on the strain data sheet
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 phenotype on the strain data sheet
009358	B6;129S2-Lats1^tm1Tx/J	Repository- Live
	Homozygous animals exhibit a lack of mammary gland development, infertility and growth retardation. Accompanying these defects are hyperplastic changes in the pituitary and decreased serum hormone levels. The reproductive hormone defects of homozygotes are reminiscent of isolated luteinizing hormone (LH)-hypogonadotropic hypogonadism and corpus luteum insufficiency in humans. Furthermore, Homozygous mice develop soft tissue sarcomas (some by 4-10 months of age) and ovarian stromal cell tumors (by 3 months of age) and are highly sensitive to carcinogenic treatments. Data demonstrates a role for this gene in mammalian tumorigenesis and specific endocrine dysfunction.
012463	B6;129S4-Foxd1^{tm1(GFP/cre)Amc}/J	Repository- Live
	Heterozygous mice are viable and fertile, normal in size and do not display any gross physical or behavioral abnormalities. The DI states that the strain is homozygous lethal. The FoxD1^GC allele expresses an eGFPCre fusion protein (EGFP and cre fusion protein) from the Foxd1 promoter/enhancer elements. When Foxd1 is induced, EGFP immunofluorescence is observed during kidney development in metanephric mesenchyme in cells fated to become stromal cells of the kidney. When FoxD1^GC mice are bred with mice containing loxP-flanked sequence, Cre-mediated recombination will result in deletion of the floxed sequences in the Foxd1-expressing cells of the offspring. These mice may be useful for studying therapeutic strategies directly targeting pericyte differentiation in vivo and may productively impact fibrotic kidney disease.
012464	B6;129S4-Foxd1^{tm2(GFP/cre/ERT2)Amc}/J	Repository- Live
	Heterozygous mice are viable and fertile, normal in size and do not display any gross physical or behavioral abnormalities. The DI states that the strain is homozygous lethal. The Foxd1^GCE allele expresses an eGFPCreER^T2 fusion protein (EGFP and creERT2 fusion protein) from the Foxd1 promoter/enhancer elements. Foxd1 is induced, and EGFP immunofluorescence is observed, during kidney development in metanephric mesenchyme in cells fated to become stromal cells of the kidney. Cre-ER^T2 fusion gene activity is inducible; observed in the same cells only following tamoxifen administration. When Foxd1^GCE mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequences in the FoxD1-expressing cells of the offspring. These mice may be useful for studying therapeutic strategies directly targeting pericyte differen ..... For more information please see the full phenotype on the strain data sheet
008752	B6;129S4-Nhlh2^tm1Irk/J	Repository- Live
	Male mice homozygous for this targeted mutation exhibit bilateral cryptochism, hypogonadism, azoospermia, low testosterone and follicle stimulating hormone levels and lack instinctual male sexual behavior. Homozygous females are hypogondal unless raised in the presence of male mice, have estrous cycle defects, and reduced fertility. No gene product (mRNA) is detected by Northern blot analysis of embryos. Initially, homozygous male mice, 4 to 7 weeks of age, have a reduced weight compared to wildtype controls. By 12 weeks of age, homozygous males are significantly heavier than wildtype, and mutants progressively increase weight with age. Female homozygotes 5 to 6 weeks of age have normal body weight, however by 7 weeks of age they are significantly heavier than wildtype controls. The increased body weight is due to increased adipose tissue, with the exception of female homozygotes more than 52 weeks of age that exhibit increased lean body mass. Male heterozygotes and homozygotes, ..... For more information please see the full phenotype on the strain data sheet
000231	B6;C3Fe 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.
010803	B6;FVB-Tg(Adipoq-cre)1Evdr/J	Repository- Live
	Mice hemizygous for this Adipoq-Cre BAC transgene are viable and fertile, with expression of a Cre recombinase directed to adipose tissue by the promoter/regulatory regions of the mouse adiponectin (Adipoq) locus on the BAC transgene. Transcription/translation from the BAC Adipoq locus is disabled, and Cre recombinase expression levels are similar to that of endogenous Adipoq expression. These mice express Cre recombinase effectively in white adipose tissue (WAT) and brown adipose tissue (BAT), but not in macrophages (including adipose-tissue resident macrophages, alveolar macrophages, or thioglycollate-stimulated peritoneal macrophages). The donating investigator reports highly efficient Cre recombinase activity, with no ectopic expression. The phenotype of homozygous mice was not determined by the donating investigator. These Adipoq-Cre BAC transgenic mice may be useful in generating conditional mutations for studying adipose tissue function and storage, obesity, ..... For more information please see the full phenotype on the strain data sheet
010576	B6;SJL-Tg(MMTV-rtTA)4-1Jek/J	Repository- Live
	The donating investigator claims homozygous mice are viable and fertile. These MMTV-rtTA mice have expression of the reverse tetracycline-controlled transactivator (rtTA) protein directed primarily to the breast epithelia of the mammary ductal system by the mouse mammary tumor virus (MMTV) promoter. The donating investigator also reports some rtTA expression in salivary glands (particularly in the males) as well as prostate glands. When mated to a mutant strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE, TetRE or tetO), expression of the target gene may be induced with administration of the tetracycline analog doxycycline (dox) in the double mutant offspring. These MMTV-rtTA mice are a Tet-On tool that allows conditional, dox-inducible expression of genes primarily in mammary gland epithelial cells and may be useful in studying the endocrine function of mammary tissues and/or breast cancer (for example).
012924	B6N;129-Egr1^tm1Jmi/J	Repository- Live
	In this strain a coding exon upstream of the DNA-binding domain of the early growth response 1 (Egr1) gene is replaced with a neo cassette, abolishing gene function. Homozygous Egr1^-/- mice are viable and normal in size. Homozygous females are sterile, are absent of corpora lutea, and display a 30% reduction in the weight of the uterus. These mice exhibit an impaired inflammatory response, impaired wound healing, and attenuated dermal fibrosis after TGF-β or bleomycin stimulation. Macrophages from Egr1^-/- mice showed reduced TNF-α secretion when stimulated with TGF-β. These mice may be useful for studying carcinogenesis, inflammation, atherosclerosis, scleroderma, ischemic injury, tissue repair, fibrosis, matrix remodeling and wound healing.
003794	BALB/cByJ-Nedd4l^andi/EiJ	Repository- Live
	Mice homozygous for the adult nephrogenic diabetes insipidus mutation can often be initially detected by a slight reduction in body size by wean age. By 4 to 6 weeks of age polyuria, polydipsia, and low urine osmolality can be detected and none of these phenotypes are responsive to DDAVP. Histology reveals highly abnormal renal tubules. Homozygotes breed but should not be relied upon to breed for as long as heterozygotes or wild-type BALB/cByJ mice because progressive hydronephrosis develops.
008172	BKS(HRS)-Ddr2^slie/JngJ	Repository- Live
	Mice homozygous for this mutation appear normal at birth. By weaning, they exhibit a reduced body mass, gain weight slower and display minor craniofacial abnormalities such as protruding eyes and a shortened snout. Bone mineral content, but not density is reduced in homozygotes. Plasma glucose levels are significantly increased while blood urea nitrogen levels are decreased in homozygotes. By six weeks, it can be seen that homozygous females lack a corpora lutea. By four months, homozygous males exhibit atrophy of spermatogonia, Sertoli and Leydig cells. This mutant mouse strain has characteristics similar to human Levi type dwarfism and may be useful in studies related to dwarfism and infertility.
008340	BKS.Cg-Lepr^db Nos3^tm1Unc/RhrsJ	Repository- Live
	These double mutant mice harbor both the Lepr^db spontaneous mutation and the Nos3 (eNOS) targeted mutation and are congenic on C57BLKS/J genetic background. Mice homozygous for both mutations (called eNOS^-/- C57BLKS/J db/db, eNOS^-/- db/db, or db/db/eNOS-/- double mutant mice) are viable with development of type II diabetes and diabetic nephropathy. The eNOS^-/- C57BLKS/J db/db mice develop type II diabetes with significant obesity and hypertension: while both mutations are associated with insulin resistance, the mutated leptin receptor in db/db mice chiefly accounts for the observed hyperglycemia and defective leptin signaling (leading to persistent hyperphagia and obesity), and the eNOS-deficiency accounts for the moderate systemic hypertension. In addition, eNOS^-/- C57BLKS/J db/db mice exhibit rapid onset and progression of pathologic ..... For more information please see the full phenotype on the strain data sheet
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 phenotype on the strain data sheet
013080	C57BL/6-Actb^{tm3.1(Sirt1)Npa}/J	Repository- Live
	Mice that are heterozygous for the targeted mutation are viable, exhibit delayed reproduction and lower body weight. No homozygotes are produced from heterozygous crosses. Fewer than expected heterozygotes are produced from heterozygote X wildtype crosses. Overexpression of gene product (protein) is detected by Western blot analysis of white adipose tissue, brown adipose tissue, MEFs, skull calvaria cells and brain tissue. Overexpression of the protein is not detected in liver or muscle tissue. Fusion gene product (mRNA) is detected in white adipose tissue by Northern blot analysis. Beta-actin protein expression is equivalent to wildtype levels. Heterozygote knock-in mice have reduced fat mass (epididymal fat pad weight), circulating free fatty acids, leptin, adiponectin and total cholesterol. Food consumption, glucose tolerance and metabolic rate (with associated higher oxygen consumption) are increased in the mutant mice. In fasted conditions, heterozygotes have lower circul ..... For more information please see the full phenotype 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. Expression of glutathione S-transferase mRNA is increased in epithelial cells in proximal tubules of hyperglycemic mutants (Fujita et al., 2001). As well, plasma concentrations of valine, leucine, isoleucine, as well as the total branched chain amino acids, alanine, citrulline and proline, were significantly higher in the Akita mice (Mochida et al., 2011). Sphingosine-1-phosphate is elevated and diabetic animals demonstrated reductions in plasma levels of omega-9 24:1 (nervonic acid)-containing ceramide, sphingomyelin, and cerebrosides. Reduction of 24:1-esterfied sphi ..... For more information please see the full phenotype on the strain data sheet
012810	C57BL/6J-Enpp1^asj/GrsrJ	Repository- Live
	Homozygotes initially appear normal but by 2 months of age they hold their forepaws closer to the body and develop a slow hobbling gait due to joint calcification. Moderate to severe hearing loss is found by 3 months of age. Homozygotes may breed, but the ability to breed and maintain a litter is curtailed by progressive physical disability.
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.
009345	C57BL/6J-Mstn^lean/J	Repository- Live
	Mice homozygous for this ENU-induced mutation, called the lean (Ln) allele of myostatin (Mstn^Ln), are viable and fertile. The Mstn^Ln allele alters mRNA splicing and results in an additional larger transcript containing a 128 basepair insert at the junction between exons 2 and 3. This insertion encodes an additional 4 amino acids before a premature stop codon (ASDNX), and is predicted to generate a truncated protein containing the Mstn signal sequence and propeptide, but lacking the ligand portion of the molecule. In addition to this abnormal splicing product, the mRNA from mutant males is also reduced in abundance by approximately 60% compared to wildtype males. When maintained on normal diet, homozygous (Mstn^Ln/Ln) mice exhibit increased muscularity. When maintained on a high fat diet, homozygotes exhibit glucose tolerance, protection against overall insulin resistance, improved muscle and liver insulin sensitivity (with decreased ..... For more information please see the full phenotype on the strain data sheet
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 phenotype on the strain data sheet
016131	C57BL/6J-Sec61a1^m1Gek/J	Repository- Live
	Mice homozygous for the ENU-induced missense mutation, called Sec61a1^Y344H, are viable and fertile. By ~4 weeks of age, homozygous males and females maintained on a high-fat diet (~58% kcal from fat) become diabetic (hyperglycemic) with hypoinsulinemia; the result of endoplasmic reticulum (ER) stress-induced apoptosis of pancreatic β-cells. In addition to diabetes, these mice exhibit other metabolic, endocrinological, and growth abnormalities (including hyperlipidemia, hepatosteatosis, hypercholesterolemia, hypertriglyceridemia, and, in older mice, hepatic cirrhosis). Homozygous mice maintained on a chow diet (~5% kcal from fat) become diabetic by ~10 weeks of age; exhibiting hyperglycemia, hypoinsulinemia, glucose intolerance, and pancreatic β-cell loss. Heterozygous mice have an intermediate hypoinsulinemic phenotype on high-fat diet. These Sec61a1^Y344H mutant mice may be useful in studying diabetes, ER protein trafficking/processing/sec ..... For more information please see the full phenotype on the strain data sheet
007082	CByJ.129S(B6)-Tnf^tm1Gkl/J	Repository- Live
	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 phenotype on the strain data sheet
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 phenotype on the strain data sheet
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. View cre expression characterization.
006654	FVB.BKS(D)-Lepr^db/ChuaJ	Repository- Live
	The congenic "FVB-db" strain differs from that previously published on other genetic backgrounds in that it presents a marked obesity/diabetes phenotype intermediate between the severe uncompensated hyperglycemia observed in C57BLKS/J and DBA2/J backgrounds and the mild, compensated syndrome reported on the C57BL/6J and 129/J backgrounds. The literature reports that obese FVB-db mice of both sexes show long-term hyperglycemia primarily due to severe insulin resistance. The hyperglycemia in the fed state persists despite continued extreme hyperinsulinemia correlated with a marked pancreatic cell hypertrophy and hyperplasia. These phenotypes have been replicated in the stock at The Jackson Laboratory. However, the diabetic nephropathy (glomerulosclerosis) reported in the literature was not evident in the stock imported to JAX at the age evaluated (24 weeks). As the phenotype varies by genetic background, these mutant mice, along with db mutants on other ge ..... For more information please see the full phenotype on the strain data sheet
008659	NOD.Cg-Rag1^tm1Mom Ins2^Akita Prf1^tm1Sdz/SzJ	Repository- Live
	Like NOD.Cg-Rag1^tm1Mom Prf1^tm1Sdz/J (004848), this strain lacks mature T and B cells. NK cells, although present, lack cytotoxic activity. Both sexes develop spontaneous hyperglycemia as early as three weeks of age, however, the phenotype is predominantly exhibited by males. Pancreatic islets have reduced insulin staining and exhibit an altered morphology with age. Human islet transplantation at doses of 4000 IEQ is successful in returning hyperglycemic males to a euglycemic state. This strain may useful in studies of human islet and beta stem and progenitor cell function.
014568	NOD.Cg-Rag1^tm1Mom Ins2^Akita Il2rg^tm1Wjl/SzJ	Repository- Live
	NRG-Akita mice, which are homozygous for the Rag1^tm1Mom and the Il2rg^tm1Wjl alleles (males are hemizygous for the X-linked Il2rg^tm1Wjl allele) and heterozygous for the Ins2^Akita allele, develop spontaneous hyperglycermia. No mature T, B or NK cells are detected in flow cytometric analysis of splenocytes from NRG-Akita mutant mice. Granulocyte and macrophage populations are similar to those seen in NRG mice (Stock No. 7799). NRG-Akita mice develop hyperglycemia between 3 and 5 weeks of age. Histological examination at 3 weeks of age reveals normal pancreas morphology, and routine insulin and glucagon staining. By approximately 32 weeks of age, NRG-Akita mice display disorganized, condensed pancreatic islet architecture, with loss of insulin-positive cells. Euglycemia is restored by subrenal transplantation of mouse or human islets or intrapancreatic transplantation of dissociated mouse islet cells. NRG-Akita ..... For more information please see the full phenotype on the strain data sheet
000726	RBF/DnJ	Repository- Live
	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.
012882	STOCK Ascl1^{tm1.1(Cre/ERT2)Jejo}/J	Repository- Live
	In Ascl1-CreERT2 mice, the entire coding region of the endogenous mouse achaete-scute complex homolog 1 (Ascl1 or Mash1) gene is replaced by a CreER^T2 fusion protein. Cre activity is induced following tamoxifen administration. As such, when Ascl1-CreERT2 mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Ascl1-expressing cells of the offspring. The creERT2 fusion protein is expressed in all Ascl1 expressing neural progenitor cells in the embryo and the adult brain, including subsets of neurons throughout central nervous system (CNS) and peripheral nervous system (PNS), and in neuroendocrine cells in lung and kidney. Homozygotes die within hours of birth due to CNS and PNS disruptions in neural development. Mice heterozygous for this allele are viable, fertile, and normal in size. These mice may be useful for studying the lineage of distin ..... For more information please see the full phenotype on the strain data sheet
012881	STOCK Ascl1^tm1Reed/J	Repository- Live
	In this strain the entire coding region of the endogenous mouse achaete-scute complex homolog 1 (Ascl1 or Mash1) gene is replaced with a nuclear localized green fluorescent protein (GFP) gene, abolishing gene function. GFP, driven by the Ascl1 promoter sequence, is expressed in all Ascl1-expressing neural progenitor cells in the embryo and the adult brain, including subsets of neurons throughout the central nervous system (CNS) and the peripheral nervous system (PNS), and in neuroendocrine cells in lung and kidney. Homozygotes die within hours of birth due to CNS and PNS disruptions in neural development. Mice heterozygous for the targeted mutation are viable, fertile, and normal in size. These mice may be useful for studying the lineage of distinct cell populations, neuronal turnover, and neuronal replacement upon traumatic injury.
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 phenotype on the strain data sheet
009340	STOCK Eif2ak3^tm1Dron/HotaJ	Repository- Live
	These mice harbor a targeted mutation of the Eif2ak3 (eukaryotic translation initiation factor 2 alpha kinase 3 [also called Perk]) locus that abolishes endogenous gene expression. To date (Feb 2010), the donating investigator has not been able to generate homozygous mice on a C57BL/6J congenic background. The following phenotype describes mice on a mixed albino Swiss Webster;129/SvEv genetic background. Heterozygous mice are viable and fertile. Homozygous (Perk-/-) mice appear runty within a few days of birth and develop a rapid and progressive decline in endocrine and exocrine pancreatic function. This results in a complex pleiotropic phenotype including hyperglycemia, exocrine pancreatic insufficiency, diabetes, growth retardation, inability to breed, and early mortality. The phenotype of the Perk-/- mice is very similar to that observed in humans with Wolcott-Rallison syndrome; the consistent feature of which is severe diabetes mellitus developing in infancy. Heterozygous mi ..... For more information please see the full phenotype on the strain data sheet
014108	STOCK Epn3^tm1.1Pdc/J	Repository- Live
	These Epn3^-/- mice lack the entire coding region of the Epsin 3 (Epn3) gene. Homozygous mice are viable, fertile, and normal in size. Epn3 is expressed specifically in in the parietal cells of the stomach as well as in keratinocytes migrating across collagen in cutaneous wounds.
001618	STOCK 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.
012620	STOCK Trp53^tm1Brd Brca1^tm1Aash Tg(LGB-cre)74Acl/J	Repository- Live
	BLG-Cre; Brca1^{F22-24/F22-24}; p53^+/- mice carry the beta-lactoglobulin (BLG)-Cre transgene, are homozygous for floxed exons 22-24 of the breast cancer 1 (Brca1) allele, and are heterozygous for p53 tumor-suppressor gene (p53) deficiency. Mice of this genotype are viable, fertile, normal in size and do not display any behavioral abnormalities. BLG-Cre; Brca1^{F22-24/F22-24}; p53^+/- females have expression of the BLG-Cre transgene during lactation; which leads to loss of Brca1 function in the mammary gland. This results in formation of mammary tumors exhibiting high grade central necrosis and metaplastic elements in the form of spindle cell and squamous cell differentiation; as seen in human basal-like breast cancers and BRCA1 mutation carriers. Heterozygosity for the mutant p53 allele accelerates the formation of mammary tumors. This strain may be useful for studying human basal-like cancer and breast ..... For more information please see the full phenotype on the strain data sheet
008755	STOCK Tg(Ins2-rtTA)2Efr Tg(teto-DTA)1Gfi/J	Repository- Live
	This strain was generated by breeding Stock No. 008168 and Stock No. 008250 together at The Jackson Laboratory. The resulting double transgenic colony was established as Stock No. 008755. The Ins2-rtTA (or RIP7-rtTA) transgene expresses the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the rat insulin 2 (Ins2) promoter. The tet-DTA (or tetO-DTA) (transgene expresses diphtheria toxin A (DTA) under the control of a tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator) and a cytomegalovirus minimal promoter. Mice harboring both of these transgenes has doxycycline-inducible expression of DTA in pancreatic beta cells; i.e. addition of the tetracycline analogue doxycycline (dox) results in ablation of pancreatic beta cells.
012462	STOCK Tg(Nr5a1-cre)7Lowl/J	Repository- Live
	These transgenic mice express Cre recombinase under the direction of the mouse Nr5a1, nuclear receptor subfamily 5, group A, member 1, promoter. The Cre recombinase activity pattern mimics the endogenous gene expression (mRNA) pattern. Cre mediated recombination is detected in steroidogenic factor-1 (SF1)-positive neurons in the ventromedial hypothalamic nucleus (VMH) as well as pituitary, gonad, and adrenal tissue. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make the strain homozygous. When crossed with a strain containing loxP site flanked sequence, Cre-mediated recombination results in tissue-specific deletion of the flanked sequence in the offspring.
014158	STOCK Tg(Pax4-cre)1Dam/J	Repository- Live
	Pax4-cre transgenic mice have the mouse paired box gene 4 (Pax4) promoter directing expression of an enhanced green fluorescent protein fused to a Tet-off cassette (EGFP/tTA). The transgene also contains a tetracycline-responsive element with a CMV minimal promoter (tetO-CMVmin) driving expression of a Cre-recombinase gene. In the absence of tetracycline/doxycycline, Cre recombinase expression is observed in Pax4-expressing cells (pancreatic progenitor cells). While designed to concomitantly allow tetracycline/doxycycline-dependant inhibition of Cre recombinase expression, the donating investigator confirms no such inhibition is observed. Also, no GFP expression is observed with or without tetracycline/doxycycline administration. Therefore, Pax4-cre transgenic mice function only for Cre recombinase expression in Pax4-expressing cells. When bred with mice containing a loxP-flanked sequence, Cre-mediated recombination will result in deletion of ..... For more information please see the full phenotype on the strain data sheet
003658	STOCK Tg(TIE2GFP)287Sato/J	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.
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 phenotype 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 phenotype on the strain data sheet
017476	129S-Ucp1^tm1Kz/J	Under Development - Now Accepting Orders
	Mice that are homozygous for this knockout allele are viable and fertile, but exhibit sensitivity to cold temperatures. The Donating Investigator notes that homozygous offspring have increased survival rates to weaning age when maintained at 25°C to 28°C. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brown adipose tissue from homozygotes. When maintained at 20°C, homozygotes are resistant to diet induced obesity with reduced white fat depot weights, exhibit a 0.1-0.3°C higher body temperature, and a slightly lowered respiratory quotient compared to controls. Notably, when maintained at 27°C, homozygous mutant mice are no longer resistant to diet induced obesity and gain weight at a rate similar to wildtype controls. An increase in the number of brown adipocytes in the inguinal fat depots is observed in mutant mice maintained at 20°C, on either diet. Homozygotes have reduced levels of plasma fatty acids, circula ..... For more information please see the full phenotype on the strain data sheet
017601	B6.129-Eif2s1^tm1Rjk/J	Under Development - Now Accepting Orders
	The Eif2a^S51A mutation in these mice prevents phosphorylation of the α subunit of eIF2. Phosphorylation of eIF2α in the endoplasmic reticulum (ER) is required for translational regulation, transcriptional induction, and survival in response to ER stress. EIF2α translational regulation is also required for the maintenance of blood glucose and pancreatic insulin content. Homozygotes die within 18 hr after birth due to hypoglycemia associated with defective gluconeogenesis. Homozygous mutant embryos and neonates displayed a deficiency in pancreatic β cells and an increase in circulating insulin. Heterozygotes are viable and fertile. On a high fat diet, heterozygous mice develop diabetes due to unregulated proinsulin translation. These mice also exhibit defective ER cargo trafficking, increased oxidative damage, reduced expression of stress response and beta-cell-specific genes, and apoptosis.
016224	B6.129S(Cg)-Id2^tm2.1Blh/ZhuJ	Under Development - Now Accepting Orders
	The Id2-EGFP knockin allele was designed to both abolish inhibitor of DNA binding 2 (Id2) gene function and express enhanced green fluorescent protein (eGFP) from the Id2 promoter/enhancer elements. No mRNA or protein expression from the Id2-eGFP allele is observed. The donating investigator reports that homozygote mice mice are runted with defective lung alveolarization. Other organ systems have not been evaluated. However, Id2-eGFP homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (including postnatal lethality and defects of the immune system, digestive tract, kidneys, adipose tissue and mammary gland development). The donating investigator also reports eGFP expression recapitulates the endogenous Id2 expression pattern. In the lungs, immunohistochemical detection of eGFP recapitulates the epithelial expression of the endogenous gene (distal tip lung epithelial multipotent precursor cells of the ..... For more information please see the full phenotype on the strain data sheet
014137	B6.129S4-Pmch^tm1Emf/J	Under Development - Now Accepting Orders
	Mice that are homozygous for this knockout are viable, fertile, and exhibit a smaller stature and increased locomotor activity when compared to wildtype controls. No gene product (mRNA or protein) is detected by RT-PCR and in situ hybridization analysis of hypothalamus tissue, RT-PCR of pancreatic islets from homozygotes and immunocytochemical analysis of brain tissue from homozygotes. Homozygotes appear smaller, are leaner than wildtype controls and when placed on a chow diet, display increased basal metabolic rates and locomotor activity. When fed a high-fat diet, the oxygen consumption ( by 15.7%) and activity levels are further increased and homozygotes do not gain as much weight as controls. The lean phenotype persists in homozygous mice more than 12 months of age. Homozygotes, 12-19 months of age, are more sensitive to insulin, have reduced aging-associated weight and visceral adiposity gain, maintain increased locomotor activity, and are resistant to aging-associated glu ..... For more information please see the full phenotype on the strain data sheet
017560	B6.FVB-Tg(Fabp4-IKBKB*)49Hxu/J	Under Development - Now Accepting Orders
	These aP2-hIKKbeta SE transgenic mice express a constitutively active form of the human inhibitor of kappaB kinase beta (IKBKB) gene in adipose tissue under direction of the mouse fatty acid binding protein 4 (Fabp4) promoter. Hemizygous mice are viable and fertile. IKBKB gene product, IKKβ, is a master kinase involved in obesity-related inflammation and insulin resistance. These mice exhibit increased food intake, reduced weight of white adipose tissue, increased energy expenditure, and reduced triglyceride contents in adipose tissue, liver and muscle. They also exhibit reduced plasma free fatty acid (FFA) levels, increased systemic and tissue inflammation, decreased blood glucose levels, and improved glucose and insulin tolerance. These aP2-hIKKbeta SE mice show a decrease in hepatosteatosis even on a high fat diet. These mice may be useful for studying the effects of inflammation on adipose tissue and metabolism.
017598	FVB/N-Sdccag8^{Tn(sb-Tyr)2161B.CA1C2Ove}/J	Under Development - Now Accepting Orders
	These OVE2161B-CA1C-2 mice harbor a mutation created by random insertion of the pT2-BART3 transposon transgene. Using inverse PCR analysis, the integration site was identified between exons 12-13 of the serologically defined colon cancer antigen 8 gene (Sdccag8) on chromosome 1. The transgene is linked to the (+) strand of DNA at position 178,833,225 bp [NCB137/mm9; L:SV40:178,833,225(+)]. The donating investigator reports that homozygous mice have complete absence of Sdccag8 transcript. All homozygous mice exhibit cleft palate, with open palate observed by embryonic day (E)15. Homozygous mice die shortly after birth with complications from cleft palate (cannot suckle). In addition, the donating investigator reports that homozygous mice exhibit preaxial polydactyly and polycystic kidney disease. Hemizygous and homozygous mice of line OVE2161B-CA1C-2 exhibit very light tan coat color and red eyes.
017632	STOCK Ncor1^tm1Anh/J	Under Development - Now Accepting Orders
	These NCoR^lox mutant mice possess loxP sites flanking exons 37-40 of the nuclear receptor co-repressor 1 (Ncor1) gene. Exons 37-40 encode two of three 5' receptor interacting domains (RIDs). NCOR1 is recruited through interactions of its RIDs to nuclear receptors, such as retinoic-acid and thyroid-hormone receptors (TR), where it acts as a transcription repressor. 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 that express tissue-specific Cre recombinase, resulting offspring will have exons 37-40 deleted in the cre-expressing tissues. For example, when bred to B6.Cg-Tg(Alb-cre)21Mgn/J mice (Stock No. 003574) deletion of the two most 5' RIDs (N2 and N3) in the liver results in the inability of NCOR1 to bind to the TR. This strain may be useful for studying the role of NCOR1 on ..... For more information please see the full phenotype on the strain data sheet
006365	129-Cckar^tm1Kpn Cckbr^tm1Kpn/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
006367	129-Cckar^tm1Kpn/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
006369	129-Cckbr^tm1Kpn/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
004166	129-Itgb5^tm1Des/J	Cryopreserved - Ready for recovery
	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.
008243	129;B6-Tff3^tm1Dkpy/J	Cryopreserved - Ready for recovery
	Mice homozygous for this intestinal trefoil factor (ITF or Tff3) mutant allele are viable and fertile with no RNA or protein expression of the targeted gene in the gastrointestinal tract. Homozygous mice exhibit impaired physiological migration of intestinal epithelium to the mucosal surface, have impaired mucosal healing and increased susceptibility to dextran sulfate sodium (DSS)- induced colitis, and are more susceptible to chemotherapy and radiation-induced mucositis. These intestinal trefoil factor (ITF or Tff3) mutant mice may be useful in studying gastrointestinal tract injury (including inflammatory bowel diseases), maintenance of the mucosal barrier, migration and turnover of the intestinal epithelium, and therapies for colon cancer.
005989	129;FVB-Tg(PTH-cre)4167Slib/J	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	Mice homozygous for the diabetes 3J spontaneous mutation (Lepr^db-3J) become identifiably obese around three to four weeks of age. Elevations of plasma insulin begin at 10 to 14 days 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. Homozygous mutant mice on the 129P3/J background exhibit severe obesity but the diabetes phenotype is much reduced.
007175	129S-Cyp4a14^tm1Jhc/J	Cryopreserved - Ready for recovery
	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 (5α-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	Cryopreserved - Ready for recovery
	*The colony at The Jackson Laboratory Repository is on a mixed 129S genetic background and may not recapitulate the phenotype originally described.* The following text reflects the phenotype reported by the donating investigator (Dr. Iris Lindberg) 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 "129Sv" genetic background exhibit Cushing's-like disease pathologies of liver, pancreas, and pituitary; including pituitary-dependent hyperadrenocorticosteronism, severe hypoglycemia, hyperproinsulinemia, adrenal hypertrophy, pitui ..... For more information please see the full phenotype on the strain data sheet
003117	129S-Sst^tm1Ute/J	Cryopreserved - Ready for recovery
	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.
011120	129S-Wwtr1^tm1Benj/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, small in size and less active than wildtype controls. Only 10-25% of the expected homozygotes are born. The Donating Investigator reports that breeding homozygous females successfully is uncommon and homozygotes usually succumb before breeding age. No gene product (protein) is detected by Western blot analysis. Homozygotes develop severe polycystic renal disease, with an onset as early as a few weeks of age, and emphysema, with swollen alveoli and breakdown of alveolar walls. Kidney size increases with age. Intestinal and pulmonary inflammation is observed in some homozygotes. Levels of protein polycystin 2 (PC2) is increased in kidney epithelial cells of homozygotes. Histological analysis reveals adipocytes are smaller than wildtype control.
000090	129S1/Sv-Oca2⁺ Tyr⁺ Kitl^Sl-J/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
000004	ABP/LeJ	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
006446	B10.Cg-H2^h4 Sh3pxd2b^nee/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the nose eyes ear mutation are runted, with proportionally smaller skeletons, shortened noses, shortened and domed skulls, reduced areal bone mineral density, diminished visceral and subcutaneous white adipose tissue, but not brown adipose tissue, and abnormal eyes and middle ears. The eyes have an enlarged anterior chamber, cloudy cornea, and severe peripheral anterior synechia of the irideocorneal angle. The middle ear shows inflammation as serous fluid with diffuse neutrophils with thickened epithelium. Elevated ABR thresholds are found in all homozygotes and homozygotes are infertile.
000593	B6 x B6CBCa A^w-J/A-Grid2^Lc T(2;6)7Ca Mitf^Mi-wh/J	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery

002048	B6 x C57BLKS-Dock7^m Lepr^db Myo15^sh2-J/J	Cryopreserved - Ready for recovery
	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 wild-type 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 (Dock7^m) and diabetes (Lepr^db) spontaneous mutations.
005543	B6(129)-Duox2^thyd/J	Cryopreserved - Ready for recovery

006564	B6(C)-Kit^W-41J Gusb^mps/BrkJ	Cryopreserved - Ready for recovery
	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. They are fertile, distinct from mice with other alleles of Kit, and have the impaired hemopoiesis causing mild, normochromic, macrocytic anemia. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They ..... For more information please see the full phenotype on the strain data sheet
000562	B6(Cg)-Tub^tub/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
008884	B6.129(Cg)-Pnlip^tm1Dyh/J	Cryopreserved - Ready for recovery
	These mice harbor a null mutation of the Pnlip (pancreatic lipase [also called pancreatic triglyceride lipase or PTL]) gene. Homozygous (PTL^-/-) mice are viable and fertile, with no protein expression from the targeted allele observed in pancreatic tissue extracts. Homozygotes exhibit mildly delayed triglyceride (also called triacylglycerol or TAG) absorption after low fat diet feeding, but significantly delayed TAG absorption on a high fat/high cholesterol diet. Homozygous mice have a significant decrease in the rate/amount of cholesterol absorption; attributed to PTL-deficiency delaying dietary fat absorption to the distal small intestine (ileum) where intestinal cholesterol uptake is less efficient. Because PLT-/- mice retain endogenous Cel (carboxyl ester lipase [also called cholesterol esterase]) expression, pancreatic extracts from PTL-/- mice retain robust TAG hydrolytic activity (albeit at lower levels than wildtype mice). This TAG hydrolytic ..... For more information please see the full phenotype on the strain data sheet
008104	B6.129(FVB)-Ptgs2^{tm2.1(Ptgs1)Fun}/J	Cryopreserved - Ready for recovery
	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.
003509	B6.129-Blmh^tm1Geh/J	Cryopreserved - Ready for recovery
	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.
006411	B6.129-Gast^tm1(INS)Ez/J	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
006201	B6.129-Scd1^tm1Ntam/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
006879	B6.129-Scd2^tm1Myz/J	Cryopreserved - Ready for recovery
	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.
002681	B6.129P2-Agt^tm1Unc/J	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	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.
008841	B6.129S2-Ccrn4l^tm1Bjc/J	Cryopreserved - Ready for recovery
	Mice homozygous for this Nocturnin (Ccrn4l or Noc) targeted mutation are viable and fertile, with no detectable Noc protein made from the targeted gene. Homozygotes are resistant to diet-induced obesity and remain lean on high-fat diets, with lower body weight and reduced visceral fat. Unlike lean lipodystrophic mouse models, Noc-deficient mice do not have fatty livers (hepatic steatosis) and do not exhibit increased activity or reduced food intake. In addition to changes in glucose tolerance and insulin sensitivity, homozygous mice may also have deficits in lipid metabolism or lipid uptake. Nocturnin-deficient mice may be useful in studying resistance to diet-induced obesity, physiologic rhythms downstream of the circadian clockwork, and post-transcriptional regulation of genes necessary for nutrient uptake, metabolism, and storage.
003114	B6.129S2-Crh^tm1Maj/J	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
005517	B6.129S4-Cyb5r4^tm1Hfb/HfbJ	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
002939	B6.129S4-Insr^tm1Dac/J	Cryopreserved - Ready for recovery
	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.
005897	B6.129S4-Ppard^tm1Rev/J	Cryopreserved - Ready for recovery
	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.
005901	B6.129S4-Ppard^tm2Rev/J	Cryopreserved - Ready for recovery
	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.
009640	B6.129S4-Vip^tm1Clw/J	Cryopreserved - Ready for recovery
	Mice that are heterozygous for the targeted mutation are viable and fertile. No gene product (protein) is detected by immunohistochemical analysis of homozygotes. Homozygous females are subfertile, 15-20% of homozygous females can have litters. Homozygotes exhibit impaired circadian rhythm generation, muscle weakness, increased motor activity and increased induced airway hyperresponsiveness and inflammation. In constant darkness, homozygotes initially display shortened circadian period. Some homozygotes develop arrhythmic circadian periods after extended darkness. Heterozygotes also display abnormal circadian rhythm. Homozygotes have both gross and microscopic anatomical abnormalities of the gastrointestinal tract. 10-15% of homozygotes die of stenosis of the gut before one year of age. Male homozygotes exhibit moderate right ventricular (RV) hypertension, RV hypertrophy, thickened and remodeled pulmonary arteries, perivascular inflammation of smaller pulmonary vessels and airways, red ..... For more information please see the full phenotype on the strain data sheet
009082	B6.129S6-Osta^tm1Pda/J	Cryopreserved - Ready for recovery
	Homozygous (Osta^-/-) mice are viable and fertile, with no mRNA or protein expression from the targeted allele. Homozygotes exhibit a small growth deficit that is ameliorated after weaning, partial impairment of intestinal bile acid absorption (impaired basolateral transport of bile acids out of the ileal epithelial cell), altered regulation of bile acid synthesis, a significantly reduced bile acid pool, intestinal lengthening and intestinal hypertrophy. Homozygous mice also have reduced hepatic Cyp7a1 expression that is inversely correlated with ileal expression of fibroblast growth factor 15 (FGF15). These mutant mice may be useful in studying cholesterol metabolism, intestinal drug absorption, intestinal bile acid absorption, bile acid synthesis, and cholesterol and bile acid homeostasis. 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 ..... For more information please see the full phenotype on the strain data sheet
002188	B6.129S7-Amh^tm1Bhr/J	Cryopreserved - Ready for recovery
	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.
006941	B6.129S7-B4galt1^tm1Shur/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
006943	B6.129S7-B4galt1^tm2Shur/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
003264	B6.129S7-Gck^tm1Ts/J	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	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.
008115	B6.129X1-Pomc^tm2Ute/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
009680	B6.B-Vps54^wr/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for this spontaneous mutation on the C57BL/6 background are viable, but infertile and die prematurely. The average lifespan is 3 months, although this can be increased if littermates are present in the cage, the Donating Investigator reports. Homozygotes exhibit progressive locomotor impairment with corresponding motor neuron and muscular degeneration. Homozygous males have defective spermiogenesis and are sterile. Homozygotes of both sexes have reduced serum estrogen. Mitochondria in motor neurons are abnormal. This mutant mouse strain may be useful in studies of Spinal Muscular Atrophy, Distal Hereditary Motor Neuronopathy and Amyotrophic Lateral Sclerosis 1.
003625	B6.C-H2-Ab1^bm12/KhEg-Mc1r^e-J/J	Cryopreserved - Ready for recovery

000495	B6.C-H38^c/By-Kit^W-56J/J	Cryopreserved - Ready for recovery

000560	B6.C-H7^b/By Kit^W-50J/J	Cryopreserved - Ready for recovery

000017	B6.C3-A^vy/J	Cryopreserved - Ready for recovery
	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.
000122	B6.C3-Kit^W-44J/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
000991	B6.C58-Kit^W-57J/J	Cryopreserved - Ready for recovery

013040	B6.Cg-Apoe^tm1Unc Ins2^Akita/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Akita spontaneous mutation are stunted and typically die postnatally 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). Apoe-null homozygotes have marked increase in total plasma cholesterol levels that are unaffected by age or sex (see the datasheet for Stock No. 002052 for additional information). These double mutant mice (Apoe-null, Akita heterozygous) may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, hypercholesterolemia, and diabetes-related macrovascular complications.
006183	B6.Cg-Col4a5^tm1Yseg/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
008608	B6.Cg-Dmc1^tm1Jcs/JcsJ	Cryopreserved - Ready for recovery
	While mice heterozygous for this meiosis-specific RecA homolog (Dmc1) mutation are viable and fertile, homozygotes are viable but sterile due to arrest of gametogenesis in the first meiotic prophase (prophase I). No RNA message from the targeted gene is observed in homozygous testis. Homozygous males have reduced testis size and no mature spermatozoa in the epididymis; spermatocytes undergo meiotic arrest from defective double strand break repair and extensive chromosome asynapsis. Homozygous females exhibit defective oogenesis due to similar aberrations occurring at the pachytene stage or earlier and thus have small, malformed ovaries with complete depletion of oocytes and follicles by adulthood. These Dmc1-mutant mice may be useful in studying gametogenesis and meiosis (including double strand breaks, chromosome asynapsis, DNA repair mechanisms, homologous recombination, and the pachytene checkpoint).
000699	B6.Cg-Dock7^m Lepr^db/+ +/J	Cryopreserved - Ready for recovery
	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 diabe ..... For more information please see the full phenotype on the strain data sheet
002644	B6.Cg-Hmga2^pg-Tg40BCha/BmJ	Cryopreserved - Ready for recovery
	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.
006580	B6.Cg-Ins2^Akita Ldlr^tm1Her/J	Cryopreserved - Ready for recovery
	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.
000133	B6.Cg-Kit^W-24J/J	Cryopreserved - Ready for recovery

000139	B6.Cg-Kit^W-25J/J	Cryopreserved - Ready for recovery

000164	B6.Cg-Kit^W/J	Cryopreserved - Ready for recovery

000124	B6.Cg-Kitl^Sl Krt71^Ca/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
006906	B6.Cg-Lep^ob Ldlr^tm1Her/J	Cryopreserved - Ready for recovery
	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.
000194	B6.Cg-Lx Kit^W-v/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
000158	B6.Cg-Mitf^Mi-wh/Mitf^Mi/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
000184	B6.Cg-Mitf^Mi-wh/Mitf^mi-rw/J	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	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. Ventricular enlargement and striatal reduction is observed in adult homozygous wa1 mice. The phenotype is more severe in males. In addition, adult males exhibit reduced hippocampal volume and impaired auditory and contextural fear learning. Both sexes demonstrate an abnormal fear response. Peripubertal mice do not exhibit behavioral deficits despite slight forebrain structural abnormalities. (Koshibu K, et al., 2005)
006200	B6.Cg-Tnks2^tm1.1Yjc/J	Cryopreserved - Ready for recovery
	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.
008247	B6.Cg-Tg(Ela1-TAg*)289Mjt/J	Cryopreserved - Ready for recovery
	Hemizygous T1-147 transgenic mice (harboring the E1-T147 transgene) are viable and fertile, with high-level expression of an N-terminal, truncated (1-147 amino acid), and mutant (does not express the small t antigen) form of simian virus 40 large T antigen (TAg) directed to pancreatic acinar cells by the rat elastase 1 (Ela1 or E1) upstream control region. Hemizygous T1-147 transgenic mice exhibit pancreatic dysplasia in the embryonic pancreas, with cancer progression after birth to primary pancreatic acinar cell tumor formation (100% penetrance). These mice have microadenomas and acinar cell carcinomas present as early as 10 weeks of age, and become moribund or show clear evidence of abdominal distention around 20-30 weeks of age. T1-147 transgenic mice with large tumors develop metastatic disease to the liver and mesenteric lymph nodes. The donating investigator reports that the cancer phenotype of these T1-147 transgenic mice is identical to that of their similar T1-127 trans ..... For more information please see the full phenotype on the strain data sheet
006086	B6.Cg-Tg(HBB-GH1)420King/J	Cryopreserved - Ready for recovery
	Mice hemizygous for this transgene are viable. While males are fertile, transgenic females are unreliable breeders and mothers. Homozygotes are sterile. In both fetal and adult tissues, erythroid-specific expression of the transgene is observed. Transgenic mice have 120-150% greater mature body mass and increased bone mass. The donating investigator also reports transgenic mice have increased dermatological stiffness and toughness. Transgenic mice have a characteristic coat with few guard hairs compared to wildtype littermates. These mice may be useful in studies of bone formation and development, dermatology, and acromegaly.
007176	B6.Cg-Tg(Pax8-rtTA2S*M2)1Koes/J	Cryopreserved - Ready for recovery
	Transgenic Pax8-rtTA mice are viable and fertile. These mice express an optimized reverse tetracycline-controlled transactivator (rtTA2^S-M2) protein under the control of the murine Pax8 promoter, which directs expression to proximal and distal tubules and the collecting duct system of both embryonic and adult kidney. The rtTA2^S-M2 variant of rtTA contains five amino acid changes in the TetR moiety (S12G, E19G, A56P, D148E, and H179R) and a synthetic optimized transactivating domain, resulting in reduced basal activity and enhanced doxycycline sensitivity compared to wild-type rtTA. When mated to a second strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE or tetO), expression of the target gene in kidney cells is induced with administration of the tetracycline analog, doxycycline (dox). These Pax8-rtTA mice provide a Tet-On tool that allows the inducible expression of genes in renal tubular epithelial ..... For more information please see the full phenotype on the strain data sheet
000171	B6.D2-Kit^W-45J/J	Cryopreserved - Ready for recovery

001563	B6.D2-Kit^W-73J/J	Cryopreserved - Ready for recovery

000772	B6.DW-Pou1f1^dw/J	Cryopreserved - Ready for recovery
	Mice homozygous mice for the dwarf spontaneous mutation (Pou1f1^dw) are characterized by severe proportional dwarfing, sterility, and hypothyroidism. Adult dwarf mice are about one-fourth to one-third the size of wildtype mice. There is a lack of growth hormone, prolactin and thyroid stimulating hormone producing cells in the anterior pituitary leading to severe endocrine deficiency of these hormones. Homozygous mutant mice show a transient loss in cortical thymocytes associated with the primary defect in anterior pituitary.
006451	B6.FVB(129X1)-Tg(Sim1-cre)1Lowl/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
001177	B6.LP-Kit^W-49J/J	Cryopreserved - Ready for recovery

004454	B6;129-Crhr1^tm1Klee/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical abnormalities. No gene product (mRNA) is detected in cerebellum tissue. No gene product receptor function is seen in treated cultured pituitary cells. Pups from homozygote crosses die within 48 hours after birth of lung dysplasia due to insufficient maternal glucocorticoid during fetal development. When corticosterone is administered by drinking water or in utero to homozygous females from embryonic day 12 through postnatal day 14, offspring have normal lung maturation. There is a reported 15% mortality in male mutant mice between 3 -12 weeks of age. Mutants have very low plasma corticosterone levels, and no diurnal rise in levels. Histological analysis reveals reduced zona fasciculata layer of the adrenal gland in mature animals. Homozygous mice display reduced anxiety response behavior. Hormonal response to stress, as measured by circulating ACTH and corticoste ..... For more information please see the full phenotype on the strain data sheet
004161	B6;129-Fgf7^tm1Efu/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted allele are viable, fertile and normal in size. No Fgf7 transcript is detected. By 2 months of age, the hair coat takes on a matted/greasy appearance that becomes more prominent with age. Homozygote kidneys are markedly smaller and posses structural anomalies. Morphometric analyses indicate a reduction (~30% of wildtype) in the total number of nephrons present. Kidney development appears to be effected as early as embryonic day 16.5. This mutant mouse strain represents a model that may be useful in studies related to kidney disease.
002963	B6;129-Pcsk2^tm1Dfs/J	Cryopreserved - Ready for recovery

012862	B6;129-Slc9a3r1^tm1Ssl/J	Cryopreserved - Ready for recovery
	In this strain exon 1 of the endogenous mouse solute carrier family 9 (sodium/hydrogen exchanger), member 3 regulator 1 (Slc9a3r1, or Nherf-1) gene is disrupted by a neomycin (neo) resistance cassette, abolishing gene function. No homozygous females are obtained in the first 3 generations of backcrosses. Nherf-1^-/- females obtained between F4 and F6 generations have 30-50% reduction in bodyweight over wildtype littermates, show impaired mobility, and some develop hydrocephaly. Most homozygous females die 30-35 days after birth due to reduced bone mineral density. Associated bone fractures are observed. Male homozygotes display an increase in urinary excretion of uric acid, a decrease in serum phosphate concentration, an increase in serum alkaline phosphatase, a 3-fold increase in urinary phosphate excretion, a slight increase in urinary magnesium excretion, but maintain normal overall renal function. Homozygotes also exhibit abnormalities in the targeting and sign ..... For more information please see the full phenotype on the strain data sheet
008678	B6;129-Ubb^tm1Rrk/J	Cryopreserved - Ready for recovery
	Mice heterozygous for the targeted allele are viable and fertile. This polyubiquitin B (Ubb) mutation is characterized by a GFP-puro^r fusion protein "knock-in" allele that also abolishes endogenous gene function. Direct visualization of GFP fluorescence is observed in ovaries, testes, hypothalamus (arcuate nucleus) and cerebral cortex. Homozygotes have no Ubb mRNA observed in the various tissues tested, and are viable but sterile due to failure of germ cells to progress through meiotic prophase I and hypogonadism. Homozygotes also exhibit a complex metabolic phenotype initially characterized by dysfunction of neurons within the central nervous system accompanied by retarded perinatal growth that progresses to adult-onset obesity linked to selective hypothalamic neurodegeneration. Homozygotes also develop adult-onset hyperleptinemia (but normal levels of circulating glucose and insulin) as a consequence of increased fat content. These Ubb-mutant mice may be useful in studyin ..... For more information please see the full phenotype on the strain data sheet
002713	B6;129S-Oxt^tm1Wsy/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Oxt^tm1Wsy targeted mutation are viable and fertile. Females are able to successfully mate, deliver and produce milk however milk injection is impaired. Pups do not successfully suckle and must be fostered to survive. Oxytocin injection restores milk injection in response to suckling. Homozygotes displayed reduced aggressive behavior relative to heterozygotes and wild-type mice.
003728	B6;129S-Sparc^tm1Hwe/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for Sparc are viable and fertile. They display decreased physical activity when handled but otherwise appear normal. Sparc transcripts and protein products are not detected in these animals. The development of cataracts and osteopenia are the predominant phenotypes. Lenticular opacity starts to develop at 1 to 2 months after birth, progressing to mature cataracts by 5-8 months of age. Intracellular vacuoles are apparent at 1-2 months, leading to a disruption of fiber cell packing. In later stages, the lens capsule ruptures and displacement of lens material into the anterior chamber is evident. At 17 weeks of age, null mice exhibit 50% less trabecular bone than that found in wild type controls. The loss is 70% at 36 weeks. Decreases in both osteoclast and osteoblast numbers are observed, the cumulative effect of which is a negative bone-balance leading to profound osteopenia.
004858	B6;129S1-Tshr^tm1Rmar/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation exhibit delayed eye opening, are runted by day 21, and will die within 1 week if weaned at day 21. Homozygotes will survive by extending weaning to 28 days but will not reproduce. Homozygotes are viable and fertile when weaned at day 21 and subsequently placed on a hormone replacement therapy diet consisting of a 100ppm desiccated thyroid powder supplement. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis of thyroid membranes. Enhanced Green Fluorescent Protein (EGFP) gene product is detected by RT-PCR and Western blot analysis of thyroid tissue. Hypothyroidism is exhibited by mutant mice that have a longer weaning period and a non-supplemented diet, as indicated by low T4 and T3 serum levels, and high thyrotropin (TSH) serum levels. Treatment with exogenous TSH does not result in a thyroid hormone release response. Mutant mice produce uniodinated thyroglobulin and do not accumulate radioactive iodide in ..... For more information please see the full phenotype on the strain data sheet
002494	B6;129S2-Cga^tm1Sac/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Cga^tm1Sac targeted mutation are viable but both sexes are infertile. They lack TSH, LH, and FSH. Homozygous mutant mice are hypogonadal and exhibit severe hypothyroidism resulting in dwarfism. Development of the thyroid gland was arrested in late gestation. However, gonadotropin releasing hormone (GNRH) neuron migration, development of secondary sex organs, and fetal and neonatal gonadal development are normal. Mice heterozygous for the Cga^tm1Sac targeted mutation appear normal.
002783	B6;129S2-Crh^tm1Maj/J	Cryopreserved - Ready for recovery
	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 (10-30ug/ml) from day 12 of gestation until weaning. Homozygous mutant mice have reduced adrenocortical secretion following stress. They may be susceptible to complications from hypoglycemia when fasting. Heterozygous mice are phenotypically indistinguishable from wildtype siblings.
002426	B6;129S4-Insr^tm1Dac/J	Cryopreserved - Ready for recovery
	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.
007675	B6;129S4-Lhx3^tm1Lmgd/J	Cryopreserved - Ready for recovery
	Mice heterozygous for this targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous mice have a perinatal phenotype and are stillborn or die within 24 hours of birth. Embryos homozygous for the mutation do not exhibit the gene product (mRNA) as detected by in situ hybridization. Homozygotes exhibit abnormal pituitary development with the posterior lobe forming normally and the anterior and intermediate lobes failing to form. Although development of Rathke’s pouch, the precursor of the anterior and intermediate lobes of the pituitary, is initially normal, by embryonic day 12.5 homozygotes exhibit marked hypoplasia and growth arrest. This mutant mouse strain may be useful in studies of pituitary development.
007203	B6;129S4-Zfand5^{Gt(ROSA)72Sor}/J	Cryopreserved - Ready for recovery
	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.
002382	B6;129S6-Ttr^tm1Wsb/J	Cryopreserved - Ready for recovery
	Mice carrying the Ttr^tm1Wsb targeted mutation are phenotypically normal, viable and fertile. They have markedly reduced levels of serum retinol, retinol-binding protein and thyroid hormone. The homozygotes can utilize stored retinol despite a defective plasma retinol transport system.
002187	B6;129S7-Amh^tm1Bhr/J	Cryopreserved - Ready for recovery
	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.
003283	B6;129S7-Fshb^tm1Zuk/J	Cryopreserved - Ready for recovery
	Males carrying the targeted mutation are fertile, have small testes, reduced sperm number and sperm motility. Homozygous mutant females are infertile due to a preantral stage block in ovarian folliculogenesis. Heterozygotes are fertile.
010816	B6;C-Ghrhr^lit Prkdc^scid/BmJ	Cryopreserved - Ready for recovery
	B6;C-Ghrhr^litPrkdc^scid/BmJ mice are deficient in growth hormone and IGF1 and are useful for determining endocrine dependence of grafted cells and tissues (Beamer et al., 1993, Cancer Research, v53:3741; Friend et al., 2001 Growth Hormone & IGF Research, v11:84).
010574	B6;SJL-Tg(Gh1-rtTA)4-3Jek/J	Cryopreserved - Ready for recovery
	The donating investigator reports that homozygous mice are viable and fertile. These GH-rtTA transgenic mice have expression of the reverse tetracycline-controlled transactivator (rtTA) protein directed to GH1-producing cells (pituitary somatotropes) by the rat growth hormone (Gh1) promoter. When mated to a mutant strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE, TetRE or tetO), expression of the target gene in GH1-producing cells may be induced with administration of the tetracycline analog doxycycline (dox) in the double mutant offspring. These GH-rtTA transgenic mice are a Tet-On tool that allows conditional, dox-inducible expression of genes in GH1-producing cells/tissues (such as pituitary somatotropes) and may be useful for studying pituitary hormone secretion and proliferation.
006043	B6;SJL-Tg(Oxt/EGFP)AI03Wsy/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
010573	B6;SJL-Tg(Prl-tTA)6-5Jek/J	Cryopreserved - Ready for recovery
	The donating investigator claims homozygous mice are viable and fertile. These Prl-tTA transgenic mice have expression of the tetracycline-controlled transactivator (tTA) protein directed to PRL-producing cells (pituitary lactotropes/mammotropes) by the rat prolactin (Prl) promoter. The donating investigator also reports some expression in testis. When mated to a mutant strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE, TetRE or tetO), expression of the target gene in the PRL-producing cells may be conditionally abolished with administration of the tetracycline analog doxycycline (dox) in the double mutant offspring. These Prl-tTA transgenic mice are a Tet-Off tool that allows dox-conditional expression of genes in PRL-producing cells/tissues (such as pituitary lactotropes/mammotropes) and may be useful for studying pituitary hormone secretion and proliferation.
000350	B6By.Cg-Kit^W-v Mitf^Mi-wh T/J	Cryopreserved - Ready for recovery
	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. 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 dilut ..... For more information please see the full phenotype on the strain data sheet
001573	B6C3Fe a/a-Mitf^Mi/J	Cryopreserved - Ready for recovery
	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.
000230	B6C3Fe a/a-Tcirg1^oc/J	Cryopreserved - Ready for recovery
	Mice homozygous for the osteosclerotic spontaneous mutation (oc) can be recognized at about 10 days by failure of eruption of the incisors, clubbed feet, and circling behavior. Homozygous mutant mice may also have a kinked tail. They grow normally for about the first 10 days of life, then lose weight or at least fail to gain.
000956	B6CB-Mitf^mi-rw/J	Cryopreserved - Ready for recovery
	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.
000504	B6EiC3Sn a/A-Cacnb4^lh/J	Cryopreserved - Ready for recovery
	Mice homozygous for the lethargic spontaneous mutation (Cacnb4^lh) are first recognizable at 15 days by their lethargic behavior with gait instability and occasional seizures. The seizures resemble human petit mal seizures. No pathological changes were found in the CNS or in skeletal muscles, but peripheral motor nerves show reduced conduction velocity and prolonged distal latency. There is early thymic involution at 3 to 4 weeks in Cacnb4^lh homozygotes, accompanied by decreased lymphocyte count, decreased cell-mediated immunity, and increased levels of serum IgG1. The defects in the immune system tend to disappear by 2 months of age in mice that survive. In addition to neurological and immunological defects, homozygous lethargic mice show pituitary-adrenal hypercorticism. Homozygotes are smaller and weaker than their normal littermates and often die before 2 months old. Survivors of both sexes may breed, but their reproductivity is low.
000553	B6EiC3Sn a/A-Egfr^wa2 Wnt3a^vt/J	Cryopreserved - Ready for recovery
	Mice homozygous for the spontaneous waved 2 mutation (Egfr^wa2) are recognizable at 2 to 3 days by curly whiskers. The first coat is waved but later coats are not; vibrissae usually remain curled and the guard hairs curved. Some homozygotes have eyelids open at birth. Fertile mutant females have impaired lactation. Mice homozygous for the vestigial tail spontaneous mutation (Wnt3a^vt) have very short tails, few presacral vertebrae, and abnormal formation of the lumbar vertebrae.
000503	B6EiC3Sn a/A-Gy/J	Cryopreserved - Ready for recovery
	Gyro (Gy) is an X-linked dominant mutation that causes circling behavior and defects in phospate metabolism. It is allelic with the hypophosphatemia mutation (Phex^Hyp). Hemizygous males and heterozygous females are characterized by hypophosphatemia, rickets, circling behavior, and inner ear abnormalities. Affected males are also sterile.
004176	BKS.B6-Tub^tub/Jng	Cryopreserved - Ready for recovery
	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 on the C57BL/6 background. 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). ..... For more information please see the full phenotype on the strain data sheet
000700	BKS.Cg-Dock7^m Lepr^db/+ +/J	Cryopreserved - Ready for recovery
	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 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. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Lepr^db/+) also have increased metabolic ..... For more information please see the full phenotype on the strain data sheet
001192	BKS.Cg-mea^J Lepr^db +/+ + Dock7^m/J	Cryopreserved - Ready for recovery
	Mice homozygous for the meander tail-J spontaneous mutation (mea^J) have variably shortened and kinked tails. At about two weeks an unsteadiness of gait, often amounting to a tremor, appears. Homozygous mutant mice are smaller and less vigorous than wild-type controls but are fertile. The anterior lobe of the cerebellum is disorganized. Purkinje cells are scattered, some cellular layers never form, and Bergmann glial processes are absent. The cytoarchitecture of the posterior lobe is normal, and the transition from normal to disorganized areas is sharply demarcated. This mutation occurred in the BKS.Cg-Lepr^db +/+ Dock7^m strain so it is also segregating for the diabetes (Lepr^db) and misty (Dock7^m) mutations. See strain description for Stock No. 000642 for more information.
000696	BKS.V-Lep^ob/J	Cryopreserved - Ready for recovery
	Mice homozygous for the obese spontaneous mutation (Lep^ob, commonly referred to as ob or ob/ob) are first recognizable at about 4 weeks old. Homozygous mutant mice increase in weight rapidly and may reach three times the normal weight of wildtype controls. In addition to obesity, mutant mice exhibit hyperphagia; a diabetes-like syndrome of hyperglycemia, glucose intolerance, and elevated plasma insulin; subfertility; and increased hormone production from both pituitary and adrenal. They are also hypometabolic and hypothermic. The obesity is characterized by both an increased number and size of adipocytes. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase body weight and is probably the result of it. Homozygotes do have an abnormally low threshold for stimulati ..... For more information please see the full phenotype on the strain data sheet
002391	BKSChpLt.HRS-Cpe^fat/J	Cryopreserved - Ready for recovery
	Mice homozygous for the fat spontaneous mutation (Cpe^fat) on a C57BLKS/J genetic background (N10) have a diabetes phenotype that is primarily restricted to males and is more severe than what is seen on the original HRS/J or C57BLKS/J (N5) genetic backgrounds. At weaning both males and female homozygous mutant mice were significantly lighter than wildtype or heterozygous littermates. Obesity develops between 6 and 8 weeks of age and mutant mice can be distinguished from wildtype littermates between 8 and 12 weeks of age. By 18 weeks fat mutant mice will reach 45-55 g and may reach 60-70 g by 6 months of age. Thus, the obesity is thus slower to develop than in the obese (Lep^ob) and diabetes (Lepr^db) mutant mice. The excess adiposity is distributed throughout the body's fat stores, in contrast to the largely axial and inguinal fat deposition of the obese and diabetes mutant mice. Hyperinsulinemia is severe by 4 weeks of age and contin ..... For more information please see the full phenotype on the strain data sheet
007810	C.129-Stat5b^tm1Hwd/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
005516	C.129S4-Cyb5r4^tm1Hfb/HfbJ	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
001768	C3.Cg-Irs1^Sml H2^b/GrsrJ	Cryopreserved - Ready for recovery
	The small mutation causes hyperinsulinemia with only mild insulin resistance, a paucity of body fat, deficiencies in bone development and homeostasis, and hearing loss. Homozygotes can be distinguished by 2 weeks of age by their smaller body size and thin short tails, and adult homozygotes are visibly smaller with a tail that is 20% shorter than in wild-type controls. Hearing loss was shown through increased ABR threshold values when assessed between 8 and 12 weeks of age. The skeletal defects include shortened femurs with smaller growth plates, decreased cortical and trabecular thickness and abnormal trabecular number, with an increase in the number of osteoclasts and osteoblasts per bone perimeter but impaired osteoblast proliferation and differentiation in culture. This spontaneous point mutation is semidominant in some aspects of phenotype, unlike targeted mutations of this gene. Heterozygotes are statistically smaller than wild-type controls, but the severity of dwarfing is not ..... For more information please see the full phenotype on the strain data sheet
000225	C3FeLe.B6 a/a-Ptpn6^me/J	Cryopreserved - Ready for recovery
	Mice homozygous for the motheaten spontaneous mutation (Ptpn6^me) 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, motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The lifespan of homozygous motheaten mice is approximately 3 weeks with death attributed to an autoimmune pneumonitis.
000291	C3FeLe.Cg-a/a Hm Kitl^Sl Krt71^Ca-J/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
000627	C3H/HeJ-Kit^W-x/J	Cryopreserved - Ready for recovery

003401	C3H/HeJ-Lpin1^fld-2J/J	Cryopreserved - Ready for recovery
	Homozygous fatty liver dystrophy (fld) mice have an enlarged, fatty liver and hypertriglyceridemia which resolve to normal during the weaning transition. However, decreased overall size, decreased lipid in the fat pads, and a peripheral neuropathy persist throughout the lifespan. This peripheral neuropathy manifests as a tremor and an unsteady gait shortly after 10 days of age and worsens with age. The fld neuropathy is specific to the peripheral nervous system. Electron microscopy of sciatic nerves revealed thin, poorly compacted myelin sheaths, hypertrophic Schwann cells, myelin debris, degenerating axons, bands of Bugner, and regenerative clusters, but no evidence of inflammation (Langner et al, 1991). Western blot analysis of sciatic nerve from two-to-three month old fld/fld mice showed a 7-13-fold reduction in myelin P₀, a vast increase in apoE, an increase in GAP-43, and no detectable myelin P₂. It was also noted that a ..... For more information please see the full phenotype on the strain data sheet
000510	C3H/HeJ-Pou1f1^dw-J/J	Cryopreserved - Ready for recovery
	Mice homozygous mice for the dwarf Jackson spontaneous mutation (Pou1f1^dw-J) have a phenotype very similar to mice homozygous for the original dwarf mutation (Pou1f1^dw). Homozygous mutant mice are characterized by severe proportional dwarfing, sterility, and hypothyroidism. Adult dwarf mice are about one-fourth to one-third the size of wildtype mice. There is a lack of growth hormone, prolactin and thyroid stimulating hormone producing cells in the anterior pituitary leading to severe endocrine deficiency of these hormones. Homozygous mutant mice show a transient loss in cortical thymocytes associated with the primary defect in anterior pituitary.
000099	C3HeB/FeJ-A^vy/J	Cryopreserved - Ready for recovery
	Homozygotes (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 AP^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 agout ..... For more information please see the full phenotype on the strain data sheet
000847	C3Sn.B6-Kit^W-39J/J	Cryopreserved - Ready for recovery

001380	C3Sn.Cg-Kitl^Sl-con/J	Cryopreserved - Ready for recovery
	Both homozygous and heterozygous mice with the contrasted induced mutation (Kitl^Sl-con) are viable. Male homozygous mutant mice are fertile but females are usually sterile. Mice heterozygous for the contrasted mutation are recognizable soon after birth by dark pigmentation of the genital papilla with the adult coat being slightly lighter than normal. Homozygous mutant mice also have dark genitalia and a markedly diluted coat and mild macrocytic anemia.
003100	C3Sn;129-Del(10AI646023-Ggt5)1Bayer/J	Cryopreserved - Ready for recovery
	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.
000233	C3Wf.Cg-Hmga2^pg/BmJ	Cryopreserved - Ready for recovery
	Mice homozygous for the pygmy mutation (Hmga2^pg) are recognizably smaller at birth, growth rate is slow, and adults weigh about one-third as much as normal mice. They are healthy and active; some are sterile, but fertility may be almost normal on genetic backgrounds favoring large size. Pituitary, thyroid, and adrenals appear normal; Normal somatomedin activity; Normal serum levels of GH and PRL, but below normal concentrations in the pituitary; Unresponsive to administration of growth hormone.
009062	C57BL/6-Magel2^tm1Stw/J	Cryopreserved - Ready for recovery
	The mouse locus 7qB4/B5 (syntenic with the Prader-Willi region at chromosome position 15q11-q13 in humans) encompasses the cluster of paternally-expressed imprinted genes Magel2, Ndn, Mkrn3, and Peg12. As maternal imprinting silences the Magel2 allele, only the paternally inherited Magel2 allele is expressed. The Magel2-lacZ knock-in allele abolishes endogenous gene function and expresses a β-galactosidase fusion protein. Under control of the upstream promoter/enhancer elements, lacZ expression is directed to the same tissues as the wildtype gene. For example, β-galactosidase expression during embryogenesis is detected in central nervous system (neural tube, forebrain, midbrain and embryonic hypothalamus), peripheral nervous system (dorsal root ganglia and peripheral neurons innervating limb and trunk muscles), and some non-neuronal tissues (genital tubercle, midgut region and placenta). Adult β-galactosidase ..... For more information please see the full phenotype on the strain data sheet
000569	C57BL/6J-A^w-J-Eda^Ta +/+ Ar^Tfm/J	Cryopreserved - Ready for recovery
	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 mutation (Eda^Ta) 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.
013633	C57BL/6J-Bicc1^b2b222Clo/J	Cryopreserved - Ready for recovery
	This c.10048T->C Bicc1 (bicaudal C homolog 1 (Drosophila)) recessive mutation was identified in an ENU screen for recessive cardiovascular development phenotypes in Dr. Cecilia Lo's laboratory, NHLBI Cardiovascular Development Consortium (CvDC). It was recovered from G1 sperm and associated with the phenotype described described here. Because G1 sperm were cryopreserved, additional ENU mutations are also segregating in this strain. Homozygotes demonstrate laterality defects, including situs inversus totalis, and heterotaxy. Congenital heart disease (CHD) is marked by double outlet right ventricle (DORV)/transposition of the great arteries (TGA), atrioventricular septal defects (AVSD), and an interrupted aortic arch (IAA). Polycystic kidney disease, as well as pancreatic, choleductal, and gonadal cysts are also found.
004109	C57BL/6J-Glra1^nmf11/J	Cryopreserved - Ready for recovery
	Early onset visible phenotype characterized by small size and severely impaired gait that becomes detectable between 18-21 days (mean 18.6 +/- 1.7 days). Gently dropping the animals from a height of 10-15cm onto a soft surface frequently induces intense seizure-like behavior that may last several minutes (generalized seizure-like episodes, including front and hind limb contractions, hind limb extensions); however the animals recover and continue to move around. Electroretinograms (ERG) showed abnormal b-waves in three (2 males, 1 female) of four mutants examined. Mutants of either gender have been produced; homozygotes are not viable. ..... For more information please see the full phenotype on the strain data sheet
000166	C57BL/6J-Kit^W-17J/J	Cryopreserved - Ready for recovery

000167	C57BL/6J-Kit^W-18J/J	Cryopreserved - Ready for recovery

000169	C57BL/6J-Kit^W-20J/J	Cryopreserved - Ready for recovery

000117	C57BL/6J-Kit^W-34J/J	Cryopreserved - Ready for recovery

000128	C57BL/6J-Kit^W-35J/J	Cryopreserved - Ready for recovery

000134	C57BL/6J-Kit^W-37J/J	Cryopreserved - Ready for recovery

000062	C57BL/6J-Kit^W-39J/J	Cryopreserved - Ready for recovery

000121	C57BL/6J-Kit^W-40J/J	Cryopreserved - Ready for recovery

000119	C57BL/6J-Kit^W-41J/J	Cryopreserved - Ready for recovery

000127	C57BL/6J-Kit^W-42J/J	Cryopreserved - Ready for recovery

000129	C57BL/6J-Kit^W-43J/J	Cryopreserved - Ready for recovery

000990	C57BL/6J-Kit^W-55J/J	Cryopreserved - Ready for recovery

001179	C57BL/6J-Kit^W-62J/J	Cryopreserved - Ready for recovery

003252	C57BL/6J-Kitl^Sl-20J/J	Cryopreserved - Ready for recovery
	Kitl^Sl-20J is a dominant allele. On the C57BL/6J background heterozygotes have a light black coat color with lighter tail and feet and a steel colored belly with a belly spot. Heterozygotes of both sexes are viable and fertile.
000060	C57BL/6J-Mc1r^e/J	Cryopreserved - Ready for recovery

002611	C57BL/6J-Mitf^mi-bws/J	Cryopreserved - Ready for recovery
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption.
006699	C57BL/6J-Pcsk1^N222D/J	Cryopreserved - Ready for recovery
	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.
010825	C57BL/6J-Ptpn6^me/SzJ	Cryopreserved - Ready for recovery
	Mice homozygous for the motheaten spontaneous mutation (Ptpn6^me) develop severe autoimmune disease. Characteristics include 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, motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The lifespan of homozygous motheaten mice is approximately 3 weeks with death attributed to an autoimmune pneumonitis.
008791	C57BL/6J-Rnl11/Pgn	Cryopreserved - Ready for recovery
	Mice homozygous for this ENU induced mutation exhibit decreased kidney function as measured by an increased albumin/creatinine ratio (ACR).
008794	C57BL/6J-Rnl20/Pgn	Cryopreserved - Ready for recovery
	Mice homozygous for this ENU induced mutation exhibit decreased kidney function as measured by an increased albumin/creatinine ratio (ACR).
008796	C57BL/6J-Rnl25/APgn	Cryopreserved - Ready for recovery
	Mice homozygous for this ENU induced mutation exhibit decreased kidney function as measured by increased blood/urea/nitrogen levels (BUN). In the F2 and F3 generations, some animals exhibited increased albumin/creatinine ratios (ACR). In succeeding generations, mice with elevated ACR were bred to establish the "A" line. Mice with elevated BUN were bred to establish the "B" line (Stock No. 016256).
008798	C57BL/6J-Rnl29/Pgn	Cryopreserved - Ready for recovery
	Mice homozygous for this ENU induced mutation exhibit decreased kidney function as measured by increased blood/urea/nitrogen levels (BUN).
008803	C57BL/6J-Rnl43/Pgn	Cryopreserved - Ready for recovery
	Mice homozygous for this ENU induced mutation exhibit decreased kidney function as measured by increased blood/urea/nitrogen levels (BUN).
000708	C57BL/6J-Utp14b^jsd/J	Cryopreserved - Ready for recovery

006422	C57BL/6J-hlb324B/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 12 week old male (born 9/30/2002) with a low bone mineral content and density as determined by DEXA analysis. Retesting at 18 weeks of age, when bone development has stabilized, confirmed this phenotype. This mutant mouse strain may be useful in studies of bone mineralization.
003711	CAST.B6-Tub^tub/Jng	Cryopreserved - Ready for recovery
	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 on the C57BL/6 background. 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). ..... For more information please see the full phenotype on the strain data sheet
000707	CBA.Cg-Dock7^m Lepr^db/+ +/J	Cryopreserved - Ready for recovery
	Lepr^db/Lepr^db mice on the CBA strain background are characterized by exocrine pancreatic necrosis and kidney lesions in aging mice. In contrast to the obesity observed in other strain backgrounds, five month old homozygous males exhibit weight loss in comparison to controls. Homozygous males develop severe hyperglycemia exhibiting blood sugar levels of +/-475 mg/dl by three months of age and increasing to +/- 517 mg/dl by five months. Five month old homozygous males do not exhibit hyperinsulinemia, however homozygous females reach levels of +/-540 uU/ml. Homozygous males do not survive beyond six months (Leiter EH et al, 1981). Because of the sterility of Lepr^db homozygotes, misty has been incorporated into stocks for maintenance of the diabetes mutation. The repulsion double heterozygote (Lepr^db +/+ Dock7^m) facilitates identification of heterozygotes for breeding, while the coupling ..... For more information please see the full phenotype on the strain data sheet
000965	CBACa.C3-Kit^W-x/J	Cryopreserved - Ready for recovery

008081	CBy.129(B6)-Sirt1^tm1Ygu/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted allele (SirT1^co/co) are viable and fertile with a loxP-flanked neomycin cassette just upstream of, and a third loxP site just downstream of exon 4 of the targeted gene. The floxed mutation does not affect the protein expression of the targeted gene in MEF's or mammary tissue from homozygotes. When bred to mice that express Cre recombinase, the resulting offspring have exon 4 (encoding a conserved Sir2 motif) deleted in the cre-expressing tissue(s) (the donating investigator reports that they observe only one recombination event; complete removal of the neomycin cassette and exon 4, leaving a single loxp site remaining). These SirT1^co/co mice may be useful in generating conditional mutations for studying the role of estrogen, insulin growth factor-1 (IGF-1), and transcription factors (including NF-kappaB) in mammary gland development, breast cancer, apoptosis, and metabolic diseases. In an att ..... For more information please see the full phenotype on the strain data sheet
000936	CBy.AK-Tg^cog/J	Cryopreserved - Ready for recovery
	The Tg^cog mutation causes the development of goiters due to failed processing of thyroglobulin. Homozygotes are smaller in overall size by 15 days of age. They display an increase in growth rate at the time of weaning but generally do not attain comparable size with their wildtype littermates. Increased thyroidal volume is apparent at embryonic day 18, and continues enlarging to an average of 5 fold higher than normal at 8 weeks of age and 20 fold normal at 10 months of age. In addition to decreased serum T3 and T4 levels, homozygotes have increased serum thyroid stimulating hormone levels, reduced levels of serum IGFBP-3, IGFBP-4, and IGFBP-2, mild anemia, and hypomyelination restricted to the cerebrum. Tg^cog is an outwardly recessive mutation, but microdissection reveals a heterozygous phenotype as well. Thyrofollicular cells of heterozygotes have swollen protein-containing vesicles similar to but more moderate than those found in homozygotes ..... For more information please see the full phenotype on the strain data sheet
000805	CBy.RF-Tshr^hyt/J	Cryopreserved - Ready for recovery
	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
001723	CByJ.A-Ttc7^fsn/J	Cryopreserved - Ready for recovery
	Homozygous fsn mice suffer from hypochromic and normocytic anemia at birth which becomes more severe with age. The anemia makes the homozygous mice distinguishable as pups because of the pale color of ears and eyes. At 2 weeks of age focal epidermal hyperplasia and inflammation is evident with psoriasiform skin lesions becoming confluent and diffuse in 3-4 week old weanlings. The skin lesions progress to generalized alopecia and shedding of thick white scales. The gross lesions are accompanied by thickening and keratinization of the skin. A progressive paplosquamous disease ensues which is a model for some forms of psoriasis. fsn/fsn mice show hematocrit levels and red blood cell counts that are significantly decreased from birth through adulthood. Consequently the heart, liver and spleen become enlarged but the thymus weight is less than half normal. As the spleen enlarges, the mice also develop a potbellied appearance aiding in homozygous fsn identification. G ..... For more information please see the full phenotype on the strain data sheet
000711	CByJ.Cg-Foxn1^nu/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
003219	D2.129P2(B6)-Nr5a1^tm1Klp/EiJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Nr5a1^tm1Klp (formerly Ftzf1^tm1Klp) targeted mutation exhibit adrenal and gonadal agenesis. There is also an absence of the ventromedial hypothalamic nucleus leading to impaired expression of gonadotrope specific markers.
013719	D2.Cg-Apoe^tm1Unc Ins2^Akita/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Akita spontaneous mutation typically die postnatally 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. 007562 for additional information). Apoe-null homozygotes have marked increase in total plasma cholesterol levels that are unaffected by age or sex (see the datasheet for Stock No. 007067 for additional information). These double mutant mice (Apoe-null, Akita heterozygous) may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, hypercholesterolemia, and diabetes-related macrovascular complications.
000253	DLS/LeJ	Cryopreserved - Ready for recovery
	Mice homozygous for the dilute-lethal spontaneous mutation (Myo5a^d-l) display a severe neuromuscular disorder characterized by convulsions and opisthotonus. Homozygous mutant mice usually die by approximately 3 weeks of age. Dilute lethal homozygotes lack smooth endoplasmic reticulum in the dendritic spine of Purkinje cells causing an absence of intracellular calcium. Loss of this intracellular calcium may be the cause of dilute-lethal neurological symptoms. Homozygous dilute-neurological mutant mice (Myo5a^d-n, Stock No. 001013) display a neuromuscular disorder, but the condition is less severe than in dilute-lethal homozygotes. In this DLS/Le inbred strain the dilute-lethal mutation is maintained in repulsion with short ear (Bmp^se), closely linked mutations on Chromosome 9.
000681	DW.C3-Mlph⁺ Pou1f1⁺/J	Cryopreserved - Ready for recovery
	This DW/J congenic strain is wildtype for both the leaden (+^Mlph-ln) and dwarf ( +^Pit1-dw) mutations and thus serves as a control strain for DW/J-Pit1^dw/+ Mlph^ln/Mlph^ln, Stock No. 000643.
000643	DW/J Mlph^ln Pou1f1^dw/J	Cryopreserved - Ready for recovery
	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.
001595	DW/J-Acd^acd/J	Cryopreserved - Ready for recovery
	acd/acd homozygotes can be distinguished from their wildtype (?/+) littermates by darkened pigmentation, short, curly vibrissae, smaller overall size, and abnormal pelage. Hair growth is retarded and lacks zigzag and guard hairs producing a sparse coat. There is heavy pigmentation in the nose, ears, body, feet and tail, and foci of melanin are also found in the skin and lymph nodes. Tail kinks or polydactyly of the hind feet are sometimes found and external genitalia are underdeveloped. It is rare for homozygotes to breed. Hydronephrosis is sometimes found in post-wean aged homozygotes resulting from focal hypertrophy of ureteral epithelium which causes ureteral blockage. The adrenals are abnormal in both males and females. Although the size of the medullary cells is normal, the cortical cells and nuclei are much larger than normal with nuclear inclusions and many mitochondria in the cytoplasm. These mitochondria have tubular cristae and cholesterol ester droplets, whic ..... For more information please see the full phenotype on the strain data sheet
000092	FL/1Re-Kit^W/J	Cryopreserved - Ready for recovery
	Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been ..... For more information please see the full phenotype on the strain data sheet
005710	FVB.129S-Mmp13^tm1Werb/J	Cryopreserved - Ready for recovery
	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	Cryopreserved - Ready for recovery
	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 o ..... For more information please see the full phenotype on the strain data sheet
002437	FVB/N-Tg(MMTV-Notch4)3Rnc/J	Cryopreserved - Ready for recovery
	Male mice transgenic for the Notch4 gene (previously called Int3) are sterile, and females fail to lactate. Mammary tissue of females does not develop completely, exhibiting dramatic inhibition of alveolar-lobular development and reduced penetration of the mammary fat pad by ductal epithelium. Glandular epithelia of tissues expressing the activated form of Notch4 generally display severe ductal hyperplasia. Salivary glands fail to differentiate completely. Male transgenic mice exhibit severe epididymal hyperplasia, which is thought to be the cause of their sterility. Both male and female mice develop focal adenomas of the mammary and salivary glands.
000255	GL/Le Edar^dl-J +/+ Ostm1^gl/J	Cryopreserved - Ready for recovery
	Mice homozygous for the grey-lethal spontaneous mutation (Ostm1^gl) are characterized by osteopetrosis. Homozygous mutant mice are anemic, have a reduced white cell count, early thymic involution, and deficient calcium regulation. Homozygotes lack the power of secondary bone resorption. Consequently, the bones cannot grow normally, they do not form normal marrow cavities, and the teeth do not erupt.
000804	HPG/BmJ	Cryopreserved - Ready for recovery
	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.
006775	NOD.Cg-Foxp3^sf/DoiJ	Cryopreserved - Ready for recovery
	Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. By 3 weeks of age, Foxp3-deficient NOD mice suffer massive lymphoproliferation and inflammatory infiltration in lungs, liver, skin, pancreas, kidneys, stomach, colon, fat and muscles and die by three weeks of age. At 14 days of age, NOD.Foxp3-deficient mice developed exocrine pancreatitis and occasional peri-insulitis; however invasive insulitis and diabetes were not observed. In a NOD.Foxp3-deficient, BDC2.5 TCR transgenic model, mice experienced markedly decreased lymphoproliferation, yet 100% were diabetic by 20 days of age. This congenic NOD scurfy model is useful to study the role of Foxp3-dependent regulatory T cells on diabetes development.
006023	NOD.Cg-H2-Ab1^tm1Gru Tg(CD4,HLA-DQA1,HLA-DQB1)N8Ell/EllJ	Cryopreserved - Ready for recovery
	This NOD congenic strain contains a targeted H2-Ab1 mutation also carries two transgenes: one expressing human CD4 under the regulation of the mouse Cd4 enhancer and a second expressing human HLA-DQ6. The latter transgene confers dominant protection to development of Type 1 diabetes in humans. These double transgenic, H2-Ab1-deficient mice are viable, fertile, normal in size, and free of both autoimmune diabetes and cardiomyopathy, a phenotype found in an NOD stock expressing an HLA-DQ8 transgene (Elliot JF et al. Proc Natl Acad Sci U S A 2003; 100:13447-52). By 55 weeks of age, 100% of the H2-Ab1-deficient, DQ6 transgenic mice develop thyroiditis and thyroid autoantibodies. Of these, 25% develop thyroid gland enlargement and goiter, and a subset of these animals develops thyroid failure with elevated serum TSH levels. This model is useful for studying autoimmune thyroid disease and to understand the role of MHC class II in au ..... For more information please see the full phenotype on the strain data sheet
006956	NOD.Cg-Vdr^tm1Ska/CmatJ	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
000993	NZB/BlNJ-Kit^W-59J/J	Cryopreserved - Ready for recovery

001000	RBD/DnJ	Cryopreserved - Ready for recovery

000807	RBJ/DnJ	Cryopreserved - Ready for recovery

010522	STOCK Acan^cmd/NKruJ	Cryopreserved - Ready for recovery
	Mice that are homozygous for this spontaneous mutation die just after birth from an in ability to breathe. Newborns exhibit cleft palate, a protruding tongue, bulging abdomen, enlarged liver and a shortened trunk, limbs, snout and tail. Long bones measure half the length of wild-type mice and the spinal column is reduced by 25%. Cartilage in homozygous mice consists of densely packed chrondocytes, little matrix, pycnotic cells and unusual amounts of collagen fibers. Mice that are heterozygous for the mutation appear normal at birth, but develop proportional dwarfism by 28 days. Aging mice exhibit spinal misalignment and degeneration followed by the sudden onset of a spastic gait and an accompanying decrease in movement. Mice die within one month following the appearance of the abnormal gait. Heterozygotes do not live beyond 19 months. This mutant mouse strain may be useful in studies of achondroplasia, disc herniation and spinal degeneration.
003118	STOCK Ces1c^e Foxn1^nu/J	Cryopreserved - Ready for recovery
	Mice homozygous for Ces1c^e are viable and fertile and exhibit no apparent defect. Ces1c^e was discovered in a screen of progeny of triethylenemelamine (TEM) treated male mice for mutations at specific loci, but appears to have pre-existed in the male. The screen employed analysis of blood and kidney homogenates by "standard starch gel electrophoresis techniques" and focused on enzymes known to differ in electrophoretic mobility between the parental strains (DBA/2J and C57BL/6J). Ces1c^e was initially thought to be a null allele, but characterization of homozygous F2 mice demonstrated presence of a faint band migrating between those of the parental strains, which was not perceived in the presence of either parental band. Thus, Ces1c^e was shown to be a hypomorphic electrophoretic variant (Soares 1979). The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1^nu, formerly <> ..... For more information please see the full phenotype on the strain data sheet
002857	STOCK Egfr^tm1Mag/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Egfr^tm1Mag targeted mutation are recognizable at 2 to 3 days by curly whiskers. The first coat is waved but later coats are not; vibrissae usually remain curled and the guard hairs curved. Fertile mutant females have impaired lactation.
001743	STOCK Gtg1^dwg/J	Cryopreserved - Ready for recovery
	Mice homozgyous for the dwarf grey spontaneous mutation (Gtg1^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.
006241	STOCK Hhip^tm1Amc/J	Cryopreserved - Ready for recovery
	Mice heterozygous for this targeted mutation are viable and fertile. Homozygotes die from respiratory failure shortly after birth. Expression of the "knocked-in" lacZ gene is detected in a pattern similar to the endogenous transcript (in lung, skeleton, stomach, duodenum, spleen, and pancreas), and serves as a faithful reporter for Hedgehog (Hh) signaling. Because Hh and fibroblast growth factor (Fgf) signaling are abnormal, homozygous mice have defects in many Hh target tissues. Although the primary lung buds form in homozygotes, lung branching morphogenesis is defect beginning at 10.5 days postcoitus (dpc), and fails to generate a complete respiratory tree. The single left lobe also is significantly reduced, and total lung size at birth is diminished 67-75% compared to wildtype. In addition, homozygous mice have delayed mineralization of the endochondral skeleton, as well as impaired pancreas morphogenesis, islet formation and endocrine cell proliferation. These mutant mice ma ..... For more information please see the full phenotype on the strain data sheet
003258	STOCK Igf1^tm1Ts/ImJ	Cryopreserved - Ready for recovery
	The majority of mice homozygous for the Igf1^tm1Tstargeted mutation die perinatally. Only ~4% of homozygotes survive beyond birth for up to 4 months of age. Heterozygotes have serum levels of IGF-1 that are 37% lower than in wild type mice. Body size is, proportionally, 10-20% smaller than that of normal wild type siblings, with no apparent histological abnormalities.
003259	STOCK Igf1^tm2Ts/ImJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Igf1^tm2Ts mutation (also referred to as the Igf1^m/m midi targeted insertion) are viable and fertile, but are small in size, reaching only approximately 60 - 65% the weight of their wild type siblings. Serum levels of IGF-1 in these mutants is 30% of wild type values. They have no gross histological abnormalities. Arterial blood pressure is higher in Igf1^m/m mice than in wild type controls
000979	STOCK Kitl^Sl-16J/J	Cryopreserved - Ready for recovery
	The steel mutations cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations. Most steel homozygous mice are severely anemic in utero and die usually at 15 to 16 days of gestation. However, compounds of two Mgf^Sl mutants (e.g. Mgf^Sl/Mgf^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable Mgf^Sl/ Mgf^Sl homozygotes and deficient in the Mgf^Sl/+ heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing age.
005994	STOCK Mbtps1^tm1Jdh/J	Cryopreserved - Ready for recovery
	These mice carry a targeted mutation in which exon 2 of the targeted gene is flanked by loxP sites. A loxP-flanked ("floxed") neomycin resistance cassette also is inserted downstream in intron 2. Homozygotes are viable and fertile, and the floxed gene appears to function normally. When homozygotes are crossed with transgenic strains expressing Cre-recombinase, cre-mediated recombination of the loxP-flanked sequences can result in one of three genotypes: a) deletion of the neo cassette only, leaving a loxP-flanked second exon and unimpaired endogenous gene function. b) Deletion of exon 2 only, leaving a loxP-flanked neo cassette and no endogenous gene function. c) Deletion of both the neo cassette and exon 2, leaving a single loxP site and no endogenous gene function. When these floxed mutant mice are bred to mice carrying the Mx1-cre transgene (for example, Stock No. 003556), liver- ..... For more information please see the full phenotype on the strain data sheet
001253	STOCK Mitf^Mi-wh +/+ Wnt7a^px/J	Cryopreserved - Ready for recovery
	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. Mice homozygous for the postaxial hemimelia spontaneous mutation (Wnt7a^px) have skeletal defects of the forelimbs. Digits 5, 4, and sometimes 3, are missing and there is a reduction or absence of the ulna. There is always a large oval foramen in the scapula. The hindlimbs are usually unaffected, but digit 5 may be absent, and occasionally the fibula is r ..... For more information please see the full phenotype on the strain data sheet
001585	STOCK Oca2^p-d/Oca2^p-25H/J	Cryopreserved - Ready for recovery
	Oca2^p-25H/Oca2^p-25H mice exhibit significant dilution of coat color with pink eyes, similar in appearance to Oca2^p/Oca2^p mice. The Oca2^p-25H phenotype also includes a slightly jerky gait with some tremor, small body size compared to control littermates, male sterility, female semisterility, and impaired maternal behavior, and the smaller-than-expected proportion of Oca2^p-25H homozygous intercross offspring implies reduced prenatal viability (Lyon et al. 1992, Phillips et al. 1977). The Oca2^p-25H mutation comprises an inversion of a segment of Chromsome 7 that alters the 5' end of the Oca2^p gene so that no detectable ptranscript is produced, accounting for the pigment-dilution phenotype (Gardner et al. 1992). The deletion also disrupts the Herc2/rjs gene proximal to Oca2^p so the transcript seq ..... For more information please see the full phenotype on the strain data sheet
006327	STOCK Pcsk1^tm1Dfs/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
005701	STOCK Pdx1^tm1Macd/J	Cryopreserved - Ready for recovery
	Mice homozygous for the targeted mutation fail to develop a pancreas. Heterozygous mice have normal pancreas development but partially impaired glucose tolerance in adulthood. The substitution of the targeted gene with tTA_off inactivates the endogenous allele and places tTA_off expression under the control of the endogenous transcriptional regulatory sequences. tTA expression from the modified locus is identical to that of the normal allele; tTA mRNA is detectable in the pancreas but not in other visceral organs or salivary glands. This mutant may be useful in studies of pancreatic endocrine/exocrine function and diabetes. Heterozygotes also can be bred with transgenic mice that express a target gene under the regulation of a tetracycline-responsive element (TRE; tetO) for pancreas-specific applications. This mutant was originally designed to be mated with mutant mice with a TRE-controlled transgene coding for the endogenous Pdx1 (Ipf1) gene alon ..... For more information please see the full phenotype on the strain data sheet
010605	STOCK Prkdc^scid Gnrh1^hpg/BmJ	Cryopreserved - Ready for recovery
	Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdc^scid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen ..... For more information please see the full phenotype on the strain data sheet
002549	STOCK Tg^cog/J	Cryopreserved - Ready for recovery
	The Tgn^cog mutation causes the development of goiters due to failed processing of thyroglobulin. Homozygotes are smaller in overall size by 15 days of age. They have an increase in growth rate at the time of weaning but generally do not attain comparable size with their wildtype littermates. Increased thyroidal volume is apparent at embryonic day 18 and continues enlarging to an average of 5 fold higher than normal at 8 weeks of age and 20 fold normal at 10 months of age. In addition to decreased serum T3 and T4 levels, homozygotes have increased serum thyroid stimulating hormone levels, reduced levels of serum IGFBP-3, IGFBP-4, and IGFBP-2, mild anemia, and hypomyelination restricted to the cerebrum. Tgn^cog is an outwardly recessive mutation but microdissection reveals a heterozygous phenotype as well. Thyrofollicular cells of heterozygotes have swollen protein-containing vesicles similar to but more moderate than those found in homozygotes. ..... For more information please see the full phenotype on the strain data sheet
000579	STOCK a tp/J	Cryopreserved - Ready for recovery
	Taupe is a recessive spontaneous mutation that causes a lightening of the coat color such that a/a tp/tp mice are slate grey. The coat color is similar to that of the ruby (Hps5^ru) mutation but the eye color is not affected and the belly fur is lighter in color with yellow at the margins. The homozygous females do not have normal nipple development, although the mammary ducts and alveoli develop normally. These females also have difficulty with pregnancy and birth. They can not rear their pups even if the pups are born alive so this strain is maintained by breeding heterozygous females to homozygous males. (Fielder, 1952; Fielder, 1950.)
000317	STOCK a/a Egfr^wa2/J	Cryopreserved - Ready for recovery
	Mice homozygous mice for the waved 2 spontaneous mutation (Egfr^wa2) are recognizable at 2 to 3 days by curly whiskers. The first coat is waved but later coats are not; vibrissae usually remain curled and the guard hairs curved. Some homozygotes have eyelids open at birth. Fertile mutant females have impaired lactation.
000302	STOCK a/a Mitf^Mi-wh +/+ Itpr1^opt/J	Cryopreserved - Ready for recovery
	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 abnormalities of both the cochlear and vestibular portions of the inner ear. Mice homozygous for the opisthotonus spontaneous mutation (Itpr1^opt) display a characteristic upward arching of head and tail. Homozygous mutant mice can be recognized at about 10 days of age by their loss of balance when standing or moving. Typical behavior of 15 to 20 day old homozygotes consists of falling over and struggling to get up. Agitation and s ..... For more information please see the full phenotype on the strain data sheet
001788	STOCK Tg(Fabp1-GH1)10Bir/J	Cryopreserved - Ready for recovery

001400	STOCK Tg(Fabp1-GH1)5Bir/J	Cryopreserved - Ready for recovery

001515	STOCK Tg(Fabp1-GH1)7Bir/J	Cryopreserved - Ready for recovery

001878	STOCK Tg(IFABP-GH)11Bir/J	Cryopreserved - Ready for recovery

001879	STOCK Tg(IFABP-GH)12Bir/J	Cryopreserved - Ready for recovery

001909	STOCK Tg(IFABP-GH)15Bir/J	Cryopreserved - Ready for recovery
	Obligate hemizygous F1 offspring from founder 54 carried approximately 60 copies of the transgene in tandem head-to-tail arrangement in a single insertion site. Expression of the reporter gene, human growth hormone, is appropriately restricted to the intestine where the duodenum and proximal jejunum show expression levels normal for intestinal fatty acid binding protein, but the distal small intestine shows reduced expression. Resultant serum human growth hormone levels were 6-38 ng/ml which is approximately 1000 times lower than in mice carrying a transgene with an extended I-FABP promoter which includes nucleotides -1178 to +28. Use of the extended (-1178 to +28) promoter also results in a more normal expression in the distal small intestine. (Sweetser et al., 1988.)
005667	STOCK Tg(Neurog3-cre)C1Able/J	Cryopreserved - Ready for recovery
	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.
006395	STOCK Tg(Sim1-cre)1Lowl/J	Cryopreserved - Ready for recovery
	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. View cre expression characterization. Of note, Sim1-Cre mice may also available on a C57BL/6J congenic background (see Stock No. 006451).
005699	STOCK Tg(tetO-Ipf1,EGFP)956.6Macd/J	Cryopreserved - Ready for recovery
	Mice hemizygous for the transgene are viable, fertile, normal in size, and do not display any behavioral abnormalities. At the Jackson Laboratory, no homozygous mice were produced from mating hemizygotes together, suggesting that homozygous transgenic animals die in utero. Expression of the bicistronic transgene is under the regulation of a tetracycline promoter element (TRE; tetO). By themselves, these transgenic mice do not express EGFP, but when these mice are mated with a second transgenic strain expressing tetracycline-transactivator (tTA) protein under the control of a tissue-specific promoter, Ipf1 and EGFP are highly expressed in the appropriate tissue of bitransgenic offspring. This mouse was originally designed to be mated to an apancreatic targeted mutant with tTA_off in place of the endogenous Ipf1 gene (see Stock No. 005701). The combined mutations allow normal pancreatic dev ..... For more information please see the full phenotype on the strain data sheet
005728	STOCK Tg(tetO-Ipf1,lacZ)958.1Macd/J	Cryopreserved - Ready for recovery
	Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Expression of the bicistronic transgene is under the regulation of a tetracycline-responsive promoter element (TRE; tetO). When transgenic mice are bred to a second transgenic strain expressing tetracycline-transactivator (tTA) protein under the control of a tissue-specific promoter, the bitransgenic offspring express Ipf1 and lacZ in the appropriate target tissue. Further, Ipf1 and lacZ expression in bitransgenic mice can be suppressed by administration of the tetracycline analog, doxycycline. All cells expressing Ipf1 coexpress the reporter, and mRNA levels of the transgenic and endogenous Ipf1 fluctuate in concert during development. This mouse was designed originally to be mated to an pancreatic targeted mutant with tTA_off in place of the Ipf1 gene (see Stock No. For more information please see the full phenotype on the strain data sheet
000161	WB.D2-Kitl^Sl-d/J	Cryopreserved - Ready for recovery
	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 phenotype on the strain data sheet
002134	C57BL/6J-Mitf^mi-vit/J	Research Strain
	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.

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New Strains Awaiting Transfer from the Donor

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Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.
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Stock Number	Strain Name Strain Description	Standard Supply
017591	B6(SJL)-Tardbp^tm1.1Pcw/J	Awaiting Transfer from the Donor
These floxed mice possess loxP sites flanking exon 3 of the Tardbp gene. Deletion results in premature death due to increased fat metabolism and leanness associated with ALS.

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New Strains Awaiting Transfer from the Donor
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The Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion.
It is VERY IMPORTANT that you register interest in strains Awaiting Transfer. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.

Additional Register Interest Strains

Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.
View a Data sheet for a Strain
Select the strain name to link to the strain data sheet.

Stock Number	Strain Name Strain Description	Standard Supply
009109	B6.CBA-Tg(CAG-CYP27A1)23Etl/J	On Hold
These CYP27 overexpressor transgenic mice (or CYP27^overexp mice) have widespread expression of human cytochrome P450, family 27, subfamily A, polypeptide 1 directed by the CAG promoter. These mice may be useful in studying the conversion of cholesterol to bile acids (bile acid synthesis) by both the classical and alternate pathways, as well as lipid and cholesterol homeostasis research.
017588	B6.129X1-Cmah^tm1Avrk/J	In Progress
These CMAH KO mice may be useful for studying the hydroxylation of sialic acids required for protein/lipid synthesis and pancreatic beta cell function. In combination with other alleles, they may also have applications in studies realted to Duchenne muscular dystrophy.
017979	B6;129S-Hsd3b7^tm1Rus/J	In Progress
These Hsd3b7 knockout mice may be useful for studying cholesterol and bile acid biosynthesis and homeostasis.
017835	STOCK Brca1^tm1Aash/J	In Progress
The Brca1^{F22-24/F22-24} allele has loxP sites flanking exons 22-24 of the Brca1 gene. These mice may be useful in generating tissue-specific BRCA1 deletions for studying basal-like cancer and breast cancer.
017343	STOCK Slc19a3^tm1Said/J	In Progress
This THTR-2^- knockout mouse line has a deletion of exons 1-2 of the Slc19a3 gene. These mice may be useful in studying the role of thiamin transporters in regulating thiamin homeostasis in different cells; including liver and kidney cells.

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JAX® Mice Strains

New Strains Awaiting Transfer from the Donor

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