JAX Mice Database - Coisogenic

Search Criteria: Strain Type is "Coisogenic"

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
000058	B6(Cg)-Tyr^c-2J/J	Level 2
	Mice homozygous for Tyr^c-2J are phenotypically identical to homozygotes for the classic albino allele. Pigment is completely absent from skin, hair and eyes. While Tyr mRNA levels of Tyr^c-2J homozygotes are similar to those of wild-type mice, there is virtually no tyrosinase protein present (Le Fur et al. 1996). Both homozygote and heterozygote mice are highly resistant to light damage and exhibit retinal degeneration (increased photoreceptor death) into young adulthood. Degeneration does not continue in adult mice (Bravo-Nuevo et al. 2004).
000642	BKS.Cg-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
001801	C57BL/10ScSn-Dmd^mdx/J	Level 3
	The X-linked dystrophin gene (Dmd) is highly expressed in muscle cells and encodes a cytoskeletal protein which localizes to the inner face of the sarcolemma. Dystrophin molecules bind to cytoskeletal F-actin and transmembrane beta-dystroglycan as part of a complex, multimolecular unit that mediates signaling between the intracellular cytoskeleton and the extracellular matrix. The structure and localization also suggest that dystrophin is important for stabilizing the plasma membrane, particularly during contraction. The mdx mutation of Dmd is recessive and heterozygous females are visually indistinguishable from wild-type mice. Females homozygous and males hemizygous for the Dmd^mdx allele retain a normal lifespan and can survive up to two years. Like human patients who suffer from one of the most common neuromuscular diseases, Duchenne muscular dystrophy (DMD), the Dmd^mdx mutants do not express dystrophin and therefore have been ..... For more information please see the full phenotype on the strain data sheet
001162	B6(C)-H2-Ab1^bm12/KhEgJ	Level 4

004353	C57BL/6-Tg(UBC-GFP)30Scha/J	Level 4
	These transgenic mice express enhanced Green Fluorescent Protein (GFP) under the direction of the human ubiqutin C promoter. Mice homozygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mice express GFP in all tissues examined. Certain hematapoetic cell types display distinct expression levels of GFP, allowing identification of different cells types by FACS analysis. GFP expression is uniform within a cell type lineage and remains constant throughout development. T cells have a 2-fold higher GFP expression than CD19⁺B220⁺ B cells or peripheral blood cells. Leukocytes and red blood cells from homozygous mice fluoresce at approximately twice the level of cells from hemizygous mice. This mutant mouse strain represents a useful tool in studies related to hematopoetic cell differentiation and in vivo tracking of leukocytes.
002020	C57BL/6J-Apc^Min/J	Level 4
	The C57BL/6J-Apc^Min/J strain is highly susceptible to spontaneous intestinal adenoma formation. Homozygous mice are not viable. It was initially reported that one hundred percent of the C57BL/6J-Apc^Min heterozygous mice raised on a high fat diet develop in excess of 30 adenomas throughout the intestinal tract and most die by 120 days of age. Heterozygotes also develop anemia. (Moser et al., 1990, Su et al., 1992). A small number of C57BL/6J-Apc^Min heterozygous female mice develop mammary tumors. A subsequent publication indicates that this strain may carry a dominant modifier (Mom2) gene that reduces the number and incidence of polyp formation in C57BL/6J-Apc^Min heterozygous mice (Silverman et al., 2002).
008569	129-Alpl^tm1(cre)Nagy/J	Repository- Live
	This strain expresses Cre recombinase from the targeted locus. When crossed with a strain containing loxP site flanked sequence, Cre-mediated recombination results in tissue-specific deletion of the flanked sequence. Recombination occurs primarily in embryonic primordial germ cells. Approximately 60% of gonadal cells isolated from embryonic day 13.5 embryos exhibit Cre recombinase activity. Mosaic ectopic recombinase activity does occur. Homozygotes are not viable. This mutant mouse strain represents a model that may be useful in studies of reproductive and endocrine systems development.
006830	129-Dysf^tm1Kcam/J	Repository- Live
	Mice homozygous for this targeted mutation are viable, fertile and show a normal growth rate. Mice develop a slowly progressive muscular dystrophy. By the age of 2 months, a few individual necrotic and centrally nucleated fibers can be detected throughout the muscle; the number increases with age. By 8 months, the muscle develops all of the pathological characteristics of muscular dystrophy (e.g. regenerating fibers, split fibers, muscle necrosis with macrophage infiltration and fat replacement). The severity of the pathology varies in different muscles. Muscle fibers are defective in Ca²⁺-dependent sarcolemma resealing/repair. No protein product from the targeted gene is detected in skeletal muscle microsomes. This mutant mouse strain represents a model that may be useful in studies of muscle disease and repair.
013762	129-Nr1h3^tm1Djm/J	Repository- Live
	Homozygous Nr1h3 (nuclear receptor subfamily 1, group H, member 3) targeted mutation mice lose their ability to respond normally to dietary cholesterol. Mice maintained on cholesterol diets fail to induce transcription of the Cyp7a1 (cytochrome P450, family 7, subfamily a, polypeptide 1) gene, a rate-limiting enzyme in bile acid synthesis, and fail to induce expression of ABCG5 (ATP-binding cassette, sub-family G (WHITE), member 5) and ABCG8 (ATP-binding cassette, sub-family G (WHITE), member 8), ATP-binding cassette transporters that are required for cholesterol secretion into bile. Large amounts of cholesterol rapidly accumulate in the liver leading to impaired hepatic function. Impaired reverse cholesterol transport from peripheral tissues is also observed. The ability to regulate lipids and carbohydrates is also lost. Defects in innate immune responses by activated macrophages have also been described. Males are not infertile, but show a significantly higher number ..... For more information please see the full phenotype on the strain data sheet
016240	129-Plk1s1^tm1Cpl/J	Repository- Live
	These mice possess loxP sites on either side of exons 5 and 6 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 these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 5 and 6 deleted in the cre-expressing tissue(s). When bred to a strain with Cre recombinase expression in primordial germ cells (see Stock No. 008569 for example), this mutant mouse strain may be useful in studies of mammalian germ cell differentiation.
012771	129-Sirt7^tm1Fwa/J	Repository- Live
	This mutant mouse line has not been characterized.
014134	129/Sv-Maoa^K284stop Maob^tm1Shih/J	Repository- Live
	This strain carries two mutant alleles, a knockout of the X-linked monoamine oxidase B (Maob) gene and a spontaneous mutation designated Maoa^K284stop in the monoamine oxidase A (Maoa) gene. The two mutations lie 24kb apart. MAO A/B deficient mice are viable, fertile, and normal in size. Maoa and Maob are mitochondrial enzymes which oxidize neurotransmitters and dietary amines. These mutants lack both MAOA and MAOB activity in the brain and liver resulting in increased levels of phenylethylamine, serotonin, dopamine, and norepinephrine. These mice exhibit increased reactivity to stress and increased aggression. These mice may be useful for studying MAOA and MAOB-related behaviors and disorders.
014133	129/Sv-Maob^tm1Shih/J	Repository- Live
	In this strain, a neomycin resistance (neo) cassette replaces exon 6 of the endogenous X-linked monoamine oxidase B (Maob) gene, abolishing gene function. Maob deficient mice are viable, fertile, and normal in size. Maob is a mitochondrial enzyme which oxidizes neurotransmitters and dietary amines. These mutants lack MAOB activity in the brain and liver resulting in increased levels of phenylethylamine. These mice exhibit increased reactivity to stress and increased aggression. These mice also show decreased susceptibility to the neurodegenerative effects of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), which induces Parkinson's disease-like symptoms when administered to mice. These mice may be useful for studying neurodegeneration and MAOB-related behaviors.
013596	129S-Batf3^tm1Kmm/J	Repository- Live
	These Batf3^-/- knockout mice have a loxP-flanking neomycin (neo) resistance cassette replacing exons 1-2 of the basic leucine zipper transcription factor, ATF-like 3 (Batf3) gene, abolishing gene function. Mice that are homozygous for this allele are viable and fertile. Batf3 is highly expressed in CD11c⁺ CD8α⁺ conventional dendritic cells (cDCs), with low to absent expression in other immune cells.The deletion of Batf3 prevents development of splenic CD8α⁺ cDCs, which are important for cross-presentation during infections. Lymph nodes and thymi of Batf3^-/- mice lack CD8α⁺ DCs, and DCs generated from Batf3^-/- bone marrow (BM) and spleens are deficient in Toll-like receptor (TLR) 3-induced interleukin (IL)-12 production. These mice also lack CD103⁺CD11b^- DCs in the lung, intestine, mesenteric lymph nodes (MLNs), dermis, and skin-draini ..... For more information please see the full phenotype on the strain data sheet
013757	129S-Batf^tm1.1Kmm/J	Repository- Live
	These knockout mice lack exons 1-2 of the basic leucine zipper transcription factor(Batf), ATF-like gene, abolishing gene function. Mice that are homozygous for this allele are viable and fertile. Batf is highly expressed in T helper (T_H) 1, T_H2 and T_H17 cells. Batf is required for the differentiation of interleukin (IL)-17-producing T_H17 cells which are CD4⁺ T cells that coordinate inflammatory responses in host defense. These mice exhibit normal T_H1 and T_H2 differentiation, but show a defect in T_H17 differentiation with a reduction in IL-17 production, but maintain normal levels of IL-2, interferon (IFN)-γ, and IL-10 under T_H17 conditions. Since T_H17 cells are the major pathogenic population in experimental autoimmune encephalomyelitis (EAE), these Batf^-/- mice are completely resistant EAE even when immunized with myelin oligodendrocyt ..... For more information please see the full phenotype on the strain data sheet
013039	129S-Spic^tm1Kmm/J	Repository- Live
	In these mutant mice a loxP-flanked neomycin resistance (neo) cassette replaces exons 2-5 of the Spi-C transcription factor (Spi-1/PU.1 related) gene (Spic), abolishing gene function. Heterozygous mice are viable and fertile, while homozygotes are born at a frequency lower than the expected Mendelian ratio and they have small litters. Spi-C is highly expressed in red pulp macrophages which are a distinct splenic subset required for red blood cell recycling and iron homeostasis. These Spi-C^-/- mice exhibit a defect in the development of red pulp macrophages, which fail to efficiently phagocytose red blood cells trapped in the spleen. They also develop an iron overload localized selectively to splenic red pulp. These mice may be useful for studying the development and function of red pulp macrophages.
008396	129S-Top2b^tm2Jcw/J	Repository- Live
	These mice possess loxP sites flanking the 3 exons encoding the active-site tyrosyl residue 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 these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have the 3 exons deleted in the cre-expressing tissue(s). When bred to a strain expressing Cre recombinase during spermatogenesis (see Stock No. 003328 for example), this mutant mouse strain may be useful in studies of neural development. When bred to a strain expressing Cre recombinase in the telencephalon and discreet head structures (see Stock No. 004337, 006084 for example), this mutant mouse strain may be useful in studies of corticogenesis.
011120	129S-Wwtr1^tm1Benj/J	Repository- Live
	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.
007844	129S4/SvJae-Gt(ROSA)26Sor^tm2(FLP)Sor*/J	Repository- Live
	Homozygous ROSA26Flpo mice are viable and fertile, with widespread expression of the mouse codon-optimized FLP recombinase (FLPo) variant of the Saccharomyces cerevisiae FLP1 recombinase gene driven by the GT(ROSA)26Sor promoter. The GT(ROSA)26Sor promoter drives expression in a constitutive fashion from preimplantation onward. When bred with mice containing a FRT site flanked sequence of interest with the FRT sites in the same orientation, FLP-mediated recombination will result in deletion of the FRT-flanked sequence(s) in the offspring. Flpo exhibits enhanced recombinase activity compared to Flpe in vivo.
010977	129S4/SvJae-Pdgfrb^tm11Sor/J	Repository- Live
	These mice possess loxP sites on either side of the exons encoding the first and second immunoglobulin domain 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 these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have the exons encoding the first and second immunoglobulin domain deleted in the cre-expressing tissue(s). When bred to a strain with Cre recombinase expression in adrenal tissue (see Stock No. 006364 for example), this mutant mouse strain may be useful in studies of steroidogenesis.
013184	129S4/SvJaeSor-Mycl1^tm1.1Rne/J	Repository- Live
	These L-Myc^flox mutant mice possess loxP sites flanking all three exons v-myc myelocytomatosis viral oncogene homolog 1 (Mycl1) 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 these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have all three Mycl1 exons deleted in the cre-expressing tissue. The donating investigator states that this strain may be useful, in combination with other Myc knock-out models, for studying early embryonic growth and organogenesis of the brain, olfactory bulb, and lungs.
010608	129X1/SvJ-Gzma^tm1Ley Gzmb^tm2.1Ley/J	Repository- Live
	Mice that are homozygous for the targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Cytotoxic T lymphocytes (CTL) and natural killer (NK cells) derived from mutant mice exhibit a decrease in cytotoxic activity against allogenic and NK-sensitive targets. This mutant mouse strain may be useful in studies of cell-mediated cytotoxicity.
006859	129X1/SvJ-Lamc2^jeb/DcrJ	Repository- Live
	Mice that are heterozygous for this mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Northern blot analysis of skin from homozygotes detects the wildtype and a dominant larger sized mutant gene product (mRNA). Homozygotes express a reduced level of gene product (protein), as detected by Western blot analysis of keratinocytes. Mean onset of progressive skin blistering disease in homozygotes on the 129X1 background is age 154 days. Homozygotes exhibit ulcerated lesions and tissue granulation in ear skin, which develops into deformed pinna; ulcerated lesions in the footpads and tail. Thickened epidermis (hyperplasia) and subepidermal separation, with little to no inflammation, occurs in the skin of the footpads and tail. Ultrastructural analysis of skin with electron microscopy reveals that the dermal-epidermal separation occurs at the lamina lucida.
006246	A/J-sunk/GrsrJ	Repository- Live
	Mice homozygous for the sunken mutation are small and have severe kyphosis with the abdomen appearing sunken in.
008657	AKR/J-agil^2J/J	Repository- Live
	Homozygotes display an abnormal, wobbling gait by 2 weeks of age and are smaller than control littermates. At 3 weeks of age dystrophic axons and vacuoles are found in the spinal cord, white matter, cerebellar peduncles, and eighth cranial nerve root.
007750	B6(C)-Mir150^tm1Rsky/J	Repository- Live
	Mice homozygous for this targeted allele (miR150^-/- or MiR-150^-/-) are viable and fertile with normal development of T cells, follicular B cells, and MZ B cells. No miR-150 is expressed in spleen, mesenteric lymph node, and thymus of homozygotes. Homozygous mice exhibit B cell expansion (CD19⁺B220loCD5⁺CD43⁺CD23^-; B1a subset) in spleen and peritoneal cavity (with reciprocal reduction in B2 cells) and enhanced humoral immune response (increased serum immunoglobulins of various classes both at steady-state and following T cell-dependent antigen exposure). Homozygous miR-150 deficiency also leads to enhanced induction of the miR-150 target protein c-Myb in activated B and T cells, but no reported change in expression of the miR-150 target genes Foxp1 or ZFP91 in resting or activated B cells. These miR150^-/- mice may be useful in mircoRNA biology, specifically to study the role of miR-150 and its target genes (inc ..... For more information please see the full phenotype on the strain data sheet
013048	B6(Cg)-Etv1^{tm1.1(cre/ERT2)Zjh}/J	Repository- Live
	The ER81-CreER (or ER81-CreERT2, Etv1-CreER, Etv1-CreERT2) knock-in allele was designed to both abolish ets variant gene 1 (Etv1) gene function and expresses CreER^T2 fusion protein from the Etv1 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when ER81-CreERT2 mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Etv1-expressing cells of the offspring. Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Although mice homozygous for other null mutations of this gene on a similar genetic background exhibit neuromuscular abnormalities, ataxia and premature lethality, the donating investigator reports that ER81-CreER homozygous mice show no gross abnormalities. ER81 mRNA or protein expression fr ..... For more information please see the full phenotype on the strain data sheet
010633	B6(Cg)-Gt(ROSA)26Sor^{tm1(CAG-taulacZ)Bene}/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. A loxP-flanked neo cassette prevents transcription of the downstream tau- beta galactosidase (tauLacZ) gene. When bred to mice that express Cre recombinase, the resulting offspring will have the neo cassette deleted in the cre-expressing tissue(s); resulting in expression of taulacZ. Upon histochemical staining with X-gal, the tau beta galactosidase activity is revealed as an intense blue precipitate found in the entire cell, regardless of cell type. When tested with an olfactory sensory neuron specific cre-expressing strain, expression of lacZ labels axon projections. This mutant mouse strain may be useful as a cre reporter.
014175	B6(Cg)-Irf8^tm1.1Hm/J	Repository- Live
	These mice possess loxP sites on either side of exon 2, which encodes the DNA binding domain. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 deleted in the cre-expressing tissue(s). When bred to a strain with Cre recombinase expression in B lymphocytes (see Stock No. 006785 for example), this mutant mouse strain may be useful in studies of B cell differentiation
004742	B6(Cg)-Ncf1^m1J/J	Repository- Live
	Peritoneal neutrophils and macrophages, bone marrow cells and neutrophils isolated from bone marrow of mice homozygous for Ncf1^m1J fail to produce superoxide upon stimulation in vitro with N-formyl-methionyl-leucyl-phenylalanine (fMLP) or phorbol 12-myristate 13-acetate (PMA), as determined by kinetic spectrophotometric analysis of cytochrome c reduction. Western blot analysis detected no full-length NCF1/p47^phox protein in cells from these mice; a faint band of slightly smaller molecular size than the wild type NCF1 protein was observed on probing with antibodies to NCF1. To exclude the possibility that the NCF1 protein is produced in cells of mutant mice but is degraded rapidly by endogenous proteases, bone marrow cells were isolated and samples prepared for western blot analysis in the presence of diisopropyl fluorophosphate (DFP); no difference was observed upon analysis of freshly prepared cell lysates made with and without DFP, indicatin ..... For more information please see the full phenotype on the strain data sheet
008771	B6(Cg)-Rorc^tm3Litt/J	Repository- Live
	These mice possess loxP sites on either side of the exon 3-6 region of the targeted gene. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of orphan nuclear receptor RORgamma, including the RORgammaT thymus-specific isoform. Germline deletion of RORgamma and RORgammaT induces an abnormality in lymphoid organ development, survival of CD4⁺ CD8⁺ double positive thymocytes, and differentiation of Th17 helper T cells.
004684	B6.Cg Nos2^tm1Lau-chtl/GrsrJ	Repository- Live
	This mutant has an overall lighter coat, tail and ears than a black +/+ control. Both males and females breed and it is maintained as a homozygous stock.
013050	B6;129-Pink1^tm1Aub/J	Repository- Live
	These mice contain a mutation designed to replace gene function of the endogenous mouse Pink1 gene with the loss-of-function mutation, G309D, and a loxP-flanked neomycin resistance cassette (neo). Mice homozygous for Pink1^-/- are viable and fertile. Mice with this mutation carry the same loss-of-function mutation found in early-onset PARK6-linked Parkinson's disease (PD). Unlike other PD models, these mice lack peripheral paralysis, and exhibit normal motor performance, coordination, anxiety, and lifespan. They also lack lewy bodies and have reduced expression of α-synuclein mRNA. As these mice age they exhibit a progressive reduction of weight, a reduction of locomotor activity, and abnormal dopamine levels. These mice show increasing mitochondrial dysfunction resulting in impaired neural activity similar to PD, in absence of overt neuronal death.
012641	BALB/c-Tg(S100a4-cre)1Egn/YunkJ	Repository- Live
	These transgenic mice express Cre recombinase under the control of the mouse S100a4, S100 calcium binding protein A4, promoter. Cre recombinase expression is detected specifically in stromal fibroblasts of tissues such as the prostate, forestomach, mammary gland. Mice that are homozygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities.
001592	BALB/cByJ-Lpin1^fld/J	Repository- Live
	The original fld (fatty liver dystrophy) mutation arose spontaneously at The Jackson Laboratory in the Animal Resources BALB/cByJ colony in 1981, and was maintained by sibling mating for 47 generations, then backcrossed once in 2001 to a male BALB/cByJ via homozygous ovarian transplant, then sibling mating resumed. Homozygotes can be identified soon after birth by an enlarged, pale liver and smaller overall body size. Although the hepatic steatosis resolves to normal at wean age, a neurological phenotype manifests by day 14 as a tremor and an unsteady gait which is most pronounced in the rear legs (Sweet et al. 1988). Both phenotypes stem from improper cellular processing of lipid. fld/fld mice are smaller than their normal littermates by three days of age and remain smaller throughout life. Hair growth is retarded and abnormal resulting in a ruffled, unkempt appearance in the adult. Homozygotes experience increased mortality between 19 and 35 days of age. A ..... For more information please see the full phenotype on the strain data sheet
002169	BALB/cByJ-Mtap7^mshi/J	Repository- Live
	Mice homozygous for the male sterility and histoincompatibility spontaneous mutation (Mtap7^mshi) are characterized by reduced testis size and sterility. The testes are highly disorganized and appear to have a block in the regulation of male germ cell proliferation. Reproduction is normal in homozygous mutant female mice. In addition to the male reproductive defects this mutation also affects histocompatibility in both sexes. Most homozygous mutant mice reject sex-matched skin grafts from BALB/cBy mice.
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.
002167	BALB/cJ-Cst6^ichq/J	Repository- Live

012624	BALB/cJ-Pld4^thss/GrsrJ	Repository- Live
	Homozygotes are smaller than normal and the coat comes in sparse and fails to fill in even in the adult.
000029	BXD29-Tlr4^lps-2J/J	Repository- Live
	The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. This subline of BXD29/Ty is homozygous for the mutation defective lipopolysaccharide response 2 Jackson, which arose spontaneously in the parental strain. The non-mutant parental strain is available as stock number 010981.
006038	C3H/HeDiSn-Dscam^2J/GrsrJ	Repository- Live
	Mice homozygous for the Dscam^2J mutation can be identified as early as 2 days of age resting on their backs instead of their stomachs and struggling to maintain balance. They develop overt thoracic kyphosis and a domed skull and appear to walk on their toes. Homozygotes fail swim tests wherein they are unable to swim in a straight line, curl up their bodies, and sink to the bottom. However, they have normal auditory brain stem responses indicative of normal cochlear hair cell function and connectivity. Degeneration of spinal joints, dystrophic axons in the lumbar spinal cord and small areas of degenerating epaxial skeletal muscle are found in aging homozygotes. On this background, in the presence of the Pde6b^rd1 mutation, the inner nuclear layer and retinal ganglion layer are disorganized, a phenotype beyond the retinal degeneration inherent in the background. Additionally, the dopaminergic amacrine cells have fasciculated neurites and are orga ..... For more information please see the full phenotype on the strain data sheet
004626	C3H/HeDiSnJ-Vamp1^lew/GrsrJ	Repository- Live
	Mice homozygous for this recessive mutation are recognized by their wasting pre-weaning lethal phenotype, they curl up, waste away and die by 21 days. Mutants do not live to breed but no lesions have been found pathologically.
004780	C3H/HeJ-agil/GrsrJ	Repository- Live
	Mice homozygous for this recessive mutation are recognized by 15 days of age by their shaky, unsteady, wobbly gait. Mutants die around three weeks of age. The agitans-like mutation maps to Chromosome 14 between D14Mit39 and D14Mit115 which are near the neurological mouse mutation agitans (ag). The agitans mutants exhibit a similar phenotype.
004476	C3H/HeJ-snol/GrsrJ	Repository- Live
	The snol homozygous mutant phenotype includes a short nose, odd face and body shape, and kinked tail. Most mutants also get malocclusion and two homozygous mutants tested at 49 days of age exhibited intermediate hearing loss ( about 25 dB above normal). The odd shape of the face can be used to distinguish the Homozygotes by 14 days of age. snol has been mapped to Chromosome 4. The most likely gene order places the mutation between D4Mit12 and D4Mit203 in 92 tested meioses. A short nosed mutation, snubnose (sno), maps in this location, but could not be tested for allelism because it is believed to be extinct. The spina bifida occulta reported in sno homozygotes is not seen in snol homozygotes.
014132	C3H/HeOuJ-Maoa^{Tg(H2-K1-Ifnb1)8Seif}/J	Repository- Live
	These H2-IFNB transgenic mice have the murine interferon beta 1 (Ifnb1) coding sequence driven by a fragment of the murine histocompatibility 2, K1, K region (H2-K1) promoter. The transgene integrated into the X-linked monoamine oxidase A (Maoa) gene, replacing exons 2-3 and abolishing Maoa gene function. Hemizygous males and homozygous females are viable, and fertile until at least 6 months. MAOA is a mitochondrial enzyme that oxidizes monoamine neurotransmitters and dietary monoamines. These mutants lack MAOA activity resulting in increased levels of serotonin, dopamine, and norepinephrine. Excess serotonin in these mice causes abnormal development of certain neural circuits, such as in the barrelfield. During the first two postnatal weeks, these mice successively exhibit increased trembling and head nodding, frantic running and falling over. Adult males exhibit increased aggression towards subordinate males, male intruders, and females during ..... 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
009045	C57BL/6-Apc^tm1Tyj/J	Repository- Live
	Mice that are homozygous for the conditional allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The 15 coding exons are flanked by loxP sites. Germline heterozygous deletion of the floxed region results in a tumor-prone mouse similar to Apc^Min animals (see Stock No. 002020). Homozygous germline deletion mice are not viable. This mutant mouse strain is useful for studies of this tumor suppressor gene and serves as a mouse model of colon cancer.
008817	C57BL/6-Arg1^tm1Pmu/J	Repository- Live
	These mice possess loxP sites on either side of exons 7 and 8 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 these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 7 and 8 deleted in the cre-expressing tissue(s). When bred to a strain with inducible Cre recombinase expression in the myeloid cell lineages (see Stock No. 004781, for example) or endothelial cells (see Stock No. 004128 , for example), this mutant mouse strain may be useful in studies of immune response to bacterial and parasitic infections.
014096	C57BL/6-Ces1c^tm1.1Loc/J	Repository- Live
	These Es1^-/- knockout mice lack exon 5 of the carboxylesterase 1C (Ces1c or Es1) gene, abolishing gene function. Mice that are homozygous for this allele are viable, fertile, and normal in size. Carboxylesterases are expressed in the liver and are found in many tissues including the intestine, lung, and in the plasma of mice, but not in the plasma of humans. To mimic the lack of ES1 in human plasma and the resulting increase in susceptibility to nerve agents and to drugs that are hydrolyzed by ES1, these mice have had plasma ES1 activity eliminated. ES1 acts as an organophosphorus (OP) bioscavenger which reduces the level of OP reaching biologically relevant targets and protects against lethal toxicity from nerve agents. Es1^-/- mice have normal acetylcholinesterase (AChE), butyrylcholinesterase (BChE), and paraoxonase plasma activity, with normal levels of carboxylesterase activity in other tissues, including the brain, lungs, liver, ..... For more information please see the full phenotype on the strain data sheet
008374	C57BL/6-Foxp3^tm1Flv/J	Repository- Live
	Mice homozygous/hemizygous for this X-linked targeted knock-in are viable and fertile and do not display any gross physical or behavioral abnormalities. Cells expressing the forkhead box P3 gene are co-marked with monomeric red fluorescent protein (mRFP). RFP expression faithfully marks gene expression in lymphocytes. This strain may be helpful in studies of forkhead box P3-expressing regulatory T cells.
013174	C57BL/6-Grn^tm1Aidi/J	Repository- Live
	These Grn floxed mutant mice possess a single loxP site upstream of the promoter region of the granulin (Grn) gene, and a second loxP site fused to a FRT-flanked neomycin/kanamycin (neo/kan) resistance cassette downstream of exon 4. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 1- 4 deleted in cre-expressing tissues. When bred with mice expressing Cre-recombinase driven by the chicken actin gene promoter (CAG-cre), granulin deficiency is widespread (see Stock No. 013175). These mice exhibit neurodegeneration as seen in human frontotemporal dementia and have an exaggerated inflammation response when exposed to microbial agents. This floxed strain may be used to generate whole mouse or tissue-s ..... For more information please see the full phenotype on the strain data sheet
007900	C57BL/6-Gt(ROSA)26Sor^{tm1(HBEGF)Awai}/J	Repository- Live
	Mice homozygous for this iDTR mutation are viable and fertile. These mice have the simian Diphtheria Toxin Receptor (DTR; from simian Hbegf) inserted into the Gt(ROSA)26Sor (ROSA26) locus. Widespread expression of DTR is blocked by an upstream loxP-flanked STOP sequence. When bred to Cre recombinase-expressing mice, the STOP sequence is deleted in tissues where Cre is present, permitting DTR expression. Cells expressing DTR are rendered susceptible to ablation following Diphtheria toxin administration. For example, when bred to a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 006785), this mutant mouse strain may be useful in studies of lymphocyte cell ablation. When crossed to a strain expressing Cre recombinase in oocytes (see Stock No. 011062), this mutant mouse strain ma ..... For more information please see the full phenotype on the strain data sheet
008517	C57BL/6-Gt(ROSA)26Sor^{tm3(CAG-MIR17-92,-EGFP)Rsky}/J	Repository- Live
	Mice homozygous for the "miR-17-92 transgene" conditional allele are viable and fertile, with a loxP-flanked Neo-STOP cassette preventing transcription of the downstream bicistronic sequences (human miR-17-92 cluster (encoding the precursor of seven miRNA molecules; miR-17-5p, miR-17-3p, miR-18a, miR-19a, miR-20a, miR-19b and miR-92) and EGFP). When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissue(s); resulting in expression of the human miR-17-92 cluster. Because the synthetic CAG promoter driven miR-17-92 transgene was targeted for insertion into the Gt(ROSA)26Sor locus, expression of the transgene is determined by which tissue(s) express Cre recombinase. EGFP fluorescence, however, is not reported following exposure to Cre recombinase (presumably due to RNaseIII excision of the stem-loop structures encoding individual miRNA destabilizing the EGFP portion of the primary transcript ..... For more information please see the full phenotype on the strain data sheet
012343	C57BL/6-Gt(ROSA)26Sor^{tm7(Pik3ca,EGFP)Rsky}*/J	Repository- Live
	Mice homozygous for the R26Stop^FLP110* conditional allele (also called P110-transgene) are viable and fertile, with a loxP-flanked Neo-STOP cassette preventing transcription of the downstream bicistronic sequences (P110 [a constitutively active form of the mouse catalytic P110α subunit of phosphatidylinositol 3-kinase] and EGFP). When bred to mice that express Cre recombinase, offspring will have the STOP cassette deleted and subsequent expression of the P110* signal molecule and EGFP fluorescence in the cre-expressing cells. Expression of P110* leads to constitutively active PIK3 heterodimer activity; resulting in the generation of downstream effectors that mediate signal transduction cascades that control cell survival and cell cycle progression (growth, and proliferation). Of note, breeding these mice to an FLP-expressing strain will result in removal of the frt-flanked IRES-EGFP cassette.
012352	C57BL/6-Gt(ROSA)26Sor^{tm8(Map2k1,EGFP)Rsky}*/J	Repository- Live
	Mice homozygous for the R26Stop^FLMEK1DD conditional allele are viable and fertile, with a loxP-flanked Neo-STOP cassette preventing transcription of the downstream bicistronic sequences (MEK1DD [a mutant form of rat MAPKK1 rendered constitutively active by two serine->aspartic acid substitutions (S218D/S222D) within the catalytic domain] and EGFP). When bred to mice that express Cre recombinase, offspring will have the STOP cassette deleted and subsequent expression of the MEK1DD signal molecule and EGFP fluorescence in the cre-expressing cells. Expression of MEK1DD leads to constitutive activity of MAP Kinase signal transduction pathways that mediate various cellular activities, including gene expression, mitosis, differentiation, proliferation, cell survival, and cell cycle progression. Of note, breeding these mice to an FLP-expressing strain will result in removal of the frt-flanked IRES-EGFP cassette.
012361	C57BL/6-Gt(ROSA)26Sor^{tm9(Rac1,EGFP)Rsky}*/J	Repository- Live
	Mice homozygous for the R26Stop^FLRACDA conditional allele are viable and fertile, with a loxP-flanked Neo-STOP cassette preventing transcription of the downstream bicistronic sequences (RACDA [Rac^G12V; a mutant form of Rac1 rendered constitutively active by a glycine->valine substitution at amino acid 12] and EGFP). When bred to mice that express Cre recombinase, offspring will have the STOP cassette deleted and subsequent expression of the RACDA signal molecule and EGFP fluorescence in the cre-expressing cells. Expression of RACDA leads to constitutive activity of Rac1-dependent signal transduction; which is associated with gene expression, proliferation, cell survival, cell cycle progression, cytoskeletal reorganization, and Rho- and CDC42-pathways. Of note, breeding these mice to an FLP-expressing strain will result in removal of the frt-flanked IRES-EGFP cassette.
014148	C57BL/6-Itgal^tm1.1Mshi/J	Repository- Live
	This strain carries an I306A knock-in mutation of the Itgal (integrin alpha L; also known as Cd11a or LFA-1) gene. This mutation was shown to perturb lymphocyte de-adhesion that is part of circulating T cell homing/rolling to lymph nodes via endothelial venules. Homozygotes are viable and fertile and do not exhibit any gross abnormalities or developmental defects except for a smaller sized peripheral lymph nodes which contain fewer lymphocytes as compared to wildtype mice. Lymphocytes from these mice show reduced expression of ITGAL, but not other integrins. These mice may be useful in studies of integrin function.
009062	C57BL/6-Magel2^tm1Stw/J	Repository- Live
	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
014165	C57BL/6-Myo3a^tm1.1Mckg/J	Repository- Live
	These Myo3a^KI/KI mice contain the nonsense mutation TAT>TAG at codon 1041 of the myosin IIIA (Myo3a) gene. This mutation introduces a premature stop codon in exon 28, analogous to a Myo3a mutation found in humans with adult on-set hearing loss (DFNB30). Homozygotes are viable, fertile, and normal in size. DFNB30 is an inherited progressive hearing loss first identified in a Middle Eastern family, Family N. Myo3a is normally expressed in the vestibular hair cells of the inner ear. These mice exhibit significant hearing loss during the third month of life, beginning at high frequencies and eventually progressing to all frequencies. The inner and outer hair cells of these mice exhibit degeneration by 10 and 17 months of age, respectively, showing greater loss towards the base of the cochlea. These mice may be useful for studying adult on-set human hearing loss DFNB30.
014557	C57BL/6-Plau^tm1.1Bug/J	Repository- Live
	These mice carry 6 nucleotide substitutions in exon 4 that result in 4 amino acid substitution mutations (Y23N, R28N, R30H, and R31W) and abolish binding interaction of the protein with its receptor: plasminogen activator, urokinase receptor (uPAR). Homozygous mutant mice express a mutant urokinase plasminogen activator protein with a 400 fold reduction in affinity to the mouse urokinase plasminogen activator receptor and a binding affinity to human urokinase plasminogen activator receptor that is similar to endogenous human PLAU affinity. The mutant protein is functional, with homozygotes exhibiting normal skin wound healing. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The nucleotide substitutions were confirmed by sequence analysis. Levels of gene product (mRNA and protein) expression are normal as detected by qPCR or Western blot analysis. Homozygotes exhibit 2.5 fold ..... For more information please see the full phenotype on the strain data sheet
008309	C57BL/6-Rag2^tm1Cgn/J	Repository- Live
	Mice homozygous for the RAG-2^fl allele are viable and fertile, with loxP sites flanking exon 3 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (coding for the entire RAG-2 protein) deleted in the cre-expressing tissue(s). These RAG-2^fl mice may be useful in generating conditional mutations for studying the role of RAG-2 in B and T cell development (including cancer and toxicology research as a xenograft/transplant host), T and B cell receptor (V(D)J) recombination, hematopoiesis, hematology, immunology, and inflammation research. For example, when bred to a strain with inducible Cre recombinase expression in liver and lymphocytes (see Stock No. 003556), this mutant mouse strain may be useful in studies of B and T cell development.
009369	C57BL/6-Zbtb7b^tm1.1Litt/J	Repository- Live
	These mice possess loxP sites on either side of exons 2 and 3 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 crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the gene. Deletion in CD4⁺CD8⁺ thymocytes (through crosses to a Cd4-cre strain) or germline deletion (through EIIa-cre crosses; see Stock No. 003724) causes mice to lose helper T cells. This strain may be useful in studies of T cell lineage commitment.
006567	C57BL/6-Tg(CAG-EGFP)131Osb/LeySopJ	Repository- Live
	This transgenic mouse line with an "enhanced" GFP (EGFP) cDNA under the control of a chicken beta-actin promoter and cytomegalovirus enhancer makes all of the tissues, with the exception of erythrocytes and hair, appear green under excitation light. The viability of homozygous mice is unknown. Of note, it has been the experience at The Jackson Laboratory that Stock No. 006567 (C57BL/6-Tg(CAG-EGFP)131Osb/LeySopJ) demonstrates the highest proportion of GFP expressing cell populations in bone marrow, thymus, spleen and peripheral blood when compared to Stock No. 003291 (C57BL/6-Tg(CAG-EGFP)1Osb/J) and Stock No. 007075 (CByJ.B6-Tg(CAG-EGFP)1Osb/J). View the pdf document on GFP Expressing Lymphocyte Populations in C57BL/6-T ..... For more information please see the full phenotype on the strain data sheet
014176	C57BL/6-Tg(CLEC4C-HBEGF)956Cln/J	Repository- Live
	BDCA2-DTR transgenic mice have a simian diphtheria toxin receptor (DTR) under the transcriptional control a human C-type lectin domain family 4, member C (CLEC4C or BDCA2) promoter. Homozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mice express DTR specifically in plasmacytoid dendritic cells (pDCs). pDCs are bone marrow-derived leukocytes that respond to viral infection by secreting interferons and chemokines. This promotes resistance to viral infection and apoptosis of infected cells as well as recruitment and activation of natural killer (NK) cells, dendritic cells (DC), T cells, and B cells. After diphtheria toxin injection, 90% of pDCs are depleted in blood, spleen, liver, and lymph nodes. These mice may be useful for studying pDC function during the adaptive and innate immune responses to viral infection.
013760	C57BL/6-Tg(Camk2a-AIDPak)21Stl/J	Repository- Live
	dnPAK transgenic mice have a mouse calcium/calmodulin-dependent protein kinase II alpha (Camk2a) promoter directing postnatal forebrain expression of the mouse dominant negative (dn) autoinhibitory domain (AID) of p21 protein (Cdc42/Rac)-activated kinase (Pak) gene (dnPAK). The AID is conserved in all three Pak genes (Pak1, Pak2, Pak3). Homozygous dnPAK mice are viable, fertile, and normal in size. Pak genes are expressed in multiple brain regions, including the cortex and hippocampus, and are critical regulators of actin remodeling. The activation of PAK catalytic activity requires the release of the catalytic domain from the AID and autophosphorylation of a gene specific threonine residue. dnPAK binds to the catalytic domain of PAK and blocks autophosphorylation, inhibiting activation of catalytic activity. dnPAK overexpression causes a decrease in the number of and increase is the size of cortical neuron dendri ..... For more information please see the full phenotype on the strain data sheet
010712	C57BL/6-Tg(Camk2a-tTA)1Stl/J	Repository- Live
	When these transgenic mice are crossed with a tissue or cell-specific cre strain to remove a floxed stop cassette, tetracycline-controlled transactivator (tTA) is expressed in hippocampal CA3 and the dentate gyrus under the control of the calcium/calmodulin-dependent protein kinase II alpha (Camk2a) promoter. When further mated to a transgenic strain that carries a gene of interest driven by a tetracycline-responsive promoter element (TRE; tetO), expression of that gene can be conditionally regulated by the presence or absence of doxycycline in the drinking water. Expression in tTA/tetO animals can be reversibly inhibited by the presence of doxycycline or induced by withdrawal of the tetracycline analog.
016097	C57BL/6-Tg(Car1-cre)5Flt/J	Repository- Live
	These transgenic mice express Cre recombinase under the control of the mouse Car1, carbonic anhydrase 1, promoter. Transgenic transcript is detected in the tissues of the large intestine (cecum, proxmial and distal colon) by RT-PCR. Low levels of transcript are detected in the liver, and no transgene transcript is detected in kidney, stomach, bone marrow, prostate, lung, thymus, liver hear, duodenum, jejunum, ileum, pancreas, spleen. Mosaic recombinase activity is detected as early as 14.5 dpc in approximately 15% of the epithelial cells of the large intestine and is observed in individual crypts from the base to lumen. When crossed with a strain containing loxP site-flanked sequences, cre-mediated recombination results in large intestine epithelial-specific deletion of the flanked sequences in the offspring. Mice that are homozygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities.
011086	C57BL/6-Tg(Cck-cre)CKres/J	Repository- Live
	A minimal Cck (cholecystokinin) promoter drives expression of Cre in this transgenic strain. These mice express Cre at high levels in the brain cortex in a pattern that is qualitatively similar to that of the wildtype Cck gene. There is virtually no expression in subcortical regions. Although a component of the transgene, DsRed2 is not expressed. This strain may be useful for various psychiatric and neuroscience studies of this neuropeptide promoter.
014639	C57BL/6-Tg(Cd4-TcraDN32D3)1Aben/J	Repository- Live
	Vα14-Jα18 transgenic mice contain CD4 promoter/enhancer elements driving expression of prearranged Vα14-Jα18 T cell receptor (TCR) cDNA from hybridoma line DN32.D3. Hemizygous mice are viable and fertile. These mice overexpress Natural Killer T (NKT) cells, or Vα14 NKT cells, in the liver, thymus, spleen, and lymph nodes. These mice may be useful for studying positive/negative selection, T cell receptor interactions, and NKT cell function.
014644	C57BL/6-Tg(Cd4-Zbtb16)1797Aben/J	Repository- Live
	CD4-PLZF transgenic mice contain CD4 promoter/enhancer elements driving expression of the zinc finger and BTB domain containing 16 (Zbtb16 or PLZF) cDNA from purified natural killer T (NKT cells). Hemizygous mice are viable and fertile. PLZF is a transcriptional regulator that is expressed in NKT cells and is required for their maturation into effector-type lymphocytes. Transgenic expression of PLZF using the CD4 promoter induces conventional CD4 T cells to acquire effector characteristics. While CD4 T cells are present at normal levels in the thymus, spleen, liver, and lungs of the CD4-PLZF mouse, they are nearly absent in the blood and lymph nodes. Greater than 98% of mature CD4 T cells display a CD44^hi/CD62L^lo effector phenotype. An increased percentage of CD4 T cells produce both interleukin-4 (IL-4) and interferon (IFN) γ upon TCR stimulation. These mice may be useful for studying the function of PLZ ..... For more information please see the full phenotype on the strain data sheet
008766	C57BL/6-Tg(Cd8a-cre)1Itan/J	Repository- Live
	Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre activity is observed in peripheral CD8⁺ T cells (CD8 α⁺CD8β⁺ αβT cells and CD8α⁺CD8β^- αβT cells, but not in CD4⁺CD8α^-CD8β^- αβT cells). When bred with a mouse containing a loxP site-flanked sequence of interest, Cre-mediated recombination results in deletion of the flanked genome in cells that normally express Cd8a.
016133	C57BL/6-Tg(Defa2-Myd88)1Lvh/J	Repository- Live
	The mouse Defa2 (defensin, alpha, 2; also known as cryptdin 2 or CR2) promoter directs expression of FLAG-tagged Myd88 (myeloid differentiation primary response gene 88) to the Paneth cells of the small intestine in this transgenic strain. Hemizygotes are viable and fertile and do not display any gross physical or behavioral abnormalities. Anti-FLAG antibodies may be used for immunohistochemical analysis. This strain may be useful in studies of microbial/immune system interactions and antimicrobial transcriptional responses at the intestinal epithelial barrier.
006474	C57BL/6-Tg(Grik4-cre)G32-4Stl/J	Repository- Live
	Mice hemizygous for this "G32-4" transgene are viable, fertile, and do not display any gross physical or behavioral abnormalities. Transgene expression (cre activity) is detectable at 14 days old in area CA3 of the hippocampus, and at 8 weeks of age, recombination is observed in nearly 100% of pyramidal cells in area CA3. Recombination is also observed in other brain areas, but at distinctly lower frequencies. If bred with mice containing a loxP-flanked sequence of interest, tissue-specific deletion of that sequence results in the offspring. Specifically, when these mice were bred with a conditional CaMKII allele (see Stock No. 006575), the resulting offspring exhibited altered neurotransmitter release. The donating investigator reports that G32-4 females may confer global Cre-mediated deletion of loxP-flanked sequences in some offspring, and recommend using male G32-4 mice exclusively for such trials. These C ..... For more information please see the full phenotype on the strain data sheet
011005	C57BL/6-Tg(H2-K^b-Tcra,-Tcrb)P25Ktk/J	Repository- Live
	These P25 TCR-Tg mice contain CD4 + T cells expressing a transgenic T-cell antigen receptor that recognizes peptide 25 (aa 240-254) of Mycobacterium tuberculosis Antigen 85B bound to I-Ab. Homozygotes are viable, fertile, and normal in size. These transgenic mice, with T cell response specific to M. tuberculosis infection, may be useful for studying the process of the adaptive immune response to M. tuberculosis infection in the lungs. These mice exhibit an immune response that is not dependant on bacteria number in the tissue, but rather on movement of bacterium into the draining nodes of the lungs.
012943	C57BL/6-Tg(Ins2-luc/EGFP/TK)300Kauf/J	Repository- Live
	C57BL/6J mice carrying tri-fusion transgene Ins2-luc/EGFP/Tk, commonly called MIP-TF, line 300 express a luciferase/enhanced green florescent protein/thymidine kinase fusion protein (luc/EGFP/Tk) under the control of mouse insulin promoter (Ins2) and are viable, fertile and exhibit no gross physical or behavioral abnormalities. Transgene expression, determined by luciferase enzymatic activity and green florescence is exclusive to the pancreas, specifically the insulin producing cells. Transgene expression appears to have no effect on weight, islet morphology, fasting blood glucose, or response to glucose challenge when compared to wild-type controls. This trifusion reporter model should enable longitudinal noninvasive imaging of beta cells in the same animal by cooled charge coupled device (CCD) and micro positron emission tomography (microPET), and identification of beta cells at the cellular level by florescent microscopy. There is a correlation between CCD and microPET signals fr ..... For more information please see the full phenotype on the strain data sheet
012906	C57BL/6-Tg(Nes-cre/Esr1*)1Kuan/J	Repository- Live
	Mice homozygous for the nestin-CreER transgene are viable and fertile, with the rat nestin enhancer/hsp68 minimal promoter directing expression of a tamoxifen-inducible Cre recombinase (Cre-ER^T1). This Cre-ERT1 fusion protein is estrogen insensitive, and is only active when it binds the estrogen analog 4-hydroxytamoxifen (OHT or tamoxifen). Following tamoxifen administration, Cre recombinase activity is reported in adult neural progenitors in the subventricular zone (SVZ), perinatal SVZ glioblasts, embryonic neural progenitors, and postnatally transformed radial glial cells. When these nestin-CreER transgenic mice are bred with mice containing a loxP-flanked sequence, tamoxifen-inducible Cre-mediated recombination is expected to result in deletion of the floxed sequences in the Cre recombinase-expressing tissues of the offspring. These mice may be useful for studying embryonic and adult neurogenesis. The Cre-ERT1 fusion protein consists of Cre recombinase f ..... For more information please see the full phenotype on the strain data sheet
008831	C57BL/6-Tg(Neurod2-Smo*A1)199Jols/J	Repository- Live
	These Smo/Smo transgenic mice express the constitutively active point mutation, SmoA1, of the mouse smoothened homolog (Drosophila) (Smo) gene, under the control of the 1kb mouse neurogenic differentiation 2 (Neurod2) promoter. Transgene expression is specific to cerebellar granule cells, as observed by His tag staining. Subclinical tumor incidence in mice homozygous for the transgene is 85% by one month of age and 94% by two months of age, with an average age of onset of clinical tumor symptoms at four months. Symptoms associated with advanced tumors include enlarged posterior fossa, and/or tilted head, and hunched posture. Weight loss and an ungroomed appearance are also common. The disease progresses to leptomeningeal metastasis of the brain and spine. Once clinical symptoms are noted, survival is one to two weeks. This mutant mouse strain may be useful in studies of medulloblastoma and metastasis.
013148	C57BL/6-Tg(Pdgfra-cre)1Clc/J	Repository- Live
	Hemizygous Pdgfra-cre mice are viable and fertile, with cre expression directed to retinal Muller glial cells by the mouse Pdgfra (platelet derived growth factor receptor, alpha polypeptide) promoter. Expression is predominantly in the cell bodies of the inner nuclear layer (INL) of the retina, but some expression may be observed in the outer nuclear layer (ONL) and in the ganglion cell layer (GCL). The donating investigator indicates that although not examined, cre may also be active in many types of central nervous system glial cells. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in the offspring.
008535	C57BL/6-Tg(Pf4-cre)Q3Rsko/J	Repository- Live
	These transgenic mice express a codon-improved Cre recombinase (iCre) under the control of the mouse Pf4 (platelet factor 4), or Cxcl4, promoter. Cre recombinase expression is detected in the majority of megakaryocytes. Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The BAC clone used to generate this strain also contains 4 other genes: Cxcl5, Cxcl7, Cxcl15 and Cxcl3. The additional copy of these chemokine genes in the BAC has no effect on blood count of the mutant mice. This strain represents an effective tool for generating megakaryocyte lineage-restricted specific-targeted mutants.
003135	C57BL/6-Tg(TRAMP)8247Ng/J	Repository- Live
	These mice harbor the Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP); PB-Tag Line 8247 transgene. Mice hemizygous for the TRAMP transgene develop progressive forms of prostate cancer with distant site metastasis and exhibit various forms of disease from mild intraepithelial hyperplasia to large multinodular malignant neoplasia. TRAMP hemizygotes can exhibit prostatic epithelial neoplasia (PIN) by 12 weeks of age. Tumors, appearing as well differentiated adenocarcinoma, can arise by 24 weeks of age, mostly in the dorsal and lateral lobes of the prostate. By 30 weeks of age, most hemizygous mice will display evidence of metastatic spread to the lymph nodes and/or lungs, phylloides appearance of some tumors, and seminal vesicle invasion. Tumors exhibit elevated levels of nuclear TRP53 and decreased androgen receptor expression. Note that pure C57BL/6 TRAMP hemizygotes may live to 52 weeks of age or longer. TRAMP mice are also available on a mixed C57BL/6 x FVB/N genet ..... For more information please see the full phenotype on the strain data sheet
006912	C57BL/6-Tg(Tcra2D2,Tcrb2D2)1Kuch/J	Repository- Live
	Mice hemizygous for this "2D2 TCR" (or MOG 35-55 specific TCR) transgene are viable and fertile. The myelin oligodendrocyte glycoprotein (MOG)-specific transgenic T cells are not deleted nor tolerized and are functionally competent. The majority of thymocytes in 2D2 TCR mice express high and intermediate levels of the transgenic T cell receptor (TCR), indicating efficient positive selection of transgenic T cells. The majority of CD4⁺ splenocytes express the transgenic TCR (as defined by Valpha3.2 and Vbeta11 expression). Cultured splenocytes are responsive to whole myelin oligodendrocyte glycoprotein (MOG) and to MOG 35-55 peptide, but not to ovalbumin (OVA) control peptides. From between 2.5 to 5 months of age, 4% of 2D2 TCR mice develop spontaneous experimental autoimmune encephalomyelitis (EAE), while within the first year 40% of 2D2 TCR mice develop spontaneous, isolated optic neuritis with neither clinical nor histological evidence of EAE. Standard EAE induction protoco ..... For more information please see the full phenotype on the strain data sheet
012769	C57BL/6-Tg(Thy1-Sncg)HvP36Putt/J	Repository- Live
	Thy1mγSN transgenic mice have the mouse thymus cell antigen 1 (Thy-1) promoter directing expression of the mouse γ-synuclein (Sncg) gene. Homozygous Thy1mγSN mice are viable, fertile, and normal in size. They develop a clasping reflex, abnormal posture and gait, and other symptoms of motor dysfunction around 6 months of age, develop limb paralysis by 9 months of age, and die by 16 months of age. Homozygotes also show a 7-fold increase of γ-synuclein mRNA in neurons compared with wild-type mice, leading to motor neuron impairment and premature death. Hemizygous mice develop this phenotype starting at 12 months of age. γ-synuclein aggregates form fibrils, much like α-synuclein, aggregates of which have been associated with neurodegeneration in diseases such as Parkinson's disease. These mice may be useful for studying the pathophysiology of Parkinson's disease, and other neurodegenerative disorders.
013729	C57BL/6-Tg(tetO-EDN1,-lacZ)9Mhus/J	Repository- Live
	These ET⁺ transgenic mice express the human endothelin (EDN1 or ET-1) gene and a β-galactosidase (lacZ) reporter, both regulated by the bidirectional tetracycline operator, tetO. Homozygous mice are viable, fertile, and normal in size. ET-1 is a vasoconstrictor expressed in endothelial cells, and is a key mediator in vascular tone and renal homeostatsis. When mated to a mutant strain expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), LacZ and ET-1 expression may be regulated with the tetracycline analog doxycycline (DOX) in the double mutant offspring. When bred to a strain expressing tTA driven by α-myosin heavy chain (α-MHC) cardiomyocyte specific (see Stock No. 003170) overexpression of lacZ and ET-1 results in left ventricular dilation, contractile dysfunction, ca ..... For more information please see the full phenotype on the strain data sheet
010713	C57BL/6-Tg(tetO-GFP/tetX)5696Stl/J	Repository- Live
	These transgenic mice express tetanus toxin (tetX) under the control of a tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator), and may be useful in generating bi-transgenic mutant mice for the reversible, inducible inhibition of synaptic transmission. Although GFP is fused to tetX, fluorescence may not be detectable.
013728	C57BL/6-Tg(tetO-NOS2,-lacZ)240iMhus/J	Repository- Live
	These iNOSβgal transgenic mice express the human nitric oxide synthase 2, inducible (NOS2 or iNOS) gene and a β-galactosidase (lacZ) reporter, both regulated by the bidirectional tetracycline operator, tetO. Homozygous mice are viable, fertile, and normal in size. NOS isoforms reduce molecular oxygen to superoxide, reactive oxygen species, and reactive nitrogen species (all of which can cause cellular toxicity and tissue damage). When mated to a mutant strain expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), LacZ and iNOS expression may be regulated with the tetracycline analog doxycycline (DOX) in the double mutant offspring. When bred to a strain expressing tTA driven by α-myosin heavy chain (α-MHC), cardiomyocyte specific overexpression of lacZ and iNOS result in embryonic lethality, cardiac enlargement, cardiomyopathy, bradyarrhythmia, and sudd ..... For more information please see the full phenotype on the strain data sheet
016181	C57BL/6-Tg(tetO-Nr1d1)1Schb/J	Repository- Live
	These transgenic mice express hemagglutinin-tagged Nr1d1 (nuclear receptor subfamily 1, group D, member 1) cDNA under the control of a tetracycline-responsive element (TRE; tetO)/minimal cytomegalovirus (CMV) promoter. When hemizygotes are bred with another transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled tranactivator protein (tTA) under the regulation of tissue-specific promoters, transgene expression can be conditionally regulated with doxycycline.
005349	C57BL/6J Tyr^c-2J-awag/GrsrJ	Repository- Live
	awag homozygotes have a distinct tremor when walking. When lifted by the tail these mutant mice do not splay their hind legs out as normal mice do, but instead hold their legs in a bowlegged umbrella manner and arch their backs. Both sexes breed and live a normal life span.
009157	C57BL/6J-Ank1^pale/GrsrJ	Repository- Live
	Pale lethal homozygotes are smaller than normal littermates, have a pale light grey skin color, evident at birth, and most die by one week of age, although some have survived to 3 or 4 weeks of age. Some prenatal lethality is implied by the fact that heterozygous crosses yield fewer than 25% homozygotes.
006926	C57BL/6J-Egfr^Vel/J	Repository- Live
	Mice homozygous for this mutation have an embryonic lethal phenotype, failing to develop past embryonic days 13.5. Heterozygous mice are viable, fertile, do not display any behavioral abnormalities and are born with open eyelids and curly vibrissae. Adult heterozygotes often have small eyes and corneal opacity with excessive secretions at the eyelid edges. MEFs (mouse embryonic fibroblasts) exhibit reduced migratory ability, approximately 53% of wildtype controls. Histological analysis of homozygous E12.5 embryos reveals placental defects. This mutant mouse strain may be useful in studies of development and as a visible dominant marker for the Egfr allelic series.
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.
017307	C57BL/6J-Krt71^Ca-17J/GrsrJ	Repository- Live
	As with other caracul mutants, heterozygotes have a very wavy coat and curved vibrissae. The mutation can be detected when the coat first comes in at about 7 to 8 days of age, is easily recognized at 3 weeks of age, and remains ruffled throughout life but is less wavy with age.
005061	C57BL/6J-Ldlr^Hlb301/J	Repository- Live
	Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This single base pair G to A transition mutation in exon 14, nucleotide 2096 was induced by ENU mutagenesis. The "Wicked High Cholesterol" (WHC) phenotype was mapped to the Ldlr, low density lipoprotein receptor, gene. Although total plasma cholesterol levels do not differ between sexes, when fed a standard chow diet for 5 weeks, homozygous WHC males exhibit higher triglyceride and HDL levels than homozygous WHC females. When fed Western diet for 5 weeks, mutant WHC males exhibit higher HDL levels than female WHC mutants. When fed an atherogenic diet for 5 weeks, WHC homozygotes of both sexes develop elevated total cholesterol levels of more than a 4 fold increase when compared to WHC homozygotes on standard chow diet. Cholesterol and HDL levels of WHC homozygotes fed atherogenic diet for 5 weeks remain elevated 1 month after resum ..... For more information please see the full phenotype on the strain data sheet
000629	C57BL/6J-Lyst^bg-J/J	Repository- Live
	Mice homozygous for the beige-J spontaneous mutation (Lyst^bg-J) are identical to the original beige mutation (Lyst^bg). The phenotype closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syn ..... For more information please see the full phenotype on the strain data sheet
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
005544	C57BL/6J-Robo3^m1J/GrsrJ	Repository- Live
	Homozygotes display impaired balance by wean age. They lean to one side and have difficulty maintaining an upright position, but are fertile and premature death has not been noted. This is a less severe phenotype than that of targeted null mice.
014106	C57BL/6J-bc^8J/GrsrJ	Repository- Live

014105	C57BL/6J-bc^9J/GrsrJ	Repository- Live

004246	C57BL/6J-sbse/J	Repository- Live

006481	C57BL/6J-Tg(ACTB-NOTCH1)1Shn/J	Repository- Live
	Transgenic mice are viable, fertile and behaviorally normal. These "CALSL-NICD (H)" mice (or simply CALSL-NICD) reportedly carry 10-20 copies of the transgene inserted into a single genomic locus. Expression of the transgene-derived intracellular domain of human NOTCH1 is prevented by a "Lox-STOP-Lox" cassette. When transgenic mice are bred to a strain expressing Cre recombinase, the "floxed stop" cassette is excised in the resulting offspring, and human NOTCH1 expression is observed in the cre-expressing tissue(s). These transgenic mice may be useful in studying early neural progenitor cell development and apoptosis, and responses to tissue-specific Notch activation. For example, when crossed to a strain expressing Cre recombinase in the nervous system (see Stock No. 003771), this transgenic mouse strain may be useful in studies of notch signaling during apoptotic cell death.
009655	C57BL/6J-Tg(Dcx-DsRed)14Qlu/J	Repository- Live
	These transgenic mice express red fluorescent protein variant (DsRed-Express) under the direction of the mouse doublecortin promoter. Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Fluorescence is first detected at embryonic day 11.5. By embryonic day 13.5 fluorescence is restricted to the CNS and mimics the endogenous doublecortin expression pattern. This mutant mouse strain may be useful in studies of neural development and visualization of developing neurons.
007567	C57BL/6J-Tg(Itgax-cre,-EGFP)4097Ach/J	Repository- Live
	Mice hemizygous for this CD11c-Cre-GFP transgene are viable and fertile. The CD11c (Itgax) promoter directs bicistronic Cre and EGFP protein expression to dendritic cells (DCs). Expression of EGFP is expected to have equimolar expression with Cre recombinase. When bred with any mouse containing a loxP-flanked sequence of interest, the resulting offspring can have Cre-mediated recombination of the flanked sequence. These CD11c-Cre-GFP transgenic mice (as well as CD11c-Cre transgenic mice (see Stock No. 008068)) may be useful for immunological studies utilizing Cre-lox technology or fluorescent protein expression in dendritic cells.
008661	C57BL/6J-Tg(Nkx2-1-cre)2Sand/J	Repository- Live
	Mice homozygous for the Nkx2.1Cre (or BAC-Nkx2.1-Cre) transgene are viable and fertile, with cre expression directed to major subgroups of brain interneuron progenitors, developing lung, thyroid, and pituitary by the Nkx2.1 promoter/enhancer regions within the BAC transgene. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in the offspring. For example, when bred with beta-galactosidase reporter mice, the first detectable Cre recombinase expression in double mutant offspring is observed on embryonic day (E)10.5 in the basal telencephalon. These Nkx2.1Cre (or BAC-Nkx2.1-Cre) transgenic mice may be useful for generating conditional mutations for studying gain or loss of function and/or fate mapping in subgroups of brain progenitors (including future major interneurons in telencephalon and hypothalamus cells), as well as developing lung, thyroid, and pituitary.
009593	C57BL/6J-Tg(Pomc-EGFP)1Low/J	Repository- Live
	Mice hemizygous for this POMC-EGFP transgene are viable and fertile, with EGFP expression directed to POMC-expressing neurons by the mouse Pomc (pro-opiomelanocortin-alpha) promoter/enhancer regions. The donating investigator reports that transcripts from the transgene encode EGFP but do not express any POMC prohormone or peptides. Direct EGFP fluorescence is observed in the arcuate nucleus of the hypothalamus (ARC), in melanotrophs/corticotrophs of the pituitary gland, and (unlike other POMC promoter-driven fluorescent mice) in a subpopulation of newly born granule neurons of the dentate gyrus of the hippocampus. EGFP expression is also observed in the nucleus of the solitary tract of the medulla. EGFP expression is downregulated as neurons mature and migrate deeper into the granule cell layer. These POMC-EGFP mice may be useful in studying neuronal signaling pathways, energy metabolism, leptin activity, obesity, seizures, depression, and epilepsy.
008239	C57BL/6J-Tg(Th-SNCAA30PA53T)39Eric/J	Repository- Live
	These hm²α-SYN-39 mice express a doubly-mutant form of human alpha-synuclein (hα-SYN) containing the A30P and A53T human mutations associated with autosomal dominant Parkinson's disease, under the control of the rat tyrosine hydroxylase promoter. Expression of hα-SYN is detected in cell bodies, axons, and terminals of the nigrostriatal system (mRNA expression in midbrain, eye, and adrenal gland, with high levels of protein expression in the cell bodies of dopaminergic neurons in the midbrain and striatum). Hemizygous mice exhibit several Parkinson's disease-related characteristics including increased density of the dopamine transporter, impairments of the ubiquitin-proteasome system, and age-related progressive loss of locomotor activity and substantia nigra pars compacta dopaminergic neurons. The Parkinson's disease-related phenotype of hm²α-SYN-39 mice is more severe than that of the control strain (hwα-SYN-5, see Stock No. > ..... For more information please see the full phenotype on the strain data sheet
002356	C57BL/6J-Tg(pPGKneobpA)3Ems/J	Repository- Live
	Homozygous neo^R transgenic mice (TgN3Ems) are viable and fertile with no apparent gross phenotype. The pPGKneobpA transgene has the mouse Pgk1 promoter directing widespread (but not necessarily uniform) expression of neo^R: this renders TgN3Ems mice highly G418-resistant and results in a 5-fold increase in the approximate lethal dose of G418 (~480 mg/kg) compared to wildtype mice (~103 mg/kg). Treatment with G418 lethal dose (or higher) in transgenic mice leads to rapid onset of decreased movement, respiratory arrest, and death within minutes. Compared to wildtype mouse embryonic fibroblasts (MEFs), TgN3Ems MEFs exhibit greatly diminished G418 sensitivity: wildtype MEFs show essentially no resistance to G418 while TgN3Ems MEFs survive approximately 20-fold higher G418 levels. Importantly, TgN3Ems heterozygotes and TgN3Ems homozygotes are equally resistant to G418. These TgN3Ems transgenic mice may be useful as source of G418-resistant feeder cells for ge ..... For more information please see the full phenotype on the strain data sheet
012441	C57BL/6J-Tg(tetO-LRRK2*G2019S)E3Cai/J	Repository- Live
	Mice hemizygous for the human leucine-rich repeat kinase 2 mutant transgene, (LRRK2G2019S), are viable and fertile. Expression of LRRK2G2019S is regulated by a tetracycline operator (tetO); also called tetracycline-responsive element (TRE, TetRE) or tet-operator). When mated to a mutant strain expressing tetracycline-controlled transactivator protein (tTA), expression of LRRK2G2019S protein may be regulated with tetracycline or its analog doxycycline (dox) in the double mutant offspring. LRRK2 protein, also known as Dardarin, contains multiple functional domains and may function as both an active GTPase and kinase. LRRK2 may regulate alpha-synuclein-mediated neuropathology through modulating the intracellular trafficking and accumulation of SNCA protein. The amino acid mutation in the kinase domain of LRRK2* may decrease proteasomal degradation of LRRK2. These mice may be useful for studying Parkinson's disease pathogenesis and neurodegenerati ..... For more information please see the full phenotype on the strain data sheet
012450	C57BL/6J-Tg(tetO-SNCA)1Cai/J	Repository- Live
	Mice hemizygous for the human synuclein (alpha-syn) transgene, (SNCA) are viable and fertile. Expression of the transgene is regulated by the tetracycline operator (tetO); also called tetracycline-responsive element (TRE, TetRE) or tet-operator). When mated to a strain expressing tetracycline-controlled transactivator protein (tTA), expression of the SNCA protein may be regulated with tetracycline or its analog doxycycline (dox) in the double mutant offspring. The formation of alpha-syn aggregates is a key step in the pathogenesis of Parkinson's disease. These aggregates cause formation of fibrillar aggregates causing various forms of cytotoxicity, including impairment of proteasomal and lysosomal activities, disruption of ER-Golgi traffic and microtubule-based transport, and dysfunction of mitochondria. SNCA mice develop age-dependent, progressive neurodegeneration. These mice may be useful for studying the Parkinson's disease pathogenesis and n ..... For more information please see the full phenotype on the strain data sheet
016211	C57BL/6N-Agtr1a^tm1Uky/J	Repository- Live
	These AT1a^flox mutant mice possess a loxP site upstream of exon 3 followed by a neomycin resistance (neo) cassette flanked by frt sites and loxP sites downstream of exon 3 of the angiotensin II receptor, type 1a (Agtr1a) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. AGTR1A is expressed in vascular cells such as endothelial cells, smooth muscle cells, and macrophages. Angiotensin II (Ang II) is a vasoconstrictor which, upon binding to AGTR1A, can induce aneurysms in the ascending aorta. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exon 3 deleted in the cre-expressing tissues. When this floxed strain is crossed to a strain expressing Cre recombinase in smooth muscle, deletion of Agtr1a had no affect on ascending aortic aneurysms (AA) after Ang II infusion. In contrast, when cr ..... For more information please see the full phenotype on the strain data sheet
016120	C57BL/6N-Lrrk1^tm1.1Youy/J	Repository- Live
	These mice lack exons 24-29 of the leucine-rich repeat kinase 1 (Lrrk1) gene, abolishing gene function. LRRK1 is a gene homolog of Lrrk2, mutations of which have been associated with Parkinson's disease. LRRK1 regulates endosomal trafficking of the EGF receptor. These mice may be useful for studying the role of Lrrk1 in the progression of Parkinson's Disease.
016121	C57BL/6N-Lrrk2^tm1.1Youy/J	Repository- Live
	These mice lack exons 39-40 of the leucine-rich repeat kinase 2 (Lrrk2) gene, abolishing gene function. LRRK2 protein, also known as Dardarin, contains multiple functional domains and may function as both an active GTPase and kinase. LRRK2 may regulate alpha-synuclein-mediated neuropathology through modulation of intracellular trafficking and accumulation of SNCA protein. These mice may be useful for studying the role of Lrrk2 in the progression of Parkinson's Disease.
015823	C57BL/6N-Pawr^tm1Rang/J	Repository- Live
	Mice homozygous for this Par4^flox allele are viable and fertile, with loxP sites flanking exon 2 of the targeted PRKC, apoptosis, WT1, regulator (Pawr or Par-4) gene. Homozygotes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. PAR4 is a pro-apoptopic protein capable of inducing apoptosis in cancer cells and causing regression of tumors in animal models. PAR4 interacts with, and inhibit, atypical protein kinase C isoforms, functioning as a negative regulator of the NF-κB pathway. When these mutant mice are bred to mice that express Cre recombinase, the resulting offspring will have exon 2 deleted in the cre-expressing tissue, resulting in inactivation of Pawr gene function. Loss of PAR4 leads to a reduction in apoptosis by increased activation of NF-κB. These mutant mice may be useful in generating conditional mutations for studying tumor development and treatment. ..... For more information please see the full phenotype on the strain data sheet
016582	C57BL/6N-Tg(Slc32a1-icre/ERT2)3Gloss/J	Repository- Live
	These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the mouse Slc32a1, solute carrier family 32 (GABA vesicular transporter), member 1, promoter. When crossed with a strain containing a loxP site flanked sequence, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeting events. Tamoxifen administration induces Cre recombination throughout the brain in neurons that structurally resemble interneurons. Homozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This Cre-ERT2 fusion protein consists of iCre recombinase (Codon-improved Cre recombinase) fused to a triple mutant form of the human estrogen receptor which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OHT or tamoxifen) and, with lesser sensitivity, ICI 18278 ..... For more information please see the full phenotype on the strain data sheet
016583	C57BL/6N-Tg(Slc6a3-icre/ERT2)2Gloss/J	Repository- Live
	These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the mouse Slc6a3, solute carrier family 6 (neurotransmitter transporter, dopamine), member 3, promoter. When crossed with a strain containing a loxP site flanked sequence, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeting events. Tamoxifen administration induces Cre recombination in dopaminergic cells of the substantia nigra and locus coeruleus. Homozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This Cre-ERT2 fusion protein consists of iCre recombinase (Codon-improved Cre recombinase) fused to a triple mutant form of the human estrogen receptor which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OHT or tamoxifen) and, with lesser sensitivity, ICI 1827 ..... For more information please see the full phenotype on the strain data sheet
004625	C57BLKS/J-Car8^wdl/GrsrJ	Repository- Live
	wdl homozygotes display a side-to-side wobble in their gait as early as two weeks of age and this persists throughout life. Despite this, they can swim in a straight line.
010970	CBA/J-Dab1^scm-4J/GrsrJ	Repository- Live
	Homozygotes can be recognized by two weeks of age by smaller body size, tremor, and leaning side-to-side gait. While some homozygotes die by three weeks of age, most live to adulthood. Poor marrow, thymic atrophy, and disorganization of the neurons of the brain were found in homozygotes.
013084	CBA/J-Dts/GrsrJ	Repository- Live
	Mice heterozygous for the dominant tail short mutation have kinked, shortened tails that range from one quarter to three quarters the length of a normal tail. The number of kinks varies and the average is slightly over 3. This mutant is also prone to hydrocephalus and aberrant cells have been found in the testis. No homozygotes have been identified to date, although predicted Mendelian segregation and complete penetrance is found in heterozygotes.
014084	CBA/J-agil^3J/GrsrJ	Repository- Live
	Mice homozygous for the agitans-like 3 Jackson mutation can be detected by 2 weeks of age by a wobbling gait and the propensity to retract the hind legs when picked up by the tail. They are smaller than their littermates and most die before adulthood. Homozygotes fail to breed.
009156	CXB5/ByJ-skp/GrsrJ	Repository- Live
	Skimpy homozygotes are smaller than their littermates, walk on their toes, have poor balance, and die by four weeks of age.
007048	DBA/2J-Gpnmb⁺/SjJ	Repository- Live
	This coisogenic strain has a functional allele of Gpnmb. Homozygous mice do not develop elevated intraocular pressure or glaucoma, although they exhibit a mild iris stromal atrophy (ISA). This strain provides a genetically matched control for DBA/2J (Stock No. 000671). The inbred strain DBA/2J is homozygous for the glaucoma-related Gpnmb^R150X and Tyrp1^isa mutations.
016193	FVB-Tg(ACTA1-PABPN1*A17)1Drub/DrubJ	Repository- Live
	Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities until roughly four months of age. At four months, hemizygotes develop a progressive muscle weakness (measured by grip strength, wire maneuver and vertical gripping tests), which progresses to late onset locomoter defects around nine months of age. At nine months mice cannot lift their own body weight. They drag their pelvis when walking. There is no difference in body weight or mortality up to 15 months of age compared to controls. Hemizygotes develop KCl-insoluble inclusions containing PABPN1 in the nuclei of skeletal muscle fibers with tubulo-filamentous ultrastructures. The proportion of myocte nuclei with aggregates increases with age. Significantly elevated numbers of TUNEL-positive myocyte nuclei can be found at six and 12 months. TUNEL staining is widely used as a cell-death marker in muscle diseases in mice and humans. Muscles of hemizy ..... For more information please see the full phenotype on the strain data sheet
013591	FVB-Tg(C3-1-TAg)cJeg/JegJ	Repository- Live
	Male transgenic mice develop prostatic hyperplasia in early life that progresses to adenoma or adenocarcinoma in about half of the animals which survive longer 7 months of age. Female animals generally develop mammary intraepithelial neoplasia with similarities to DCIS by 3 months of age with subsequent development of mammary adenocarcinoma by 6 months of age in 100% of the animals. About 10 - 15% of female mice develop lung metastases, although lung metastases from prostate cancer is extremely rare. Bone metastases have not been observed. The phenotype for this transgene has been most extensively studied in the FVB/N background.
008450	FVB-Tg(CAG-luc,-GFP)L2G85Chco/J	Repository- Live
	Mice homozygous for the CAG-luc-eGFP L2G85 transgene are viable and fertile, with widespread expression of firefly luciferase and enhanced green fluorescence protein directed by the CAG promoter (human cytomegalovirus immediate early promoter enhancer with chicken beta-actin/rabbit beta-globin hybrid promoter). Bioluminesence is detected in heart, spleen, muscle, pancreas, skin, thymus and bone marrow. Luciferase activity is not detected in mature erythrocytes, although low levels are detected in erythrocyte precursors and varying levels of activity in all leukocyte subsets tested. Homozygotes have no reported gross physical or behavioral abnormalities. Following luciferin injection, luciferase expression is generally greater in males than females. GFP fluorescence is detected in skin (upper epidermal layers) by fluorescence microscopy. The Donating Investigator reports that for the FVB-Tg(CAG-luc,-GFP)L2G85Chco/J (STOCK#8450) strain, no GFP fluorescence is detected in hematopoiet ..... For more information please see the full phenotype on the strain data sheet
013585	FVB-Tg(Cdh5-tTA)D5Lbjn/J	Repository- Live
	These transgenic mice express tetracycline regulated transactivator under the direction of the mouse Cdh5, cadherin 5, promoter. When these VE-Cadherin-tTA mice are bred with mice carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE, TetRE or tetO), expression of that gene in blood vessel endothelial cells may be conditionally inactivated with administration of the tetracycline in the double mutant offspring. Tetracycline was used by the Donating Investigator in the original publication Proc Natl Acad Sci 2005;102:128-33. When crossed with a strain carrying a tetracycline-responsive promoter driven lacZ transgene, beta-galactosidase is expression is observed in VEGFR-2, CD31 expressing cells in the blood vessels of bi-transgenic day 13.5 aged embryos. Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
006774	FVB-Tg(Col2a1-cre/ERT)KA3Smac/J	Repository- Live
	Mice hemizygous or homozygous for the Col2CreER^T transgene are viable and fertile. Mice from this founder line (line K from founder mouse A3) have strong tamoxifen-inducible cre expression directed to cells of the chondrogenic lineage (cartilage), with minimal (<0.1%) cre activity in the absence of tamoxifen. The CreER^T protein consists of Cre recombinase fused to a mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligand 4-hydroxytamoxifen. Restricted to the cytoplasm, CreER^T can only gain access to the nuclear compartment after exposure to tamoxifen. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone may be coadministered. When these Col2CreER^T mice are bred with mice containing a loxP-flanked ..... For more information please see the full phenotype on the strain data sheet
006954	FVB-Tg(Ddx4-cre)1Dcas/J	Repository- Live
	Mice hemizygous for this Vasa-Cre transgene are viable and fertile. Transgenic cre activity is directed to male and female germ cells starting at embryonic day (e)15-e18. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the flanked sequence. In such breedings, occasional hemizygous mice may exhibit variegated cre expression in skin epithelium or global cre expression (<20% incidence). Differential parent-of-origin transgene expression is observed. When the mother harbors Vasa-Cre, virtually all progeny undergo global Cre-mediated recombination, even those that do not inherit the transgene (which may be useful in converting a "floxed" allele to a null while obviating the need to perform additional crosses to remove the transgene). To achieve germ-line specific Cre-mediated recombination in offspring, paternal Vasa-Cre mice should be used. In crosses with some floxed alleles, gl ..... For more information please see the full phenotype on the strain data sheet
003718	FVB-Tg(GadGFP)45704Swn/J	Repository- Live
	Mice homozygous for the TgN(GadGFP)45704Swn transgene express Enhanced Green Fluorescent Protein (EGFP) under the control of the mouse Gad1 (GAD67) gene promoter. Homozygous mice exhibit no apparent physical or behavioral defects. Transgene expression occurs in a specific subpopulation of hippocampal and cortical GABAergic interneurons that express somatostatin. This subset of interneurons has been shown to be prone to injury during epilepsy, ischemia, and Alzheimer's disease. These transgenic mice are useful for the morphological identification and study of these interneurons in both living and fixed brain tissue. Of note, this strain is one of many fluorescent GABAergic neuron strains, each with unique labeling characteristics (see Stock No. 006334 and Stock No. 006340).
005515	FVB-Tg(ITGAM-DTR/EGFP)34Lan/J	Repository- Live
	Mice that are homozygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice have a diphtheria toxin (DT) inducible system that transiently depletes macrophages in various tissues. The transgene insert contains a fusion product involving simian diphtheria toxin receptor and green fluorescent protein under the control of the human ITGAM (integrin alpha M) promoter (CD11b). RT-PCR analysis of bone marrow macrophages detects specific transgene expression. Cytological analysis of thioglycollate treated peritoneal cells shows the absence of macrophages. Intraperitoneal injection of DT ablates monocyte/macrophage cells in the peritoneal cavity. Macrophage populations within various tissues demonstrate differential susceptibility DT induced deletion. Following DT administration macrophages are ablated in the peritoneum, kidney and ovary. Macrophage population is restored by day 4 following a single intr ..... For more information please see the full phenotype on the strain data sheet
008099	FVB-Tg(KRT14-rtTA)F42Efu/J	Repository- Live
	Mice that are hemizygous or homozygous for this transgenic insert are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the human keratin 14 (KRT14) gene promoter (active in embryonic and postnatal basal cells of the skin). When mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (tetO), expression of the target gene may be regulated by the tetracycline analog, doxycycline (dox); in the presence of dox, transcription of the target gene is induced in cells where rtTA is expressed. This strain provides a Tet-On tool that allows the inducible expression of genes in cells expressing KRT14 for hair and skin research.
008679	FVB-Tg(MECP2)1Hzo/J	Repository- Live
	As hemizygotes, these human methyl CpG binding protein 2 transgenic mice express the gene at ~2-fold wildtype levels in the brain. Enhanced motor and contextual learning, and enhanced hippocampal synaptic plasticity phenotypes begin around 10 weeks of age. After 20 weeks of age, the mice progressively develop neurological impairments, seizures, become hypoactive (characterized by a freezing-like behavior), and ~30% die by one year of age. Forepaw clasping, aggressiveness, and kyphosis are also characteristic in these mice. This strain may be useful in studies of X-linked delayed-onset neurobehavioral disorders, including MECP2 duplication syndrome, mental retardation, and autism.
005038	FVB-Tg(MMTV-Erbb2)NK1Mul/J	Repository- Live
	These transgenic mice express the activated rat Erbb2 (c-neu) oncogene under the direction of the mouse mammary tumor virus promoter. The activated, or transforming, version of the rat Erbb2 (c-neu) oncogene has a valine to glutamic acid substitution at acid 664, (Val⁶⁶⁴ to Glu⁶⁶⁴). Non-uniform and random transgene expression is detected by RNase protection assay in mammary gland epithelium from hemizygous mice. Tumor formation is multifocal, stochastic and matches the expression pattern of the transgene. While no transgene expression is detected at 5 and 8 weeks of age in normal mammary gland tissue, it is detected in adenocarcinomas from older (23 week old) mice. The donating investigator indicates that 50% of transgenic mice derived from the TG.NK founder line, develop tumors within 6-12 months of age. Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. This mutant mouse strain may be useful in studies of bre ..... For more information please see the full phenotype on the strain data sheet
016570	FVB-Tg(Myh6-TRPC3*)6.6Jmol/J	Repository- Live
	The dnTRPC3 transgene contains amino acids 1-302 of the human transient receptor potential cation channel, subfamily C, member 3 (TRPC3) gene under the control of the mouse myosin, heavy polypeptide 6, cardiac muscle, alpha (Myh6) promoter. Hemizygotes are viable, fertile and normal in size. TRPC3 is a nonselective monovalent cation channel which is activated by oxidative stress in endothelial cells. These mice express a dominant-negative form of TRPC3. They only express the N-terminus of the gene and lack the transmembrane and cytosolic carboxy terminal domains. TRPC3 transgenic mice exhibit an increase in cardiac calcineurin-nuclear factor of activated T cells (NFAT) transcriptional activity, cardiac hypertrophy, and cardiomyopathy. They show a dosage-dependent increase in cardiac hypertrophy following neuro-endocrine agonist or pressure overload stimulation.
016571	FVB-Tg(Myh6/tetO-Gata6)2Jmol/J	Repository- Live
	These Gata6 transgenic mice contain the GATA binding protein 6 (Gata6) sequence regulated by a tetracycline operator (tetO), driven by myosin, heavy polypeptide 6, cardiac muscle, alpha (Myh6 or α-MHC) promoter/enhancer elements. Hemizygotes are viable, fertile, and normal in size. α-MHC limits overexpression of GATA6 to the heart. GATA6 is a zinc-finger-containing transcription factor expressed in mesoderm and endoderm derived tissues such as heart, liver, lung, gonad, and gut. Along with GATA4, GATA6 is necessary for the development of the embryonic heart and cardiac hypertrophy in the adult heart. When mated to a mutant strain expressing tetracycline-controlled transactivator protein (tTA), expression of GATA6 protein may be regulated with tetracycline or its analog doxycycline (dox) in the double mutant offspring. When bred to mice expressing tTA driven by the α-MHC promoter, double transgenic an ..... For more information please see the full phenotype on the strain data sheet
014155	FVB-Tg(Myh6/tetO-Itpr1)22.3Jmol/J	Repository- Live
	In this transgenic strain, a conditional Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha )/tetO promoter drives expression of a recombinant mouse "IP3 sponge". The IP3 binding domain encoded by amino acid residues 224-604 of mouse type 1 IP₃R (Itpr1 (inositol 1,4,5-triphosphate receptor 1); also called mIP₃R1) is fused to glutathione S-transferase (GST). This enables expression of high affinity IP3 chelator fusion protein when the strain is crossed with a driver strain encoding tetracycline transactivator (tTA).
014153	FVB-Tg(Myh6/tetO-Itpr2)3.11Jmol/J	Repository- Live
	These transgenic animals carry the mouse Itpr2 (inositol 1,4,5-triphosphate receptor 2) gene driven by a conditional Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha)-tetO cardiac-specific promoter. When crossed with a driver strain encoding the tetracycline transactivator (tTA), a 12-fold increase in protein expression is observed. Overexpression in the heart generates mild baseline cardiac hypertrophy at 3 months of age, but no greater signs of heart disease past 10 months of age. Increased hypertrophic response occurs following pathological/physiological stimuli.
014154	FVB-Tg(Myh6/tetO-Itpr2)4.9Jmol/J	Repository- Live
	These transgenic animals carry the mouse Itpr2 (inositol 1,4,5-triphosphate receptor 2) driven by a conditional Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha)-tetO cardiac-specific promoter. When crossed with a driver strain encoding the tetracycline transactivator (tTA), a 5-fold increase in protein expression is observed. No phenotype is observed at baseline, but increased hypertrophic response occurs following certain types of stumuli. Administration of doxycline (Dox) causes near complete extinguishment of ITPR2 expression.
013732	FVB-Tg(NPEPPS)1Skar/J	Repository- Live
	These mice express a human aminopeptidase puromycin sensitive (hPSA or NPEPPS) gene directed by its endogenous promoter/enhancer regions on a BAC transgene. Mice hemizygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. PSA is a cytosolic aminopeptidase that hydrolyzes N-terminal amino acids. PSA is considered to have neuroprotective qualities due to its ability to degrade certain proteins associated with neurodegenerative diseases (TAU and polyglutamine expansion repeat-containing proteins). hPSA overexpression is seen in the cerebral cortex, spinal cord, cerebellum, hippocampus, and brain stem at a 2-3 fold greater level than endogenous PSA. hPSA activity is also increased in muscle, kidney, and liver. These mice may be useful for studying PSA protection in neurodegenerative disorders.
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.
006421	FVB-Tg(Pomc1-hrGFP)1Lowl/J	Repository- Live
	Hemizygous mice are viable and express humanized Renilla Green Fluorescent Protein (hrGFP, Stratagene) under control of the mouse pro-opiomelanocortin-alpha (Pomc1) promoter. As such, UV light-exposed transgenic brain tissues show GFP fluorescence patterns consistent with the endogenous Pomc1 gene, specifically POMC expressing neurons. The donating investigator reports that hrGFP is more stable and resistant to signal fading compared to other GFP's. The donating investigator reports that transgenic males have smaller seminal vesicles, and breeding transgenic males results in infrequent and very small (<2 pups) litter sizes. When non-transgenic males are crossed with transgenic females, fertility is normal. These POMC-GFP transgenic mice may be useful for studies of neurobiology, energy metabolism, obesity, seizures, and epilepsy.
005688	FVB-Tg(Rag2-EGFP)1Mnz/J	Repository- Live
	Mice hemizygous for the NG-BAC transgene are viable and fertile, with expression of enhanced green fluorescent protein (EGFP) directed by the Rag2 promoter. EGFP expression is high in pro-B cells and decreases during B cell maturation. Similarly, EGFP induction in T cells occurs in the late CD4/CD8 double negative stage and expression decreases during maturation. While mature cells do not express EGFP, lingering protein can be detected. The transgene does not hinder B cell function or T cell proliferation. These NG-BAC transgenic mice can be used in studies of B and T cell development as EGFP fluorescence reflects Rag2 protein expression.
013778	FVB-Tg(tetO-Cacnb2)1Jmol/J	Repository- Live
	Expression of Cacnb2 (calcium channel, voltage-dependent, beta 2 subunit) is regulated by a tetracycline operator (tetO); also called tetracycline-responsive element (TRE, TetRE) or tet-operator) in this transgenic strain. When mated to a mutant strain expressing tetracycline-controlled transactivator protein (tTA), expression of CACNB2 protein may be regulated with tetracycline or its analog doxycycline (dox) in the double mutant offspring. When crossed with a Myh6-tTA strain (e.g. Stock No. 003170), double transgenic mice show increased Ca²⁺ influx through cardiac L-type Ca²⁺ channels resulting in Ca²⁺ overload, myocyte disorganization, interstitial fibrosis, and cell death. Compound mutant animals show a 7.4-fold increase in CACNB2 expression. This strain may be useful in studies of cardiomyopathy.
013780	FVB-Tg(tetO-Cib1)1Jmol/J	Repository- Live
	Expression of Cib1 (calcium and integrin binding 1 (calmyrin)) is regulated by a tetracycline operator (tetO); also called tetracycline-responsive element (TRE, TetRE) or tet-operator) in this transgenic strain. When mated to a mutant strain expressing tetracycline-controlled transactivator protein (tTA), expression of CIB1 protein may be regulated with tetracycline or its analog doxycycline (dox) in the double mutant offspring. When crossed with a Myh6-tTA strain (e.g. Stock No. 003170), double transgenic mice show enhanced cardiac hypertrophy in response to pressure overload or calcineurin signalling. This strain may be useful in studies of cardiac hypertrophy.
012387	FVB-Tg(tetO-Ppargc1a)1Dpk/J	Repository- Live
	These transgenic mice express Ppargc1a (peroxisome proliferative activated receptor, gamma, coactivator 1 alpha) and a myc-his tag regulated by the tetracycline operator (tetO; also called tetracycline-responsive element (TRE, TetRE) or tet-operator). When mated to a mutant strain expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), tissue Ppargc1a expression may be regulated with the tetracycline analog doxycycline (dox) in the double mutant offspring. This strain may be useful for studies of metabolism, cardiomyopathy, and mitochodrial function.
012630	FVB/N-Tg(GFAP-HTT*160Q)31Xjl/J	Repository- Live
	HTT-160Q-31 transgenic mice have the human glial fibrillary acidic protein (GFAP) promoter directing expression of the human huntingtin (HTT) gene in astrocytes, a glial cell that removes extracellular glutamate in the brain. Hemizygous GFAP-HD mice are viable and fertile. HTT-160Q-31 mice exhibit weight loss, deficient motor function, and die earlier than control mice. HTT-160Q-31 binds with Sp1 transcription factor decreasing the expression of glutamate transporter in astrocytes by reducing the association of Sp1 with the glutamate transporter promoter. This leads to a decrease in extracellular glutamate uptake by glial cells and may cause the glutamate excitotoxicity associated with Huntington's disease. These mice may be useful for studying the pathology and neurodegeneration associated with glutamate excitotoxicity in Huntington's disease.
003257	FVB/N-Tg(GFAPGFP)14Mes/J	Repository- Live
	Transgenic mice overexpress Green Fluorescent Protein under the control of the astrocyte-specific glial fibrillary acidic protein promoter. Bright fluorescence is observed in the cell bodies and processes of unfixed or fixed astrocyte preparations throughout the CNS of hemizygous mice. In addition retinal Mullers cells expressed the GFP transgene in response to degeneration of neighboring photoreceptors. These mice provide a method to follow changes in astrocyte morphology during development or disease processes.
008197	FVB/N-Tg(HTT*97Q)IXwy/J	Repository- Live
	Mice hemizygous for the BACHD transgene are viable and fertile. Under the control of endogenous human htt regulatory machinery, BACHD mice have relatively high expression levels of a neuropathogenic, full-length human mutant Huntingtin (fl-mhtt) modified to harbor a loxP-flanked human mutant htt exon 1 sequence (containing 97 mixed CAA-CAG repeats encoding a continuous polyglutamine (polyQ) stretch). Prior to Cre recombinase exposure, BACHD mice exhibit progressive motor deficits, neuronal synaptic dysfunction, and selective late-onset neuropathology without somatic polyQ repeat instability in the aged brain. Moreover, BACHD mice reproduce a mhtt aggregation pattern reminiscent of that in adult-onset Huntington's disease (HD). Importantly, a relatively steady-state level of predominantly fl-mhtt and a small amount of mhtt N-terminal fragments present in both the nucleus and cytoplasm, are responsible for the onset and progression of neuropathology. Upon exposure to ..... For more information please see the full phenotype on the strain data sheet
008232	FVB/N-Tg(Ins2-IAPP)RHFSoel/J	Repository- Live
	Mice homozygous for the RIPHAT transgene are viable and fertile, with expression of human islet amyloid polypeptide (h-IAPP) under the regulatory control of the rat insulin II promoter. While h-IAPP RNA from the transgene is observed in pancreas, kidney, and stomach, h-IAPP protein is reported only in pancreas tissues. Hemizygous mice show no symptoms of spontaneous disease. Homozygous males spontaneously develop diabetes mellitus due to beta-cell death, associated with impaired insulin secretion (hypoinsulinemia), hyperglycemia, and abnormal intracellular aggregates of h-IAPP (the donating investigator reports that extracellular aggregates are not found on this strain background). Homozygous male onset is between 4-8 weeks of age with death around 16 weeks of age. Homozygous females exhibit a less severe phenotype. These RIPHAT transgenic mice may be useful in studying the beta-cell destruction and islet amyloid deposition associated with non-insulin-dependent diabetes mellitus (NIDDM ..... For more information please see the full phenotype on the strain data sheet
009610	FVB/N-Tg(LRRK2)1Cjli/J	Repository- Live
	Mice hemizygous for the BAC LRRK2 transgene are viable and fertile, with expression of a wild-type human leucine-rich repeat kinase 2 (LRRK2) gene directed by its endogenous promoter/enhancer regions on the BAC transgene. These BAC LRRK2 mice (also called WT-OX mice) "overexpress" the wildtype human LRRK2 protein in cortex, cerebellum, striatum and ventral midbrain at an approximately five- to ten-fold greater level than endogenous mouse Lrrk2, and are a control strain for the BAC LRRK2^R1441G Parkinson's disease strain (Stock No. 009604). Contrary to the hypokinetic motor deficit of the BAC LRRK2^R1441G Parkinson's disease mice, WT-OX mice exhibit slightly increased motor activities compared to nontransgenic wild-type controls.
009609	FVB/N-Tg(LRRK2*G2019S)1Cjli/J	Repository- Live
	Mice hemizygous for the BAC LRRK2 (G2019S) transgene are viable and fertile, with expression of a mutant form of human leucine-rich repeat kinase 2 (LRRK2G2019S) associated with autosomal dominant, late-onset Parkinson's disease directed by the endogenous LRRK2* promoter/enhancer regions on the BAC transgene. The phenotype of these LRRK2G2019S mice is not yet characterized. These mice represent an in vivo* model for studying the Parkinson's disease pathogenesis and neurodegeneration elicited by the dominant toxic effects of mutant LRRK2*G2019S expression.
009604	FVB/N-Tg(LRRK2*R1441G)135Cjli/J	Repository- Live
	Mice hemizygous for the BAC LRRK2^R1441G transgene are viable and fertile, with expression of a mutant form of human leucine-rich repeat kinase 2 (LRRK2R1441G) associated with autosomal dominant, late-onset Parkinson's disease directed by the endogenous LRRK2* promoter/enhancer regions on the BAC transgene. LRRK2^R1441G mice from founder line RP135 express the mutant protein in cortex, cerebellum, striatum and ventral midbrain at an approximately five- to ten-fold greater level than endogenous mouse Lrrk2. LRRK2^R1441G mice exhibit multiple late-onset and progressive characteristics of Parkinson's disease; including hypokinetic motor deficits (reversible with administration of levodopa or apomorphine [a direct-acting dopamine agonist]), progressive dopaminergic neuron dysfunction and degeneration, axon injury pathology, and hyperphosphorylated tau. These LRRK2^R1441G mice recapitulate the motor behavioral, neurochemical, and histopa ..... For more information please see the full phenotype on the strain data sheet
012460	FVB/N-Tg(Myh6-Gnaq)40Gwd/J	Repository- Live
	Mice hemizygous for the Myh6-Gnaq allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The donating investigator states that hemizygous females develop peripartum cardiomyopathy. Expression of Gαq is regulated by an α-myosin heavy chain (Myh6) promoter, which leads to overexpression of Gαq in the heart. This overexpression results in cardiac hypertrophy, defined as a conserved program of fetal gene expression, increased heart weight, and increased cardiomyocyte size, which severely compromises systolic cardiac function, and results in overt cardiac failure. Upon experimental pressure overloading, the mice progress rapidly to heart failure. These mice may be useful for studying the biochemical and physiologic phenotype resembling both the compensated and decompensated phases of human cardiac hypertrophy.
006143	FVB/N-Tg(Thy1-cre)1Vln/J	Repository- Live
	Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre activity is observed in nearly all neurons in cortex and hippocampus. When bred with any mouse containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in postnatal, neuron-specific deletion of the flanked genome. These mice may be useful in studies of the nervous system, including Alzheimer's disease. View cre expression characterization.
009090	FVB/NJ-Tg(Slc6a3-PARK2*Q311X)AXwy/J	Repository- Live
	Hemizygous Parkin-Q311X(A) mice are viable and fertile, with expression of a FLAG-tagged, C-terminal truncated human parkin-Q311X mutation associated with Turkish early-onset Parkinson's disease directed to dopaminergic neurons of the substantia nigra pars compacta (SNc) and ventral tegmentum area (VTA) by the mouse Slc6a3 promoter/enhancer sequences. Parkin-Q311X(A) mice (derived from founder line A) have expression of the FLAG-tagged parkin-Q311X protein in dopaminergic neurons at a level that is approximately equivalent to or just below that expected from a heterozygous endogenous parkin allele. Parkin-Q311X(A) mice exhibit multiple late-onset and progressive hypokinetic motor deficits, progressive dopaminergic neuron dysfunction and degeneration, and age-dependent accumulation of proteinase K-resistant endogenous alpha-synuclein. Compared to founder line D, Parkin-Q311X(A) mice have a higher transgene copy number that results in more robust and earlier onset of hypokinetic m ..... For more information please see the full phenotype on the strain data sheet
006825	MRL/MpJ-Fas^lpr/2J	Repository- Live
	The current colony (as of fall 2006) of MRL/MpJ-Fas^lpr/J has experienced a progressive loss of lymphoproliferative phenotype over the past several years, as reported by some of our customers and as observed by our technical staff. This loss of phenotype has been manifested by reduced enlargement of brachial and mesenteric lymph nodes, and poor splenomegaly. Also, the life spans of the mice in the current colony have also been found to be much longer than the historically observed and reported 17 weeks for females and 22 weeks for males. However, genotyping continues to show that all the mice in the colony remain homozygous for the Fas^lpr mutation, and the SNP profile in the region of the mutation on Chromosome 19 has not changed. In an effort to regenerate the desired phenotype, we recovered mice from our embryo archive cryopreserved in 1993. The sixteen-week old cryo-recovered mice have lymph nodes that were 4.5 (females) to 10.1 times (male) la ..... For more information please see the full phenotype on the strain data sheet
008694	NOD/ShiLt-Tg(Foxp3-EGFP/cre)1cJbs/J	Repository- Live
	Mice hemizygous for the Foxp3-EGFP/cre BAC transgene are viable and fertile. They express an enhanced green fluorescent protein and codon optimized "humanized" cre under the control of the mouse Foxp3 promoter. Transgene expression is specific to Cd4⁺Cd25 ^highCd127 ^low T cells from the lymph nodes, spleen and thymus. GFP expression is restricted to FoxP3⁺ cells. This mutant mouse strain may be useful for fluorescently labeling Foxp3+ T-cells to study regulatory T-cell function in autoimmunity specifically, type 1 diabetes.
005362	RB156Bnr/Ei-rul/GrsrJ	Repository- Live
	The phenotype of this mutation can be identified at about 10 days of age by a ruffled looking coat, which is different than the smooth coat of control littermates. The hair of mutant mice is sparse and has some curling. The ruffled looking coat is maintained throughout the animal's lifespan, unlike the caracul and caracul-like mutants who lose some of their curly coat with age. Mice homozygous for the ruffled mutation have a normal lifespan and both sexes breed normally.
014631	SWR/J-curt/GrsrJ	Repository- Live

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.
004766	C57BL/6J-Pde6b^rd1-2J/J	Research Strain
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Pde6b^2J entry.
005296	C57BL/6J-nmf246/J	Research Strain
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf246 entry.
000516	C57BLKS-Rpl24^Bst/J	Research Strain
	Belly spot and tail (Rpl24^Bst) is a semidominant, homozygous in utero lethal mutation. Adult heterozygotes are viable and fertile although a reduced birth rate for heterozygotes has been reported. This may reflect incomplete penetrance, or, more likely, prenatal mortality. The Rpl24^Bst mutation has variable expressivity and the heterozygous phenotypic traits include shortened and kinked tail, white feet and belly spot, malocclusion, smaller body size, exencephaly, abnormalities of the spine, ocular defects, and polydactyly. Polydactyly is found predominantly in the right rear paw, occasionally in the left front paw and rarely in the left rear or right front paws. Approximately 50-60% of the heterozygotes have a reduction in pupillary light reflex in one or both eyes due to an underlying optic nerve atrophy. Ontological studies showed a delay in the developmental fusion of the optic fissure, a disruption of the retinal layers by embryonic day 1 ..... For more information please see the full phenotype on the strain data sheet
012440	DBA/2J-Tg(RP24-180N9)2Kjn/Kjn	Research Strain
	The Tg(RP24-180N9)2Kjn transgene gives expression of Fscn2 and rescues the Fscn2^ahl8 related early onset hearing loss on the DBA/2J background. At one month of age the 16 kHz ABR threshold of the hemizygote is close to that of DBA/2NCrl controls, a subline that does not have Fscn2^ahl8. This transgenic rescue is similar to that found in the congenic rescue in D2.B6-Fscn2⁺/Kjn (stock #012438).
004334	NOD/ShiLt-Tg(TcraAI4)1Dvs	Research Strain

004335	NOD/ShiLt-Tg(TcrbAI4)1Dvs	Research Strain

008669	129-Daxx^tm2Led/J	Cryopreserved - Ready for recovery
	These mice possess loxP sites on either side of exon 2 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 these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 deleted in the cre-expressing tissue(s). These Daxx (Fas death domain-associated protein) conditional (floxed) mutant mice may be useful in generating conditional mutations for studying apoptosis and regulation of gene transcription.
012561	129-Zic1/Zic4^tm1Kjmi/J	Cryopreserved - Ready for recovery
	Mice heterozygous for mutations in both genes exhibit two distinct phenotypes. Similar to mice heterozygous for Zic4^tm2Kjmi, 85% of mice have grossly normal cerebellar anatomy, while the remaining 15% develop severe cerebellar size and foliation defects, disproportionate hypoplasia of the vermis, ataxia, reduced body weight, abnormal righting reflexes and do not survive past weaning. Cerebellar abnormalities in these mice resemble those seen in human Dandy Walker malformation, which is identifed by reduced cerebellar vermis size and is often accompanied by cerebellar ataxia and increased patient morbidity. Homozygous mice survive for approximately 2-3 weeks. This mutant mouse strain may be useful in studies of cerebellar development and as a model for Dandy-Walker malformation. 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 w ..... For more information please see the full phenotype on the strain data sheet
012560	129-Zic4^tm2Kjmi/J	Cryopreserved - Ready for recovery
	Mice that are heterozygous for the targeted mutation are viable, fertile, and normal in size. Heterozygous mice have posterior cerebellar hypoplasia and mild anterior foliation defects. Retinogeniculate projections from the lateral geniculate nucleus exhibit an altered topographic patterning. Homozygous mice are viable and fertile. This mutant mouse strain may be useful in studies of cerebellar development and Dandy-Walker malformation. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
007659	129S-Atp8b3^tm1Gar/J	Cryopreserved - Ready for recovery
	Both male and female homozygotes are fertile, but the average litter sizes from homozygous males are slightly smaller than observed with wildtype males. Sperm morphology and motility are unaffected, but tests show that phosphatidylserine (PS) already exists in the outer membrane leaflet before sperm capacitation. When the zona pellucida (ZP) is removed from eggs, fertilization rates are normal; although when the extracellular matrix is intact, fewer spermatozoa bind tightly or penetrate the ZP, and fewer undergo acrosome reactions. Homozygous mice do not express protein as determined by Western blot analysis of testis tissues and immunostaining of mature spermatozoa. This published information is based on studies of mixed background C57BL/6 and 129S6 background animals; the line offered here is on a pure 129S6 background. This strain may be useful in studies of male fertility.
009083	129S-Dvl3^tm1Awb/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. Homozygous null mice have a perinatal lethal phenotype. Neonates have breathing difficulties and are often cyanotic. Homozygous embryos exhibit cardiac conotruncal abnormalities such as persistent truncus arteriosis (PTA) and double outlet right ventricle (DORV), and cochlear defects (disoriented stereociliary bundles). This mutant mouse strain may be useful in studies of cardiac development, neural tube formation and development of the inner ear.
009043	129S-Gt(ROSA)26Sor^{tm3(CAG-luc)Tyj}/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. In the absence of Cre, there is low level expression of Luciferase-SIY H2^b antigen expression. After Cre activity, the recombined locus has high expression of Luciferase-SIY fusion protein. This mutant mouse strain may be useful in studies of immune response to a self-antigen or over-expressed tumor-associated antigen when used in combination with tumor-prone models. This mouse is also useful as a reporter for Cre activity.
008668	129S-Hba-a1^tm1Led/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable and fertile, but are anemic. Reduced levels of gene product (mRNA) are detected by Northern blot analysis of homozygous embryos (due to compensatory expression of the α2-globin gene). Homozygous crosses yield smaller litters. Homozygotes exhibit increased platelet number, reduced hemoglobin concentration and mean corpuscular volume. Heterozygotes are viable, fertile, normal in size and exhibit an intermediary phenotype. This mutant mouse strain may be useful in studies of erythropoiesis, α-Thalassemia and hemoglobin defects.
008667	129S-Hba-x^tm1Led/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for this targeted mutation have an embryonic lethal phenotype. No gene product (mRNA) is detected by Northern blot analysis of homozygous embryos. α-globin mRNA expression is also reduced in homozygous embryos. Homozygous embryos (12 day pc) are anemic, pale, small in size, with peripheral blood anisocytosis, poikilocytosis, and polychromasia and reduced hemoglobin concentration and mean corpuscular volume. Heterozygotes are viable, fertile, and normal in size. Heterozygotes exhibit increased platelet number, and an intermediary phenotype of reduced hemoglobin concentration and mean corpuscular volume. This mutant mouse strain may be useful in studies of erythropoiesis, α-Thalassemia and hemoglobin defects.
009084	129S-Mnt^tm1Awb/J	Cryopreserved - Ready for recovery
	These mice possess loxP sites flanking exons 4-6 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 these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 4 through 6 deleted, the loxP site flanked hygro resistance cassette deleted, or both excised in the cre-expressing tissue(s). When bred to a strain with Cre recombinase expression in a wide range of tissues (see Stock No. 003314 for example), this mutant mouse strain may be useful in studies of Miller-Dieker syndrome, embryonic development and craniofacial defects. When bred to a strain with Cre recombinase expression in a wide range of tissues, especially mammary gland (see Stock No. 003553 for example), this mutant mouse ..... For more information please see the full phenotype on the strain data sheet
007587	129S-Park2^tm1Rpa/J	Cryopreserved - Ready for recovery
	Mice carrying this mutation are viable, fertile, and display no apparent defects or abnormalities. Mutations in the human homolog of this gene are associated with autosomal juvenile parkinsonism, a heritable form of Parkinson's disease.
010831	129S-Per1^tm1Drw/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 gene product (mRNA or protein) is detected by Northern or Western blot analysis of superchiasmatic nuclei. Homozygotes housed in constant darkness exhibit gradual circadian arrhythmicity (rhythmicity is not lost initially). Homozygotes exhibit phase shift responses to light. This mutant mouse strain may be useful in studies of circadian rhythm and sleep pattern.
010832	129S-Per2^tm1Drw/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. Abberant gene products (mRNA) are detected by RT-PCR and RACE analysis of brain total RNA. No gene product (protein) is detected in homozygous mutant mice by immunohistochemical staining of superchiasmatic nuclei over a 24 hour period. Western blots of liver reveal a deletion mutant protein product is produced. When housed in constant darkness, homozygotes have a short circadian period initially, and then exhibit gradual loss of rhythmicity. Homozygotes exhibit phase shift responses to light. This mutant mouse strain may be useful in studies of circadian rhythm and sleep patterns.
010833	129S-Per3^tm1Drw/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 gene product (protein) is detected by Western blot analysis of whole brain minus cerebellum and hypothalamus, whole hypothalamus, and anterior hypothalamus containing SCN, from homozygotes. Immunoprecipitation analysis of brain lysates from homozygotes does not detect any gene product (protein). Abberant gene products (mRNA) are detected by Northern blot analysis and RT-PCR, and have rhythmic expression. Under conditions of constant darkness, homozygous males exhibit a shorter free running period. A subset of mice exhibit progressive shortening of the period length in extended constant darkness. This mutant mouse strain may be useful in studies of circadian rhythm and sleep patterns.
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
008652	129S-Trp53^tm2Tyj/J	Cryopreserved - Ready for recovery
	These mice carry a conditional point-mutant allele of the transformation related protein 53 gene (p53R172H; structural mutant homologous to human p53 codon 175). The conditional allele is functionally equivalent to a null mutation. Mice have all the phenotypic issues of p53 knockout mice and therefore have some decreased viability of homozygotes. Cre-mediated recombination leads to deletion of a transcriptional termination sequence (Lox-Stop-Lox) and expression of the oncogenic protein.
008651	129S-Trp53^tm3Tyj/J	Cryopreserved - Ready for recovery
	These mice carry a conditional point-mutant allele of the transformation related protein 53 gene (p53R270H; contact mutant homologous to human p53R273H). The conditional allele is functionally equivalent to a null mutation. Mice have all the phenotypic issues of p53 knockout mice and therefore have some decreased viability of homozygotes. Cre-mediated recombination leads to deletion of a transcriptional termination sequence (Lox-Stop-Lox) and expression of the oncogenic protein.
008715	129S-Ywhae^tm1Awb/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. Most homozygotes die at birth, less than 1% of homozygotes survive to adulthood. Survivors remain smaller in size than wildtype controls. No gene product (protein) is detected by immunoblot analysis of brain tissue from homozygotes. Homozygotes exhibit hippocampal defects with thinning of the cortex, hippocampal pyramidal cell layer disorganization and neuronal migration abnormalities. Heterozygotes exhibit less severe hippocampal defects. Mutants have increased apoptosis in the brain. This mutant mouse strain may be useful in studies of Miller-Dieker Lissencephaly Syndrome and neuronal migration during brain development.
008180	129S/Sv-Kras^tm4Tyj/J	Cryopreserved - Ready for recovery
	This strain carries a point mutation (G12D) whose expression is blocked by the presence of a loxP-flanked stop codon. Homozygotes die in utero. Cre-mediated recombination can excise the stop codon and permit the oncogenic protein to be expressed. Intranasal infection with an adenovirus encoding Cre results in a very high frequency of lung tumors and permits controlled timing of tumor initiation and tumor multiplicity. This strain may be useful in studies of cancer and development. When bred to a strain expressing Cre recombinase under the control of a tetracycline-responsive promoter element and a strain expressing a tetracycline-controlled activator protein in lung epithelial cells (see Stock No. 006234 and 006235 respectively), this mutant mouse strain may be useful in studies of lung development. When bred to a strain expressing Cre recombinase in th ..... For more information please see the full phenotype on the strain data sheet
008077	129S1/Sv-Bche^tm1Loc/J	Cryopreserved - Ready for recovery
	Mice homozygous for this BChE mutant allele are viable and fertile with no reported spontaneous abnormalities. All tissues and plasma from homozygous mice are devoid of BChE activity. As BChE (butyrylcholinesterase) is a bioscavenger molecule protecting acetylcholinesterase (AChE) activity against nerve agents and organophosphates, homozygous BChE-deficiency leads to impaired protection from toxic compounds. These BChE mutant mice are a model for human butyrylcholinesterase deficiency and may be useful for studying metabolic effects of organophosphorus toxicants or nerve agents, neurotransmitter function, and anti-Alzheimer's drug therapies. Of note, the donating investigator has multiple strains available that may be useful for testing toxic compounds, including the AChE-deficient (Stock No. 005987), G117H BChE transgenic (Stock No. 007577), and BChE-deficient (see Stock ..... For more information please see the full phenotype on the strain data sheet
007859	129S1/Sv-Sufu^tm1Aeb/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. Homozygous null mice have an embryonic lethal phenotype, failing to develop past embryonic days 9.5 to 10. No gene product (protein) is detected by Western blot analysis. Truncated gene product (mRNA) is detected by Northern blot analysis. Homozygous embryos at 9 to 9.5 embryonic day exhibit growth retardation, incomplete embryonic turning, abnormal somite development, abnormal heart looping (due to abnormal left-right axial patterning) and open neural tubes. This mutant mouse strain may be useful in studies of the Hedgehog signaling pathway and embryonic development.
008109	129S4/SvJae-Shank1^tm1Shng/J	Cryopreserved - Ready for recovery
	Homozygous targeted mutant mice show altered postsynaptic density (PSD) protein composition (depletion of Shank-associated proteins guanylate kinase-associated protein (GKAP) and homer homolog 1 (HOMER)), reduced size of dendritic spines, smaller and thinner PSD's, and weaker basal synaptic transmission in the brain. Synaptic plasticity, including long-term potentiation (LTP), long-term depression (LTD), and late-phase LTP (L-LTP) is normal. Behaviorally, they have increased anxiety-related behavior and impaired contextual fear memory. Homozygous targeted mutant mice have enhanced performance in a spatial learning task, however long-term memory retention is impaired. This strain may be useful in studies of cognitive processes, a feature that may be relevant to human autism spectrum disorders.
005358	129S6/SvEvTac-Car3^tm1Gkim/J	Cryopreserved - Ready for recovery
	Mice homozygous for the targeted allele are viable, fertile, normal in size and life span and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected. Histological examination of tissues discerns no anomalies. Similarly, gas chromatography-mass spectrometry analysis of the fatty-acid distribution in serum, muscle, liver, and fat reveal no differences between mutant and wildtype mice. When exposed to an atmosphere of 100% oxygen homozygous mice display similar mean survival times as wildtype (~ 70 hours). The contractile properties of soleus muscle derived from mutant mice exhibit some differences from wildtype mice. Mutant mice display shorter relaxation and half-relaxation times for single and tetanic twitches and a minor reduction tetanic force. Microarray analysis detects an increase (~30%) in carbonic anhydrase 13 expression.
008862	129X1-Stat3^tm1Desi/J	Cryopreserved - Ready for recovery
	These mice carry a mutant allele that has mutations in exon 23 (YIIITG) which disrupt an internal splice acceptor thereby preventing production of the beta isoform. These mice express only the alpha isoform. No beta isoform protein is detected in hepatic tissue or MEFs from homozygotes by RT-PCR. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygotes are more susceptible to bacterial endotoxicity. Mutant mice are less likely to recover from LPS challenge than wildtype mice. This mutant mouse strain may be useful in studies of inflammatory response and septic (endotoxin) shock.
005445	A.B6 Tyr⁺-Cyba^nmf333/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf333 entry.
006026	A.B6 Tyr⁺-Pde6a^nmf282/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf282 entry.
002768	A/J-Hk1^dea/J	Cryopreserved - Ready for recovery
	Severe pallor is a distinguishing feature of Hk1^dea homozygotes and is evident at birth. Decreased hexokinase activity is found in the spleen, kidney, and red blood cells, but not the liver. Peripheral blood smears reveal anisocytosis, hypochromia, polychromatophilia, in addition to the presence of echinocytes and a morphologic anomaly of red cells deemed "split cell" in which they pull into halves tethered by thin strands of membrane. Spheroctyes are not found. These homozygotes are smaller than normal, die prematurely, and females are infertile. The phenotype includes reduced red blood cell count, hemoglobin, hematocrit, and red blood cell mean corpuscular hemoglobin content. Circulating reticuloctyes are 83% rather than the normal 3.1%, red blood cell mean corpuscular volume is increased, and total bilirubin is increased. Splenic weight is increased, the red pulp is enlarged, and there is heightened iron accumulation in the kidney tubules and liver but not in ..... For more information please see the full phenotype on the strain data sheet
003485	A/J-frg/J	Cryopreserved - Ready for recovery
	Mice homozygous for the froggy mutation have a smaller body size and a shortened face with wide set eyes.
005136	A/WySnJ-ctl/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the ctl mutation are easily recognizable at birth by their curly or bent tails.
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.
005895	B10.Cg-Thy1^a H2^d Tg(TcraCl1,TcrbCl1)1Shrm/J	Cryopreserved - Ready for recovery
	Male mice that are hemizygous for the Clone-1 TCR (also called Clone 1 Thy1.1 TCR or Cl.1 TCR) transgene are viable, fertile, and normal in size. Females are very weak and have low fecundity. The donating investigator reports that all transgenic mice are prone to tumor development by 5-6 months of age. The transgene encodes a rearranged low avidity T cell receptor that recognizes an influenza virus hemagglutinin epitope (HA_518-526) restricted by MHC class I H-2K^d. Flow cytometric analysis shows appropriate skewing towards the CD8⁺ T cell compartment in thymocytes and peripheral lymphocytes. Both naive and activated clone 1 T cells exhibit decreased responsiveness when presented with their cognate antigen in vitro and when transferred into mice expressing HA on pancreatic beta cells. CD8⁺ T cells can be induced to exhibit both effector function and antitumor activity. This mouse is further modified with the Thy1.1 allele, rather than th ..... For more information please see the full phenotype on the strain data sheet
002225	B10.M-H2^f/nMob Fmn1^ld-2J/J	Cryopreserved - Ready for recovery

003483	B6 x B10.D1-H2^q/SgJ-Nox3^het-2J/J	Cryopreserved - Ready for recovery

003561	B6 x B10.PL-H2^u/(73NS)Sn-Hxl/J	Cryopreserved - Ready for recovery
	Hxl is a dominant mutation with 100% penetrance. Heterozygotes and homozygotes have polydactyly.
002995	B6 x C.B10-H2^b/LiMcdJ-Fbn2^fp-2J/J	Cryopreserved - Ready for recovery
	Mice homozygous for the recessive fused phalanges 2 Jackson mutation (Fbn2^fp-2J) have syndactyly of the second, third, and/or the fourth digits of the hindlimbs with <20% showing involvement of all three digits. This syndactyly likely results from defective mesenchyme differentiation rather than failed interdigital apoptosis (Arteaga-Solis et al., 2001). This mutant has a less severe phenotype than other Fbn2 mutants do, and shows no involvement of the digits of the forelimbs. Whether this is due to the allele or the genetic background has not been determined. (Chaudhry et al., 2001.)
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.
005292	B6(129S2)-Sobp^jc-2J/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
002016	B6(Cg)-A^w-J Eda^Ta-6J Chr Y^B6-Sxr/EiJ	Cryopreserved - Ready for recovery

007694	B6(Cg)-Cd79b^tm168Mnz/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted insertion are viable and fertile and do not display any gross physical or behavioral abnormalities. This strain carries a targeted insertion of an 18 bp I-SceI (S. cerevisiae) endonuclease recognition site in intron 2 of the gene. Infection of B lymphocytes with a retrovirus encoding for the I-SceI meganuclease produces Igh (immunoglobulin heavy chain )-IgB (Cd79b) chromosomal translocations with breakpoints at the I-SceI sequence on the mutant allele.
007693	B6(Cg)-Myc^tm37Mnz/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted insertion are viable and fertile and do not display any gross physical or behavioral abnormalities. This strain carries a targeted insertion of an 18 bp I-SceI (S. cerevisiae) endonuclease recognition site in intron 1 of the gene. Infection of B lymphocytes with a retrovirus encoding for the I-SceI meganuclease produces Igh (immunoglobulin heavy chain )-Myc chromosomal translocations with breakpoints at the I-SceI sequence on the mutant allele.
007692	B6(Cg)-Myc^tm39Mnz/J	Cryopreserved - Ready for recovery
	In B lymphocytes, the targeted mutant allele does not translocate to the Igh (immunoglobulin heavy chain) locus upon stimulation of splenocytes with LPS (lipopolysaccharide) and IL4 (interleukin 4). Homozygous animals are not viable (time of death not established) and heterozygous females produce small litters.
008149	B6(Cg)-Snord116^tm1.1Uta/J	Cryopreserved - Ready for recovery
	Mice homozygous for this Snord116del (1-loxP or knockout) allele are viable and fertile. As the Snord116 gene cluster is imprinted and expressed only from the paternal allele, mice with paternal inheritance of the deletion lack expression of the targeted Snord116 small nucleolar RNAs (snoRNAs) gene cluster in brain tissues. Similarly, paternal transmission of the mutant allele is required to obtain the mutant phenotype in offspring. Affected heterozygotes (paternal deleted/maternal wildtype) recapitulate a subset of Prader-Willi syndrome (PWS) characteristics, including early-onset postnatal growth retardation, delayed sexual maturation, increased anxiety, motor learning deficit and hyperphagia (but not obesity). Other reported abnormalities include altered metabolic fuel usage, prolonged meal time, and increased levels of circulating ghrelin. These Snord116del mice may be useful in studying growth and feeding regulation, mechanisms of obesity, and pa ..... For more information please see the full phenotype on the strain data sheet
008118	B6(Cg)-Snord116^tm1Uta/J	Cryopreserved - Ready for recovery
	Mice homozygous for this 2-loxP (floxed) allele are viable and fertile, with loxP sites flanking the Snord116 small nucleolar RNAs (snoRNAs) gene cluster. When bred to mice that express Cre recombinase, the resulting offspring will have this gene cluster deleted in the cre-expressing tissue(s). Because the Snord116 gene cluster is imprinted and only expressed from the paternal allele, breeding 2-loxP males with cre-expressing females may be required to generate deleted offspring with the knockout phenotype. The donating investigator reports that the distance between the two loxP sites (~140 kb) may reduce the recombination efficiency in somatic cells. As deletions of the Snord116 cluster are associated with Prader-Willi syndrome (PWS), mice carrying the 2-loxP (floxed) allele may be useful in generating conditional mutations for studying the role of Snord116 in growth and feeding regulation, mechanisms of obesity, and patho ..... For more information please see the full phenotype on the strain data sheet
005565	B6(V)-chtl^2J/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for this spontaneous recessive mutation are recognized by a diluted coat color that appears chocolate brown. This color dilution also lightens the eyes, feet, ears, and tail of affected animals.
003625	B6.C-H2-Ab1^bm12/KhEg-Mc1r^e-J/J	Cryopreserved - Ready for recovery

006559	B6.C-H2-K^bm1/ByBir-Gusb^mps/BrkJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Gusb^mps allele exhibit skeletal dysplasia as well as cognitive, hearing and visual deficits. Lifespan of the homozygotes is approximately six months. Homozygotes lack the lysomal enzyme, beta-glucoronidase, and, as a result, glycosaminoglycans accumulate in tissues throughout the body. Female homozygotes rarely conceive and do not lactate. This strain is a model for the human lysomal storage disease, mucopolysaccharidosis type VII.
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
008300	B6.Cg-Tg(CMV-Klc1)73Gsn/J	Cryopreserved - Ready for recovery
	The transgene in this strain encodes a protein in which a TAP (Tandem Affinity Purification) moiety is fused to the carboxyl-terminal end of murine kinesin light chain 1. Expression is driven by the CMV-IE promoter from pCDNA3. Female pups may be smaller than male pups, but no overt phenotype has been associated with this transgene. Levels of kinesin light chain 1 protein expression in the brain are higher in this line (line 73) than in mice from line 90 (see Stock No. 008301). Expression is seen in both brain and spinal cord. This strain may be useful in biochemical studies of kinesin function and axonal transport.
008301	B6.Cg-Tg(CMV-Klc1)90Gsn/J	Cryopreserved - Ready for recovery
	Hemizygotes are viable and fertile. Female pups may be smaller than male pups, but no overt phenotype has been associated with this transgene. Levels of kinesin light chain 1 protein expression are lower in the brains of mice from this line (line 90) than in mice from line 73 (see Stock No. 008300). Expression is seen in both brain and spinal cord. This strain may be useful in studies of axonal transport.
004852	B6;129-Crb1^rd8/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Crb1^rd8 (Crb1^nmf144) entry.
014651	B6;CBA-Tg(Thy1-spH)21Vnmu/J	Cryopreserved - Ready for recovery
	These transgenic mice express spH, the pH-sensitive variant of the green fluorescent protein (superecliptic pHluorin) fused to the mouse synaptic vesicle-associated membrane protein 2 (Vamp2), under the control of the mouse thymus cell antigen 1 (Thy1) promoter. In founder line spH21, transgene expression is detected in glutamatergic or excitatory neurons of many brain regions, including the cortex and the hippocampus. Synaptic activity, as determined by fluorescence, is detectable starting at approximately 14 days in vitro in cultured hippocampal neurons.
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.
002432	B6J x B6.C-H2-K^bm1/ByJ-Cdh23^v-J/J	Cryopreserved - Ready for recovery
	Mice homozygous for the waltzer Jackson spontaneous mutation (Cdh23^v-J) exhibit the circling, head-tossing, deafness, and hyperactivity typical of circling mutants. Homozygous mutant mice are very similar to other waltzer mutants (Cdh23^v and Cdh23^v-2J). Most homozygotes are deaf from birth. Abnormalities of the inner ear include degeneration of the organ of Corti, spiral ganglion, stria vascularis, and saccular macula. Double heterozygotes with shaker-1 (Cdh23^v/+ Myo7a^sh1/+) become deaf by 3 to 6 months of age. Double heterozygotes show degeneration in the organ of Corti, stria vascularis, and spiral ganglion similar to that of Cdh23^v-J homozygotes, but less severe and with much later onset. Viability and breeding ability are somewhat reduced.
001274	BALB/c-Krt71^Ca-9J/J	Cryopreserved - Ready for recovery

005852	BALB/c-Phex^Hyp-Duk/J	Cryopreserved - Ready for recovery
	This mutant offers a model for X-linked dominant hypophosphatemic rickets. The serum phosphorus (2.95 mg/dL) in hemizygous males is lower than that found in hypophosphatemia, hypophosphatemia 2 Jackson, or gyro hemizygous males. The skeletal defects include shortened long bones and craniofacial defects and hemizygous males have cochlear degeneration and a heightened auditory brainstem response threshold, higher than that in other Phex mutants. The heightened ABR threshold is dependent upon a modifier that is absent in BALB/cByJ. Consistent with vestibular dysfunction, approximately half of the hemizygous males and some of the heterozygous females display circling behavior, and in hemizygous males head bobbing or unstable gait have also been noted. Hemizygous males are mildly growth retarded, with a squared and shortened body, and shortened hind limbs and tail. While some heterozygous females display circling and growth retardation, not all do and they are more difficult to d ..... For more information please see the full phenotype on the strain data sheet
004317	BALB/cBy-Gulo^sfx/J	Cryopreserved - Ready for recovery
	The sfx phenotype is not apparent until shortly after weaning age. By 26-30 days of age, homozygotes display decreased mobility, diminished weight gain, and more scruffy appearance than their heterozygous or wildtype siblings. Dissection reveals smaller spleen and thymus and increased kidney and brain weights. A reduction in bone mass is accompanied by a paucity of mature osteoblasts on bone surfaces, a subtle reduction of chrondrocytes in epiphyseal-plate columns, growth plate arrest in long bones, and other architectural abnormalities. Bone analysis shows sponteneous fractures both in large bones and smaller ones such as metacarpals. Serum analysis shows a decrease in calcium, inorganic phosphate, alkaline phosphatase, osteocalcin, and insulin-like growth factor 1. These homozygotes also have a reduction in the number of both the red and white blood cells. Homozygotes are fragile and must be handled with great care. (Beamer et al., 2000.)
005348	BALB/cByJ Agtpbp1^pcd-3J-Bmp5^cfe-se6J/GrsrJ	Cryopreserved - Ready for recovery
	The ear pinnae of homozygotes are ragged around the edges, yet uniform, and smaller than normal.
003922	BALB/cByJ-Clcn1^adr-mto2J jgl/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the jagged tail-like (jgl) mutation are easily characterized by their kinked tails that are recognizable by 10 days of age. Full body X-rays revealed exostosis of the vertebrae near the tail tip and in the phalanges of all 4 feet and abnormal vertebral bodies were also reported in two 5 month old homozygotes. Both female and male reproductive organs are smaller than normal with the males showing severe atrophy of the seminiferous tubules and hyperplasia of Leydig cells. Although most homozygotes are not fertile, a few have produced litters. Homozygotes also have atrophic spleens, particularly the white pulp.
010637	BALB/cByJ-oar/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the oarleg mutation display improper orientation of one or both hind limbs and when lifted by the tail they point their toes straight outward and hold the hind limbs stiffly in a manner that makes the appendage resemble an oar. An abnormal gait appears by approximately 2 weeks of age. Despite this, no obvious aberrations of the skeleton have been found and these mutants can orient and swim in water.
002026	BALB/cHeA-Foxe3^dyl/J	Cryopreserved - Ready for recovery
	Dysgenetic lens (Foxe3^dyl) was originally characterized as an autosomal recessive mouse mutant but Foxe3 haploinsufficiency can also yield a similar phenotype characterized by defective lens development and cataracts. Homozygotes are viable and fertile. The most prominent abnormality is the irregular shape and reduced size of the lens. The pupil is also smaller and exhibits abnormal reactivity. The major morphological hallmark of homozygous Foxe3^dyl mice is the persistent attachment of the lens to the corneal epithelium. The iris can also be fused with the lens but the retina remains unaffected. The lens contains fewer secondary fibers but when present, these fibers are very disorganized and the tissue contains large vacuoles. The developing lens initially forms properly as the lens placode is induced within the anterior neural ectoderm but around embryonic day 10 the mutant lens vesicle does not completely close and detach from the ..... For more information please see the full phenotype on the strain data sheet
005226	BALB/cJ-Mbp^shi-J/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the shiverer Jackson mutation can be identified at 12 days of age by a generalized tremor during locomotion and the severity of the phenotype progresses with age and includes a loss of coordination of the hindlimbs. Deficiency of myelin from the central nervous system has been found at 7 weeks of age, the earliest time-point assessed.
007971	BALB/cJ-Ppp1r13l^wa3-J/J	Cryopreserved - Ready for recovery
	Homozygotes have a coat that is sparse but not wavy. They are born with their eyelids open and develop vascular corneas. They also develop early-onset cardiomyopathy, which leads to congestive heart failure. Female homozygotes have not successfully bred and male homozygotes have significantly reduced fertility, producing one or two litters in their lifetime at best.
004546	BALB/cJ-Trf^hpx/JUthHmsJ	Cryopreserved - Ready for recovery
	Mice homozygous for the hpx allele exhibit refractory iron-deficient, hypochromic, microcytic anemia with iron-loading in the liver, pancreas, heart and brain. Homozygotes usually die within 2 weeks after birth with hypochromic anemia and very low serum transferrin. The mutant condition is evident in 13-day embryos, which have severe transferrin deficiency and hepatic iron loading. Heterozygotes have normal blood values but half normal concentrations of transferrin and show minor increases in iron stores. The condition closely resembles human atransferrinemia.
013715	BALB/cJ-psds1l/GrsrJ	Cryopreserved - Ready for recovery
	psds1l homozygotes can be identified when their first coat grows in by the dirty white coat color and sparse hair. Hair is usually absent from around the eyes, which often have a crusty growth around them, and hair loss is commonly found around the cervical area.
006019	BALB/cJ-ssl/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the small swaying lethal mutation are smaller than control littermates and ataxic such that they lean and fall over on their side. This is evident by 12 to 15 days of age. They do not survive beyond 4 to 5 weeks of age.
005736	BKS(Cg)-calre/GrsrJ	Cryopreserved - Ready for recovery
	The curly coat of this spontaneous homozygous mutant mouse (BKS.Cg m +/+ Lepr^db /J-calre/J) is recognized at 10-12 days of age when hair is fully covering the body. At 2 weeks of age the coat of homozygous mutants looks very curly, and the mutants also have curly vibrissae. After several weeks, the curly phenotype is reduced; the hair becomes fuzzy in appearance, and the vibrissae straighten out and appear normal. Some mutant mice have no whiskers at wean age. Also, in older homozygous and heterzygous mice more whiskers are lost, and homozygous mutants lose more hair as they age. Homozygous mutant mice live normal life spans and breed normally.
006816	BXA7/Pgn-Slc26a4^pdsm/J	Cryopreserved - Ready for recovery
	Mice homozygous for the pdsm mutation display head bobbing, circling, and occasional head tilt, evident by 3 weeks of age. The inner ear defects include diminished or absent otoconia, hair cells and spiral ganglion cells, malformed tectorial membrane, a reduction in the number of cochlear turns, degeneration of the organ of Corti, and displacement of Reissner's membrane resulting in enlarged scala media. Serum chemistry and histology failed to detect any signs of hypothyroidism.
000509	C3.Cg-Lyst^bg-2J/J	Cryopreserved - Ready for recovery
	Mice homozygous for the beige 2J spontaneous mutation (Lyst^bg-2J) display characteristics very similar to the original beige mutation (Lyst^bg). The mouse phenotype closely resembles Chediak-Higashi syndrome in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to a ..... For more information please see the full phenotype on the strain data sheet
005327	C3.Cg-a Zfp191^hmcns/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the hmcns mutation have diminished myelin in the central nervous system, although peripheral axons appear normally myelinated. There are abundant late-stage process-extending oligodendrocytes, but these fail to myelinate the central nervous system and have diminished expression of an array of myelin-related genes. Homozygotes can be identified by approximately 14 days of age by a tremor and tonic seizures. At 14 days of age the brain and spinal cord appear smaller than normal and lack white matter. Most homozygotes die by 25 days of age.
001276	C3H/HeJ-Atp2b2^dfw/J	Cryopreserved - Ready for recovery
	Mice homozygous for the deaf waddler spontaneous mutation (Atp2b2^dfw) are deaf, walk with a hesitant, wobbly gait, and bob their heads. Both sexes are fertile.
004965	C3H/HeJ-Clic5^jbg/J	Cryopreserved - Ready for recovery

000784	C3H/HeJ-Fasl^gld/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Fasl^gld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasl^lpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks.
008676	C3H/HeJ-Hmx1^mpe/J	Cryopreserved - Ready for recovery
	Mice homozygous for the misplaced ears mutation have low set, laterally protruding ears. Fewer homozygotes than standard Mendelian genetics predicts are produced from heterozygous intercrosses. This strain is a model for oculo-auricular syndrome.
003161	C3H/HeJ-Hps3^coa-6J/J	Cryopreserved - Ready for recovery

000627	C3H/HeJ-Kit^W-x/J	Cryopreserved - Ready for recovery

004806	C3H/HeJ-Mfs/J	Cryopreserved - Ready for recovery
	Both male and female mice homozygous or heterozygous for the Mfs mutation have a striped pattern in their coats that is visible by 3 weeks of age.
000809	C3H/HeJ-Mgrn1^md-2J/J	Cryopreserved - Ready for recovery

000223	C3H/HeJ-Mgrn1^md/J	Cryopreserved - Ready for recovery

000513	C3H/HeJ-Oca2^p-J/J	Cryopreserved - Ready for recovery
	Oca2^p-J/Oca2^p-J mice exhibit significant dilution of coat color with pink eyes, a phenotype similar to that produced by Oca2^p/Oca2^p. The Oca2^p-J mutation is a partial deletion of the gene that completely ablates Oca2^p function (Oakey et al. 1996).
007782	C3H/HeJ-Pofut1^cax/J	Cryopreserved - Ready for recovery

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.
003128	C3H/HeJ-Slc4a1^wan/J	Cryopreserved - Ready for recovery
	Mice homozygous for the wan mutation are extremely pale at birth with very reduced red blood cell, hematocrit, and hemoglobin counts, and die by 72 hours after birth. At embryonic day 15 fetal red blood cell counts are decreased, there are fewer than normal reticulocytes and a considerable number of spherocytes. Newborns have spherocytic red blood cells but no reticulocytes in peripheral blood.
001294	C3H/HeJ-Tyr^c-a/J	Cryopreserved - Ready for recovery

001588	C3H/HeJ-jd/J	Cryopreserved - Ready for recovery

001544	C3H/HeJ-ruf/J	Cryopreserved - Ready for recovery

004407	C3H/HeJCrl-Kcnq1^vtg-2J/J	Cryopreserved - Ready for recovery
	Kcnq1^vtg-2J homozygotes exhibit circling and head-tossing behavior. Both clickbox and acoustic brainstem response (ABR) testing revealed that they are deaf by 8 weeks of age, while age matched heterozygotes have good hearing. This mutation was shown to be an allele of Kcnq1 by complementation testing with the original vertigo mutation, Kcnq1^vtg.
000120	C3H/HeSn-Rab27a^ash/J	Cryopreserved - Ready for recovery
	Ashen mice have a lightened coat color that is gray on a non-agouti background similar to that of dilute (Myo5a^d) or leaden (ln) mutants. Lane and Womack reported that on an agouti background the yellow pigment is more dilute in ashen mice resulting in a grayer agouti than that found in dilute or leaden mice, but Wu et al. subsequently reported that dilute and ashen mice have identical degrees of coat color dilution. This pigment dilution results from defective trafficking of melanosomes that are normally found throughout the dendrites of melanocytes. Similar to that seen in leaden mutants, ashen melanosomes are clumped around the nucleus and sparse in the dendrites where normally they are released. Melanosome trafficking from the melanocyte cell body to the ends of the dendrites results from a microtubule-based bidirectional transport. MYO5A is essential for retaining the melanosomes in the ends of the dendrites and preventing their retrograde transport back t ..... For more information please see the full phenotype on the strain data sheet
000775	C3H/HeSn-bc^3J/J	Cryopreserved - Ready for recovery

001431	C3H/HeSn-ocd/J	Cryopreserved - Ready for recovery

001272	C3H/HeSnJ-A^hvy/J	Cryopreserved - Ready for recovery
	The dominant A^hvy allele has the broadest array of expressivity of any of the agouti alleles. Carriers' coat colors range from mostly yellow to almost completely black and the color is usually patchy or striped. Mice with coats on the yellow end of the spectrum tend to develop obesity while those with more black coats do not. Homozygotes are viable and fertile, and are more likely to have yellow or mostly yellow coats than are heterozygotes. A^hvy is recessive to A^y, dominant to a and a^e, and results in an increase in the yellow pigment in the belly coat of A^hvy/a^t and A^hvy/A^w mice.
004683	C3H/HeSnJ-Slc12a6^gaxp/GrsrJ	Cryopreserved - Ready for recovery
	Giant axonopathy (gaxp) is an autosomal recessive mutation that arose spontaneously in the Mouse Mutant Resource colony at The Jackson Laboratory. It occurred in a strain bearing another mutation on the C3H/HeDiSnJ background. Homozygous mutants exhibit ataxia of the hind legs with a slight side - to - side wobble. Histopathologic studies showed pale staining, vacuolated structures measuring between 20 and 150 micra in deep cerebellar nuclei, pons, lateral vestibular nuclei and dorsal root and trigeminal ganglia. Ultrastructurally these structures were often bounded by a few layers of myelin, suggesting that they are swollen axons. gaxp has been mapped to Chromosome 2. The most likely gene order places the mutation between D2Mit128 and D2Mit102 in 174 meioses tested.
001310	C3H/HeSnJ-Slc7a11^sut/J	Cryopreserved - Ready for recovery

002261	C3H/HeSnJ-Sox18^Ra-J/J	Cryopreserved - Ready for recovery
	The Sox18^Ra and Sox18^Ra-J alleles cause a less severe phenotype than the Sox18^Ra-Op allele. The Sox18^Ra and Sox18^Ra-J alleles are similar mutations and give a very similar phenotype. The Sox18^Ra allele has been more broadly described in the literature and will be covered here. Heterozygotes are viable and fertile. Heterozygotes have developmentally retarded sinus hair growth apparent at embryonic day 16.5 and retarded development of pelage follicles apparent by embryonic day 17.5. Thus, heterozygotes have slightly shorter vibrissae evident at birth, and can be distinguished at three days of age by their pink skin which, due to the abnormally sparse development of the coat, fails to darken like that of wildtype siblings. A paucity of fur is apparent by nine days of age and persists throughout life. Compared with the wild type pelage, Sox18^Ra/+ coats have l ..... For more information please see the full phenotype on the strain data sheet
001767	C3H/HeSnJ-wl^vmd/J	Cryopreserved - Ready for recovery
	Mice homozygous for the vestibulomotor degeneration spontaneous mutation (wl^vmd) can be identified at 20 days of age by their small size, shaky behavior, ungroomed coat, and emaciation. Homozygous mutant mice tend to sit hunched with rear feet and limbs tucked in towards the body and exhibit a generalized tremor. When startled, they jump sideways. They clasp their hind feet when picked up by the tail. Most mutants die by 30 days of age, probably from inability to feed and starvation. There is no apparent difference between the wabbler lethal (wl) and vestibulomotor degeneration mutant phenotypes.
001576	C3HeB/FeJ-Atp7b^tx-J/J	Cryopreserved - Ready for recovery

004951	C3HeB/FeJ-Cacnb4^lh-3J/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for lethargic 3 Jackson are recognizable at 14 days of age. They exhibit a behavior characteristic of lethargic with a wobbly gait resembling an unsteady wide legged shuffle. Some Cacnb4^lh-3J homozygotes also have a stargazing phenotype, but seizures have not been reported. The homozygotes are smaller than their wildtype littermates but live a normal lifespan. Both sexes may breed but they produce smaller litters or stop breeding earlier than heterozygous sibs.
006045	C3HeB/FeJ-Eif3c^Xsl/GrsrJ	Cryopreserved - Ready for recovery
	Xsl heterozygotes are smaller than normal at 3 weeks of age but catch up to normal size by 6 weeks of age. They have a belly spot and extra digits at the thumb position on one or both front paws.
001292	C3HeB/FeJ-vs/J	Cryopreserved - Ready for recovery

001002	C57BL/10SnJ-Tyr^c-11J/J	Cryopreserved - Ready for recovery

008825	C57BL/6-Aicda^tm3.1Mnz/J	Cryopreserved - Ready for recovery
	These mice carry a serine 38 to alanine (S38A) phosphorylation site mutation in exon 2 of the activation-induced cytidine deaminase gene. Homozygotes are developmentally normal. B cells are impaired but not ablated in their ability to undergo class switch recombination and somatic hypermutation. These mice also have larger germinal centers in their lymph nodes than wildtype animals.
005684	C57BL/6-Ap3b2^tm1Bur/J	Cryopreserved - Ready for recovery
	Homozygotes are viable with diminished fertility. A truncated transcript encoding of the first 120 amino acids followed by 63 extra residues is expressed in brain tissue. Antibodies against C terminal epitopes show no endogenous protein. Homozygous mice have complex neurological and behavioral impairments including tonic-clonic seizures and increased locomotor activity after handling. Compared to wildtype, mutant mice have significantly diminished adaptor complex 3 (AP-3) in dendritic processes and 62% less presynaptic zinc storage in the CA1 stratum oriens (total 25% decrease throughout the brain). The synaptic vesicle targeting of membrane proteins involved in zinc uptake (ZnT3 and ClC-3) is compromised. This mutant may be useful in studies of neuron biology, specifically membrane protein assembly and storage in synaptic vesicles.
007662	C57BL/6-Arc^tm1Stl/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. A destabilized form of GFP (d2EGFP) is expressed under the control of the endogenous Arc promoter which is activated by neuronal stimulation in forebrain regions. The half-life of EGFP expression is shortened to approximately two hours which is comparable to the decay time of ARC protein. Homozygous mice have a reduced orientation specificity in the visual cortex. The loss of Arc mRNA expression in homozygous mice was verified by RT-PCR analysis of brain total RNA preparations. This strain may be useful in studies of cortical functions.
012371	C57BL/6-Bdkrb2/Bdkrb1^tm1Mki/J	Cryopreserved - Ready for recovery
	Mice homozygous for the targeted mutation, commonly referred to as B1RB2R -/-, are viable, fertile and display no major defects. At 4 months of age non-manipulated B1RB2R -/- mice exhibit no significant differences in blood pressure or kidney function when compared to Bdkrb2 deficient mice (Stock No. 006860). Fasted B1RB2R -/- mice exhibit significantly lower levels of plasma nitrite/nitrate compared to Bdkrb2 deficient mice. Post-ischemic B1RB2R -/- mice exhibit significantly higher plasma levels of urea nitrogen and creatinine, higher levels of oxidative nuclear and mitochondrial DNA modification, and increased rates of apoptosis and mortality than either wildtype or Bdkrb2 deficient mice. Histological evaluation of the kidney indicates that post ischemic B1RB2R -/- mice exhibit more severe histological changes in the renal proximal tubules than either wildtype or Bdkrb2 deficient mice (Kakoki, et al, 2007). This Bdkrb1/Bdkrb2 targeted ..... For more information please see the full phenotype on the strain data sheet
006575	C57BL/6-Camk2a^tm1Vyb/J	Cryopreserved - Ready for recovery
	Mice homozygous for this "falpha-CaMKII" allele are viable and fertile with no reported neurological abnormalities. These mutant mice have loxP sites flanking exon 2 of the endogenous gene. When bred to Cre-recombinase expressing mice, exon 2 is deleted in the resulting offspring dependent on the tissue specificity of the promoter of the cre transgene. For example, when crossed with transgenic mice expressing Cre-recombinase in hippocampal CA3 pyramidal cells (see Stock No. 006474), the resulting offspring show altered neurotransmitter release. These "floxed" mice may be useful for neurological studies such as calcium/calmodulin-dependent protein kinase activity.
006940	C57BL/6-Cd22^tm1Lam /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 expression of the targeted gene's protein product is detected on the cell surface, as determined by flow cytometry analysis of splenocytes from homozygotes. Mutants exhibit a reduction in recirculating mature B cells in the bone marrow and fewer transitional B cells in the spleen. Splenic and peripheral B cells express lower levels of membrane bound IgM than wildtype. B cell activation is abnormal in mutant mice, with enhanced Ca²⁺ mobilization after stimulation. Lipopolysaccaharide (LPS) challenge results in an increased proliferative response. CD22 deficient B cells have a shorter than average lifespan when compared to wildtype B cells. T-cell independent immune responses are impaired. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, B cell development and T cell inde ..... For more information please see the full phenotype on the strain data sheet
006468	C57BL/6-Chrm1^tm1Stl/J	Cryopreserved - Ready for recovery
	Homozygotes are viable and fertile with complete absence of the wildtype allele mRNA in forebrain tissues. Mice homozygous for this M1 muscarinic acetylcholine receptor deficiency have elevated dopaminergic transmission in the striatum, significantly increased locomotor activity, increased response to the stimulatory effects of amphetamine. These mutant mice may be useful in neurological studies, including the regulation of dopaminergic transmission by the M1 receptor and M1 dysfunction in psychiatric disorders.
009155	C57BL/6-Cldn6^tm1(cre)Dkwu/J	Cryopreserved - Ready for recovery
	This targeted strain expresses Cre under the control of the claudin 6 promoter. When bred to a floxed reporter strain, broad expression throughout the epiblast is seen at E6.5. By E9.5, expression is restricted to the endoderm-derived structures such as the oral cavity, digestive tract, and lung. In addition, it is expressed in mesonephros and otic vesicle. Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities.
008591	C57BL/6-Cxcr7^tm1Litt/J	Cryopreserved - Ready for recovery

010683	C57BL/6-Enam^tm1.1Jcch/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Enam-null/lacZ knock-in allele (Enam^- or Enam^lacZ) are viable and fertile, with a nuclear-localized β-galactosidase (NLS lacZ) translation initiation site and coding region replacing the Enam translation initiation site and 5'-coding region. This abolishes endogenous gene function; no enamelin protein is observed in homozygous mice. Under control of the upstream promoter/enhancer elements, lacZ expression is directed to ameloblasts (the enamel-forming cells in developing teeth) during the secretory stage of dental enamel formation. Enam-deficiency results in improper tooth enamel matrix organization/mineralization, altered gross tooth morphology, and premature tooth structural loss. Homozygous mice exhibit no true enamel covering the dentin and a high degree of occlusal wearing (even when fed moistened chow). Heterozygous mice have a milder phenotype primarily evident in the mandibular incisors. These Enam^lacZ ..... For more information please see the full phenotype on the strain data sheet
007895	C57BL/6-Fas^tm1Cgn/J	Cryopreserved - Ready for recovery
	Mice homozygous for this "Fas^fl" conditional allele are viable and fertile, with loxP sites flanking exon 9 of the targeted gene. When bred to mice that express Cre recombinase, exon 9 (which encodes the death domain) is deleted in the cre-expressing tissues in the resulting offspring. These Fas^fl mice may be useful in generating conditional mutations for studying many aspects of immune function. For example, when Fas^fl mice are crossed to a strain expressing Cre recombinase in B lineage cells (see Stock No. 004126 or 006785 ), this mutant mouse strain may be useful in studies of lymphoproliferative disorder. Similarly, when Fas^fl mice are crossed to an interferon inducible strain with widespread Cre recombinase expression (see Stock No. 003556, ..... For more information please see the full phenotype on the strain data sheet
012637	C57BL/6-Gt(ROSA)26Sor^{tm5(Map3k14)Rsky}/J	Cryopreserved - Ready for recovery
	Mice homozygous for the NIK-wt allele are viable and fertile, with a loxP-flanked Neo-STOP cassette preventing transcription of the downstream bicistronic sequences (NIK [a wt form of the mouse NF-kappaB inducing kinase] and EGFP). When bred to mice that express Cre recombinase, offspring will have the STOP cassette deleted and subsequent expression of the NIK-wt molecule and EGFP fluorescence in the cre-expressing cells. Expression of NIK-wt leads to overexpression of NIK in mouse B lymphocytes, amplifying alternative NF-kappaB activation and peripheral B cell numbers, in a B cell-activating factor of the TNF family receptor (BAFF-R) dependent manner. BAFF-R binding is required to sustain the NIK p100 subunit processing needed for B cell survival, and is implicated in human multiple myeloma. Of note, breeding these mice to an FLP-expressing strain will result in removal of the frt-flanked IRES-EGFP cassette. When bred to a strain expre ..... For more information please see the full phenotype on the strain data sheet
012638	C57BL/6-Gt(ROSA)26Sor^{tm6(Map3k14)Rsky}*/J	Cryopreserved - Ready for recovery
	Mice homozygous for the NIK-deltaT3 allele are viable and fertile, with a loxP-flanked Neo-STOP cassette preventing transcription of the downstream bicistronic sequences (NIKdeltaT3 [a constitutively active form of the mouse NF-kappaB inducing kinase] and EGFP). When bred to mice that express Cre recombinase, offspring will have the STOP cassette deleted and subsequent expression of the NIKdeltaT3 molecule and EGFP fluorescence in the cre-expressing cells. Expression of NIK-deltaT3 leads to uncoupling NIK from tumor necrosis factor receptor-associated factor 3 (TRAF3)-mediated control causing maximal p100 processing and dramatic hyperplasia of B cell-activating factor of the TNF family receptor (BAFF-R)-independent B cells. BAFF-R binding is required to sustain the NIK p100 subunit processing needed for B cell survival, as implicated in human multiple myeloma. Of note, breeding these mice to an FLP-expressing strain will result in removal of the > ..... For more information please see the full phenotype on the strain data sheet
008711	C57BL/6-H2-T3^tm1Luc/J	Cryopreserved - Ready for recovery
	The mouse thymus leukemia (TL) antigen is a nonclassical MHC class I molecule encoded by a locus within the MHC complex harboring two genes; H2-T3 and H2-T18. TL binds with high affinity to the CD8αα molecule expressed on the vast majority of intraepithelial lymphocytes (IEL), and the interaction of CD8αα with TL is important for lymphocyte regulation in the intestine. The C57BL/6 genetic background normally has the functional H2-T3^d allele and a mutant H2-T18^b allele known to result in no expression on the surface of intestinal epithelial cells (IEC). Because these mutant mice harbor a targeted mutation of the H2-T3 gene that abolishes gene function, expression of TL protein (antibody staining) and RNA (RT-PCR) from either locus is absent in IEC and small/large intestine, respectively. These TL-deficient mice may be useful in studying thymus leukemia (TL) antigen-deficiency on CD8αα intraepith ..... For more information please see the full phenotype on the strain data sheet
002400	C57BL/6-Igkc^tm1Cgn/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Igkc^tm1Cgn targeted mutation are viable and fertile. The number of B cells expressing l chain is increased 2-fold in heterozygotes and 7-fold in homozygotes.
010501	C57BL/6-Itga4^tm1Mshi/J	Cryopreserved - Ready for recovery
	Mice homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Lymphocytes exhibit increased basal adhesiveness to VCAM1 and MAdCAM1 under physiological conditions as well as reduced transmigration across VCAM1 and MAdCAM1 substrates and endothelial monolayers under shear stress. Homing of mutant lymphocytes to the gut is reduced by approximately 50%. In addition, fewer lymphocytes are found in the gut and Peyer's Patches are smaller in size than wild-type. This mutant mouse strain may be useful in studies of leukocyte migration and homing.
007707	C57BL/6-Itgb7^tm1Mshi/J	Cryopreserved - Ready for recovery
	Mice homozygous for this β₇ (D146A) targeted mutation are viable and fertile. DNA sequencing confirms an aspartate (D) to alanine (A) substitution at position 146 of the targeted β₇ integrin gene. As such, homozygotes have a mutant ADMIDAS (adjacent to metal ion-dependent adhesion site) cation binding/exchange site in the β₇ integrin head (A-domain). The resulting imbalance between the non-adhesive and adhesive states of leukocyte integrins skews toward a persistently adhesive state. Homozygous mutants exhibit impaired leukocyte migration, perturbed lymphocyte trafficking in the gut, and reduced T- and B-cell numbers in small/large bowel and gut-associated lymphoid tissues (less T-cells in Peyer's patches (PP), fewer intraepithelial lymphocyte (IEL) and lamina propria lymphocyte (LPL) compartments in the small intestine; and less B-cells in PP and the large intestine). In addition, CD4⁺CD45RB^high T cells isolated fro ..... For more information please see the full phenotype on the strain data sheet
010684	C57BL/6-Klk4^tm1.1Jpsi/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Klk4-null/lacZ knock-in allele (Klk4^- or Klk4^lacZ) are viable and fertile, with a nuclear-localized β-galactosidase (NLS lacZ) translation initiation site and coding region replacing the Klk4 translation initiation site and coding region. This abolishes endogenous gene function. Under control of the upstream promoter/enhancer elements, lacZ expression is directed to ameloblasts (the enamel-forming cells in developing teeth) during the transition and maturation stages of dental enamel formation. Klk4-deficiency results in improper dental enamel matrix biomineralization, altered gross tooth morphology, and premature tooth decay. Homozygous mice exhibit malformed enamel that is rapidly abraded after weaning (even when fed moistened chow) and a tendency for all teeth to fracture at points of contact. Heterozygous mice appear indistinguishable from wildtype mice. These Klk4^lacZ mice may be useful for studyi ..... For more information please see the full phenotype on the strain data sheet
008304	C57BL/6-Nras^tm1Tyj/J	Cryopreserved - Ready for recovery
	This targeted mutant strain carries a loxP-flanked stop element in exon 1 and a G12D activating mutation in exon 2 of the neuroblastoma ras oncogene (Nras). This mutation functions as a null allele and has no apparent phenotype. Homozygotes are viable. Cre mediated excision of the floxed stop element causes a significant increase in GTP-bound N-Ras production. This conditional mutant strain may be helpful in further studies of this oncogene. For example, when crossed to a strain expressing Cre recombinase in epiblast and ectoderm-derived tissues (see Stock No. 003755), this mutant mouse strain may be useful in studies of the role of NRAS in leukemogenesis. When crossed to a strain expressing interferon-induced Cre recombinase (see Stock No. 003556), this mutant mouse strain may be useful in studies of leukemia.
011068	C57BL/6-Pmaip1^tm1Ast/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 gene product (mRNA) is detected by RT-PCR analysis of irradiated thymocytes from homozygotes and Northern blot analysis of testis, lung and spleen from homozygotes. Thymocytes from homozygous mice exhibit increased resistance to DNA-damage induced apoptosis after treatment by etoposide. NK cells from homozygotes survive better than wildtype controls when cultured without IL-15.
006581	C57BL/6-Ppp3r1^tm1Stl/J	Cryopreserved - Ready for recovery
	Mice homozygous for this "fCNB1" mutant allele are viable and fertile with no reported neurological abnormalities. These mutant mice have loxP sites flanking exons 2-4 of the endogenous gene. When bred to transgenic mice expressing Cre recombinase, exons 2-4 are deleted in the resulting offspring in only those tissues expressing cre. For example, when crossed with transgenic mice expressing Cre recombinase specifically in the forebrain (similar to Stock No. 005359), the resulting offspring show abnormalities that are strikingly similar to those described for schizophrenia. These "floxed" mice may be useful in studies of calcineurin function in T cells (via NFAT transcription of cytokine genes) and in the central nervous system in, for example, neurite extension, synaptic plasticity, learning and memory, and schizophrenia pathogenesis.
010711	C57BL/6-Ptrh2^tm1Eruo/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. This mutant mouse strain may be useful in generating conditional mutations to study anoikis /apoptosis.
010540	C57BL/6-Rev3l^tm1Rsky/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. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. Excision of the floxed fragment in B cells results in chromosomal instability, impaired B cell proliferation, reduced class switch recombination, reduced frequency of somatic mutations and increased frequency of DNA breaks. This mutant mouse strain is useful in studies of genome instability, DNA break repair and class switch recombination. For example, when crossed to a strain expressing Cre recombinase in Mature B cells (see Stock No. 006368), this mutant mouse strain may be useful in studies of class switch recombination and DNA break repair.
008158	C57BL/6-Serpinb9^tm1Arp/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 gene product (mRNA) is detected by RT-PCR analysis of myeloid and lymphoid cells. After experimental viral infection, homozygous mice have lower (five to nine-fold reduction) numbers of virus specific cytotoxic T lymphocytes (CTLs) and increased apoptosis of virus specific CD8 T cells when compared to wildtype controls. Mutant mice have impaired Lymphocytic Choriomeningitis virus (LCMV) infection clearance. Granzyme A and granzyme B specific activity is reduced in cytotoxic granules and increased in CTL cytoplasm. Mutant CTLs have a three-fold increase in the number of granules lacking granzyme B. This mutant mouse strain may be useful in studies of viral immune response and inflammation, and the exocytosis pathway in CTL apoptosis.
010724	C57BL/6-Trim21^tm1Hm/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. EGFP expression is observed at high levels in lymph node, spleen, and thymus and at lower levels in kidney, heart and liver. Very low EGFP expression occurs in brain. Stimulated (LPS or polyI:C) embryonic fibroblasts derived from these mice exhibit enhanced expression of proinflammatory cytokines (TNFA, IL6 and CXCL10). A similar response is not observed in bone marrow dendritic cells or macrophages. Dendritic cells (CD11c+) generated from homozygous bone marrow are reduced by 25% as compared to controls, although, numbers of bone marrow macrophages are not altered. This mutant mouse strain may be useful in study of NFKB regulation and inflammatory responses.
006662	C57BL/6-Tg(ACTB-MAP2K1*K97M)1Stl/J	Cryopreserved - Ready for recovery
	Hemizygous mice are viable and fertile. These "dnMEK1" mice express a dominant-negative mutant (K97M) form of human MEK1 (synonym: MAP2K1) following Cre-mediated removal of the upstream "Lox-STOP-Lox" cassette; when transgenic mice are bred to a cre-expressing strain, the "floxed stop" cassete is excised in the resulting offspring, and mutant MEK1 expression is observed in the cre-expressing tissue(s). In the absence of Cre recombinase, transgene expression is not detectable in the brains of these "floxed" mice Because the MEK1 mutation abolishes the protein's kinase activity but preserves its ability to interact with ERK1 and ERK2, these transgenic mice may be useful in studying MEK-dependent activation and regulation of ERK, the ERK-MAPK signaling pathway, and neurological studies involving synaptic plasticity and memory. When bred to a strain expressing Cre recombinase in the CA1 pyramidal cell layer of the hippocampus (see Stock No. For more information please see the full phenotype on the strain data sheet
007744	C57BL/6-Tg(APOE-DGAT2)24Far/J	Cryopreserved - Ready for recovery
	Mice hemizygous for this LivLE6-DGAT2 transgene are viable and fertile, with human DGAT2 expression directed to the liver by the hepatic promoter/enhancer sequences from the human apolipoprotein E gene. Mice from founder line 24 (referred to as Liv-DGAT2-low) have an approximately 2-fold increase in total hepatic DGAT2 mRNA/protein expression, with no reported overexpression in kidney, brain, or skeletal muscle. As DGAT2 is one of two enzymes that catalyze the final step of triacylglycerol (TG) biosynthesis, transgenic mice develop hepatic steatosis with increased hepatic TG and insulin signaling lipid (diacylglycerol, ceramide and unsaturated Fatty AcylCoA) content. Liv-DGAT2-low mice also exhibit increased transcription of fatty acid synthesis genes (SREBP-1c, fatty acid synthase, and stearoyl CoA desaturase 1). Fasted mice show a 65% decrease in plasma TG, but are not insulin resistant (blood glucose and insulin are similar to wildtype). Liv-DGAT2-low mice challenged with a high-fat ..... For more information please see the full phenotype on the strain data sheet
006579	C57BL/6-Tg(Camk2a-Bdnf)A9Stl/J	Cryopreserved - Ready for recovery
	Hemizygous mice are viable and fertile, although the donating investigator reports that hemizygous mice have breeding problems likely resulting from a social anxiety-related phenotype. These "BDNF (line A9)" mice express the rat brain-derived neurotrophic factor (BDNF) primarily in forebrain regions, including the neocortex and hippocampus. Weak transgenic BDNF expression is detected also in cerebellum. Within the primary visual cortex, transgene expression is highest in the superficial layers. Hemizygous mice exhibit accelerated maturation of GABAergic innervation and inhibition, earlier termination of the critical period for ocular dominance plasticity, and accelerated development of visual acuity. These transgenic mice may be useful for studies involving BDNF overexpression and synaptic maturation and plasticity in the visual cortex.
008833	C57BL/6-Tg(Camk2a-UBB)3413-1Fwvl/J	Cryopreserved - Ready for recovery
	These transgenic mice express the mutant human ubiquitin B, UBB⁺¹, under the direction of the mouse Camk2a, calcium/calmodulin-dependent protein kinase II alpha, promoter. In hemizygotes, mutant transcript is expressed at 49% of the endogenous levels. The transgene is expressed in neurons of the cortex, hippocampus, amygdala and striatum. Hemizygous transgenic mice exhibit diminished ubiquitin-proteasome system activity with a resulting increase in ubiquitinated proteins in the cortex. Transgenic mice display a reduced synaptic plasticity in the hippocampus and impaired spatial learning. Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical abnormalities. This mutant mouse strain may be useful in studies of neurodegenerative diseases such as Alzheimer's and Huntington disease.
012895	C57BL/6-Tg(Cd4-Il17rb)5Cdon/J	Cryopreserved - Ready for recovery
	These transgenic mice express the mouse interleukin 17 receptor B under the direction of the mouse CD4 antigen promoter/enhancer. 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. The transgene is expressed in all T cells. When treated with IL25, T cells from transgenic mice have reduced numbers of IFN-gamma producing cells, reduced IL4 and IFN-gamma levels and increased IL5 and IL13 levels when compared to wildtype. Transgenic mice challenged with intranasal allergens exhibit higher levels of inflammatory cell infiltration than wildtype controls.
006781	C57BL/6-Tg(Ckm-DGAT2)10Far/J	Cryopreserved - Ready for recovery
	Mice hemizygous for this MCK-DGAT2 transgene are viable and fertile. Under direction of the mouse muscle creatine kinase (MCK) promoter, these mice overexpress human acyl CoA:diacylglycerol acyltransferase 2 (DGAT2) in striated skeletal muscles, specifically glycolytic (rather than oxidative) muscle. DGAT2 overexpression leads to increased lipid deposition (triacylglycerol, ceramide, and fatty acyl CoA) in glycolytic muscle. This lipid accumulation leads to impaired insulin signaling (insulin resistance), glucose uptake, and glucose tolerance in this tissue, as well as whole-body glucose intolerance. These MCK-DGAT2 transgenic mice may be useful in studying lipid accumulation in skeletal muscle, insulin and glucose metabolism, obesity, and type 2 diabetes. Of note, these mice may also be useful in conjunction with Liv-DGAT2-low transgenic mice (Stock No. 007744) which exhibit DGAT2 overexpression directed to hepatic tissue.
008231	C57BL/6-Tg(Ckm-Ppargc1a)31Brsp/J	Cryopreserved - Ready for recovery
	These transgenic mice express mouse peroxisome proliferative activated receptor, gamma, coactivator 1 alpha under the direction of the mouse muscle creatine kinase promoter. Transgene expression is specific to skeletal muscle. The increased levels of the transgene product induces expression of energy and mitochondrial oxidative metabolism genes such as cytochrome c oxidase II and IV. Muscle fibers from transgenic mice exhibit a more type II oxidative phenotype than wildtype mice. Isolated extensor digitorum longus muscle from transgenic mice exhibit increased fatigue resistance when compared to wildtype. Muscle fiber diameter loss in response to denervation and fasting is less severe in transgenic animals when compared to controls. Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of muscle physiology and disease, exercise and oxidative capacity, ..... For more information please see the full phenotype on the strain data sheet
008314	C57BL/6-Tg(HBB-cre)12Kpe/J	Cryopreserved - Ready for recovery
	These transgenic mice express Cre recombinase under the control of the human beta hemoglobin (HBB) promoter and intron 2-enhancer fragment, and the human beta hemoglobin locus control region (LCR). Cre recombinase expression is detected in blood, brain, gonads, spleen and liver by RT-PCR analysis and in blood by RNAse protection assay analysis. During development Cre activity is restricted to erythroid tissues. The Donating Investigator reports that recombination occurs at 50-100% efficiency in erythroid/megakarycytic cell lineages beginning at onset of hematopoiesis at approximately embryonic day 7.5. When crossed with a strain containing a loxP site-flanked sequence, Cre-mediated recombination results in deletion of the flanked sequence in erythroid tissues. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This strain represents an effective tool for generating tissue speci ..... For more information please see the full phenotype on the strain data sheet
008870	C57BL/6-Tg(Hspa2-cre)1Eddy/J	Cryopreserved - Ready for recovery
	Mice hemizygous for the Hspa2-Cre transgene are viable and fertile, with expression of Cre recombinase directed to the developing male germ cells by the mouse Hspa2 (heat shock protein 2 [Hsp70-2]) promoter. The Hspa2-Cre sequences of the transgene are flanked by Acrv1 (acrosomal vesicle protein 1 [SP-10]) insulator elements (which are believed to tether the Acrv1 gene to the nuclear matrix in somatic cells [preventing transcription]). When these transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination is expected to result in deletion of the floxed sequences in leptotene/zygotene spermatocytes of the male offspring. The donating investigator reports that expression of Hspa2-Cre may be "leaky" and recombination of loxP-flanked sequences can occur in some cells in somatic tissues. These Hspa2-Cre mice may be useful to generate conditional mutations for studying mammalian spermatocyte development, g ..... For more information please see the full phenotype on the strain data sheet
002030	C57BL/6-Tg(Igh-3/Igh-6VD93)1241Ust/J	Cryopreserved - Ready for recovery

007691	C57BL/6-Tg(Igk-Aicda)6Mnz/J	Cryopreserved - Ready for recovery
	Mice carrying this transgene are viable and fertile and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain to remove the floxed stop cassette, the transgene is expressed in B lymphocytes.
002029	C57BL/6-Tg(Igl-2MOPC315)1275Ust/J	Cryopreserved - Ready for recovery

008842	C57BL/6-Tg(Lck-VIPR2)1Ejg/J	Cryopreserved - Ready for recovery
	These "VPAC2 R TG mice" (or VPAC₂R Tg mice) are viable and fertile, harboring the LCK-huVPAC2 transgene. This transgene has the murine lymphocyte protein tyrosine kinase (Lck) proximal promoter directing persistently high expression of huVPAC₂R (human vasoactive intestinal peptide G-protein-coupled receptor 2 [VIPR2 or VIPR₂]) primarily to CD4⁺ T cells (T-helper/inducer cells). As such, expression of huVPAC₂R mRNA and protein is highest in spleen and thymus, but also observed in other tissues at much lower levels. The constitutive high huVPAC₂R expression on CD4⁺ T cells is characteristic of levels usually observed only after maximal TCR stimulation. Transgenic mice have elevated blood IgE, IgG1, and eosinophil levels. The effector T cell phenotype is altered; with Th2-bias cytokine profiles (increased IL-4, IL-5, c-maf and junB) associated with altered hypersensitivity states (increased immedi ..... For more information please see the full phenotype on the strain data sheet
012890	C57BL/6-Tg(Scgb1a1-Il17f,GFP)1Cdon/J	Cryopreserved - Ready for recovery
	These transgenic mice overexpress the mouse interleukin 17F, Il17f, under the direction of the lung specific mouse, Scgb1a1, secretoglobin, family 1A, member 1 (uteroglobin), promoter. Transgene expression elevates Il17f mRNA by at least 5 fold in the lung. Starting at 5 months of age, transgenic mice exhibit increased mucus production, macrophage infiltration of the lung, and lymphocyte infiltration of peribronchial and perivascular regions. Some severely affected mice exhibit Charcot-Leyden-like crystal structures in the airway. 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.
006140	C57BL/6-Tg(TERT)C10Hode/J	Cryopreserved - Ready for recovery
	Hemizygous transgenic mice are viable, fertile, and display no gross anatomical or behavioral abnormalities. This "hTERT" transgene carries the complete human telomerase reverse transcriptase (TERT) gene, including at least 11 kb of upstream and 1.5 kb of downstream sequences. The tissue specificity of transgene expression in hemizygous mice recapitulates that of the endogenous hTERT in humans rather than that of the endogenous mouse Tert (mTERT) gene with one exception: in brain, hTERT expression follows the expression profile of the endogenous mTERT gene. These transgenic mice may be useful in studies of telomerase function, organ-specific, differential cis-regulation of mouse versus human genes, as well as in studies of DNA replication and repair mechanisms, human aging, and carcinogenesis.
008389	C57BL/6-Tg(THY1-SNCA)1Sud/J	Cryopreserved - Ready for recovery
	This transgenic strain carries a human THY1 promoter driving expression of the human synuclein, alpha (SNCA) gene. Levels of expression show a 5-fold increase in the brain and a 10-fold increase in the spinal cord. Hemizygotes are viable and fertile and unlike some similar mutant transgenic lines, do not display any Parkinson-like phenotype upon aging.
010800	C57BL/6-Tg(Thy1-PTGS2)300Kand/J	Cryopreserved - Ready for recovery
	Mice hemizygous for the human Thy-1-COX-2 transgene (hCOX-2 transgene) are viable and fertile, with expression of human COX-2 (PTGS2 or PGE2) directed primarily to neurons of the amygdala, striatum, cerebral cortex, and hippocampus by the murine Thy1.2 expression cassette. These moderate overexpressing C57BL/6J COX-2 transgenic line 300 mice have PGE2 levels that are ~10-12-fold greater than non-transgenic controls (compared to ~25-40-fold overexpression in line 303; see Stock No. 010703). At approximately 12 months of age, COX-2 transgenic mice develop an age-dependent deficit in spatial memory. Around 20 months of age, a less pronounced, but significant deterioration in performance of non-spatial memory tasks develops. Further progressive memory impairments are observed over time. These cognitive deficits are associated with parallel age-dependent increases in cortical neuronal apoptosis and glial activation. Transgenic m ..... For more information please see the full phenotype on the strain data sheet
010703	C57BL/6-Tg(Thy1-PTGS2)303Kand/J	Cryopreserved - Ready for recovery
	Mice hemizygous for the human Thy-1-COX-2 transgene (hCOX-2 transgene) are viable and fertile, with expression of human COX-2 (PTGS2 or PGE2) directed primarily to neurons of the amygdala, striatum, cerebral cortex, and hippocampus by the murine Thy1.2 expression cassette. These overexpressing C57BL/6J COX-2 transgenic line 303 mice have PGE2 levels that are ~25-40-fold greater than non-transgenic controls (compared to ~10-12-fold overexpression in line 300; see Stock No. 010800). At approximately 12 months of age, COX-2 transgenic mice develop an age-dependent deficit in spatial memory. Around 20 months of age, a less pronounced, but significant deterioration in performance of non-spatial memory tasks develops. Further progressive memory impairments are observed over time. These cognitive deficits are associated with parallel age-dependent increases in cortical neuronal apoptosis and glial activation. Transgenic mice exhib ..... For more information please see the full phenotype on the strain data sheet
010505	C57BL/6-Tg(Vav1-NUP98/HOXD13)G2Apla/J	Cryopreserved - Ready for recovery
	These transgenic mice express the fusion gene consisting of the amino-terminal region of the human nucleoporin 98kDa (NUP98) fused to the homeodomain of the human homeobox D13 (HOXD13) under the control of the mouse vav1 oncogene (Vav1) regulatory elements. The transgene is expressed specifically in hematopoietic tissues and is detected in thymus, spleen, and bone marrow and not in brain, liver, and kidney by Northern blot analysis of total RNA. The fusion gene product (protein) is detected in thymocytes from transgenic mice by Western blot analysis. Hemizygous transgenic mice develop myelodysplastic syndromes (hematopoietic stem cell disorder) with peripheral blood cytopenia and dysplasia and normocellular to hypercellular bone marrow. By 7 months of age, hemizygotes exhibit leukopenia and anemia. By 14 months of age a subset of hemizygotes succumbs to malignant leukemia or severe anemia and leucopenia. This mutant mouse strain may be useful in studies of myelod ..... For more information please see the full phenotype on the strain data sheet
006618	C57BL/6-Tg(tetO-COX8A/EYFP)1Ksn/J	Cryopreserved - Ready for recovery
	Hemizygotes are viable and fertile. These transgenic mice express a mitochondrial-specific EYFP fusion protein under the control of a tetracycline-responsive promoter element (TRE;tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoter, tissue-specific expression of EYFP in mitochondria of the bitransgenic offspring can be regulated with the tetracycline analog, doxycycline. When bred to a strain expressing rtTA or tTA in forebrain neurons (see Stock No. 003010 for example), this mutant mouse strain may be useful in studies of neuronal mitochondrial dysfunction.
000258	C57BL/6J-Aⁱ/a/J	Cryopreserved - Ready for recovery

000774	C57BL/6J-A^sy/a/J	Cryopreserved - Ready for recovery

005469	C57BL/6J-Agrn^nmf380/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf380 entry.
005011	C57BL/6J-Agtpbp1^pcd-6J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Agtpbp1^pcd-6J entry.
006153	C57BL/6J-Akt3^Nmf350/JFrk	Cryopreserved - Ready for recovery
	Mice carrying this dominant missense point mutation in the thymoma viral proto-oncogene 3 (Akt) gene exhibit a low seizure threshold in response to electroconvulsive threshold testing or pentylenetetrazol (PTZ) administration, sporadic tonic-clonic seizures, brain enlargement and ecotopic neurons in the dentate hilus and molecular layer of the hippocampus. This mutant mouse strain may be useful in studies of AKT signalling and epilepsy.
005921	C57BL/6J-Aqp2^F204V/J	Cryopreserved - Ready for recovery
	Mice homozygous for this mutation are viable with normal body size and lifespan. Homozygotes are fertile, but females usually die during labor. The predicted valine for phenylalanine substitution at amino acid 204 of the mutant protein (F204V) leads to an enrichment in kidney cells of a normally short-lived, intermediately glycosylated 31 kDa isoform and to a reduction in the mature, glycosylated protein level. The mutant AQP2^F204V protein is mis-localized in kidney collecting duct cells, and fails to translocate to the apical cell surface in response to desmopressin. Homozygous mice exhibit excessive water consumption and urination, normal plasma glucose levels, and no glucose in the urine. Mutant mice are unable to concentrate urine and exhibit severe hydronephrosis. The presence of some mature, glycosylated protein and a defective, but not completely absent, desmopressin response in homozygous mutant mice likely permits their survival. Heterozygous mice are viable and fer ..... For more information please see the full phenotype on the strain data sheet
005598	C57BL/6J-Arsb^m1J/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Arsb^m1J mutation have a combination of delayed muscle and nerve degeneration along with a skeletal phenotype consisting of a shortened snout, wide-set eyes and shortened limbs that becomes more noticeable with age. Mutants can be poor breeders yielding small litters. Of 10 litters the average number of pups was 3.9.
004764	C57BL/6J-Cdh23^v-8J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Cdh23^v-8J entry.
004819	C57BL/6J-Cdh23^v-9J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Cdh23^v-9J entry.
008131	C57BL/6J-Celf4^Ff/Frk	Cryopreserved - Ready for recovery

005253	C57BL/6J-Clcn1^adr-mto6J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Clcn1^adr-mto6J entry.
005465	C57BL/6J-Clcn1^adr-mto7J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Clcn1^adr-mto7J entry.
005095	C57BL/6J-Clcn2^nmf240/J	Cryopreserved - Ready for recovery
	Homozygotes exhibit grainy retinas by 3 weeks of age which progresses into large white patches distributed across the entire retina by 12 weeks of age. At 10 days of age the apical processes of the retinal pigment epithelium are abnormally elongated, by 14 days of age the retinal outer nuclear layer is reduced in thickness and contains pyknotic nuclei and the photoreceptor outer segments are disorganized and shortened. By 3 weeks of age the photoreceptor layer is reduced to one to two layers of cells and the outer segments are not visible. Both dark and light adapted flash electroretinograms show reduced amplitude responses as early as 14 days of age and this worsens progressively to near zero by 26 days of age. Male infertility is associated with decreased weight of the testes and epididymides and azoospermia as early as 6 weeks of age with severe degradation of spermatogenesis. Progressive leukoencephalopathy is also found, with vacuoles in the white matter tracts and cerebellum ..... For more information please see the full phenotype on the strain data sheet
005255	C57BL/6J-Cldn9^nmf329/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf329 entry.
002923	C57BL/6J-Clock^m1Jt/J	Cryopreserved - Ready for recovery
	Mice heterozygous for this Clock^delta19 mutation (also called Clock^mut or Clock^m1Jt) show a lengthening of their circadian period by about 1 hour. Homozygous mice show a lengthening of 4 hours followed by a loss of circadian rhythm. Homozygous mice are viable. Male homozygotes are fertile, but female homozygotes appear to have reduced fertility.
013612	C57BL/6J-Dnahc5^b2b002Clo/J	Cryopreserved - Ready for recovery
	This c.13169T>C Dnahc5 (dynein, axonemal, heavy chain 5) point 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 incidental 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), atrioventricular septal defects (AVSD), superior-inferior ventricles, and likely other structural heart defects.
000519	C57BL/6J-Dsg3^bal/J	Cryopreserved - Ready for recovery

004829	C57BL/6J-Dst^dt-36J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Dst^dt-3J entry.
005560	C57BL/6J-Dst^dt-37J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Dst^dt-37J entry.
000536	C57BL/6J-Glra1^spd-ot/J	Cryopreserved - Ready for recovery

005447	C57BL/6J-Grid2^ho-16J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf334 entry.
005718	C57BL/6J-Grid2^ho-17J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf408 entry.
000527	C57BL/6J-Grid2^ho-5J/J	Cryopreserved - Ready for recovery

005561	C57BL/6J-Grm1^nmf373/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Grm1^nmf373 entry.
005521	C57BL/6J-Grm1^rcw-3J/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the recoil wobbler 3 Jackson mutation have a slightly smaller body size and a wobbly gait, causing loss of balance when walking, usually visible by 2 weeks of age.
005322	C57BL/6J-Gusb^mps-3J/J	Cryopreserved - Ready for recovery

005691	C57BL/6J-Hlb280/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) after 5 weeks on atherogenic high fat diet identified a 13 week old female (born 9/9/2002) with a 4 hour fasted plasma HDL of 136 mg/dl and total cholesterol of 486 mg/dl, which is approximately 174% and 485% (respectively) higher than controls. This mutant mouse strain may be useful in studies of hypercholesterolemia.
005060	C57BL/6J-Hlb290/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 an 8 week old male (born 11/25/2002) with a 4 hour fasted plasma glucose of 516 mg/dl, which is approximately 137% higher than controls. Two siblings were similarly affected. This mutant mouse strain may be useful in studies of diabetes and hyperglycemia.
008507	C57BL/6J-Hlb320/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 an 8 week old female (born 1/5/2003) with a 4 hour fasted plasma total cholesterol of 35 mg/dl and an HDL of 26 mg/dl, which is approximately 58% and 48% lower than controls, respectively. One female sibling was similarly affected. This mutant mouse strain may be useful in studies of hypercholesterolemia.
008411	C57BL/6J-Hlb426/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 atherogenic diet for 1 week identified a female (born 3/31/2004) with a a systolic blood pressure of 142 +/- 12 mmHg, which is approximately 30% higher than controls. Retest 6 weeks later confirmed the phenotype. This mutant mouse strain may be useful in studies of hypertension.
008509	C57BL/6J-Hlb446/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 6 week old male (born 5/27/2002) with a 4 hour fasted plasma high density lipoprotein (HDL) of 112.2 mg/dl. Retesting one week later confirmed this observation with a reading of 120.6 mg/dl. This mutant mouse strain may be useful in lipoprotein studies.
006423	C57BL/6J-Hlb468/J	Cryopreserved - Ready for recovery
	Mice carrying 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 11 week old male (born 1/19/2005) with a heart rate of 854 bpm. Repeat testing on week later measured a heart rate of 870 bpm confirming the phenotype. This mutant mouse strain may be useful in studies of tachycardia.
008263	C57BL/6J-Hlb476/J	Cryopreserved - Ready for recovery

008504	C57BL/6J-Hlb477/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 8 week old male (born 3/18/2005) with a 4 hour fasted plasma high density lipoprotein (HDL) of 106 mg/dl. Retesting one week later confirmed this observation with a reading of 107 mg/dl. This mutant mouse strain may be useful in lipoprotein studies.
008506	C57BL/6J-Hlb529/J	Cryopreserved - Ready for recovery
	Mice homozygous for this ENU induced mutation exhibit elevated HDL cholesterol.
008505	C57BL/6J-Hlb561/J	Cryopreserved - Ready for recovery
	Mice homozygous for this ENU induced mutation exhibit elevated HDL cholesterol.
008503	C57BL/6J-Hlb586/J	Cryopreserved - Ready for recovery
	Mice homozygous for this ENU induced mutation exhibit elevated plasma HDL cholesterol.
008499	C57BL/6J-Hlb589/J	Cryopreserved - Ready for recovery
	Mice homozygous for this ENU induced mutation exhibit elevated HDL cholesterol.
008500	C57BL/6J-Hlb592/J	Cryopreserved - Ready for recovery
	Mice homozygous for this ENU induced mutation exhibit elevated plasma HDL cholesterol.
008262	C57BL/6J-Hlb594/J	Cryopreserved - Ready for recovery

007711	C57BL/6J-Hps3^coa-8J/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the cocoa 8 Jackson mutation have hypopigmentation resulting in a diluted coat color and pale ears, feet and tail.
000542	C57BL/6J-Hps5^ru2-J/J	Cryopreserved - Ready for recovery

005342	C57BL/6J-Il7^hlb368/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 an 8 week old male (born 4/7/2003) with a CBC of 1.50 x 103 WBC/ul (84% lower than controls); testing two weeks later produced a result of 2.51 WBC/ul (74% lower than controls). This mutant mouse strain may be useful in studies of leukopenia.
004820	C57BL/6J-Kcne1^2J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Kcne1^2J entry.
005748	C57BL/6J-Kcnq1^vtg-3J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Kcnq1^vtg-3J entry.
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

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.
005094	C57BL/6J-Lama1^nmf223/J	Cryopreserved - Ready for recovery
	Homozygotes have retinal vasculopathy, characterized by vitreal fibroplasias and vessel tortuosity. There is thinning of the peripheral inner nuclear layer and variable cell loss in the retinal ganglion cell layer, along with reduced dark and light adapted electroretinogram amplitudes. There is abnormal migration of retinal astrocytes into the vitreous and the persistence of hyaloid vaculature. While targeted disruption of the alpha 1 laminin gene causes a more severe phenotype, including the absence of the inner limiting membrane, this hypomorph nevertheless displays ectopic cells and blood vessels within the vitreous indicative of reduced integrity of the inner limiting membrane.
005635	C57BL/6J-Lama2^dy-7J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Lama2^dy-7J entry.
000529	C57BL/6J-Lbr^ic-J/J	Cryopreserved - Ready for recovery
	Lbr^ic-J/Lbr^ic-J homozygotes can be identified at 2 weeks of age due to sparse fur and at 3-4 weeks of age scales develop on the tail and, to a lesser degree, on the trunk. These mutants are smaller than their wild type siblings. The mutants develop mild epidermal hyperplasia with orthokeratotic hyperkeratosis and dilation of the piliary canals. Homozygotes have an increased incidence of syndactyly and hydrocephaly, and a high prenatal mortality rate. Aberrant morphology of nuclear heterochromatin occurs in lymphocytes, neutrophils, eosinophils, intestinal epithelium, and cerebellar granule cells. Electron microscopy reveals clumps of heterochromatin at the periphery of the nucleus within splenic lymphocytes. These mice are a model for Pelger-Huet anomaly, which is associated with mutations in LBR, although the skin pathology is specific to the mouse mutation. (Eicher, 1976; Hoffmann et al., 2002; Shultz et al., 2003.)
000974	C57BL/6J-Lgi4^clp/J	Cryopreserved - Ready for recovery

005638	C57BL/6J-Lhfpl5^hscy-2J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Lhfpl5^hscy-2J entry.
005579	C57BL/6J-Lta^hlb382/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)identified a non-fasted female (born 10/9/2003) with an increased white blood cell count of 15.39 x 103 cells/ul, which is approximately 92% higher than controls. This mutant mouse strain may be useful in studies of leukocytosis.
000060	C57BL/6J-Mc1r^e/J	Cryopreserved - Ready for recovery

005124	C57BL/6J-Mpl^hlb219/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 6 week old female (born 8/14/2002) with a platelet count of 106 x 103 cells/ul, which is approximately 91% lower than controls. This mutant mouse strain may be useful in studies of thrombocytopenia.
005749	C57BL/6J-Myo6^sv-3J/J	Cryopreserved - Ready for recovery

005468	C57BL/6J-Myo7a^sh1-11J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Myo7a^sh1-11J entry.
004851	C57BL/6J-Nmf128/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Nmf128 entry.
005007	C57BL/6J-Nmf191/J	Cryopreserved - Ready for recovery
	At 12 weeks of age, the retinas of Nmf191 carriers were found to be grainy, although electroretinographic recordings were normal. View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Nmf191 entry.
004832	C57BL/6J-Nmf220/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Nmf220 entry.
005014	C57BL/6J-Nox3^het-4J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf250 entry.
004817	C57BL/6J-Npc1^nmf164/J	Cryopreserved - Ready for recovery
	Npc1 is a transmembrane protein involved in endosomal lipid sorting and trafficking. The nmf164 allele is a point mutation, which results in partial functional loss of the protein. In comparison to mice carrying Npc1^spm (Stock #002760) and Npc1^m1N (Stock #003092), the nmf164 phenotype has a delayed onset and models a more slowly progressing form of human Niemann-Pick C disease. Mice exhibit age-dependent ataxia, impaired motor and strength capabilities, shortened lifespan (112 +/- 4 days), weight loss, progressive accumulation of sphingomyelin and glycosphingolipids in the liver and spleen (sphingomyelinosis), and abnormal cholesterol levels in liver. In the brain, phenotypic characteristics include: loss of cerebellar Purkinje cells, an increase in the GM2 and GM3 gangliosides, abnormal astrocyte and microglial cell activation, abnormal cholesterol levels in neurons, and acoustic startle response abnormalities. This mutant mou ..... For more information please see the full phenotype on the strain data sheet
005008	C57BL/6J-Nphp4^nmf192/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf192 entry.
008188	C57BL/6J-Npr3^lgj-3J/GrsrJ	Cryopreserved - Ready for recovery
	Homozygotes can be detected by 5 to 7 weeks of age due to their elongated bodies, kinked tails, and conical extension of the body. With age, homozygotes appear thinner than normal with thoracic kyphosis. Their digits are often banded, twisted and deformed. A hearing deficit is also found in homozygotes assessed between 3 and 5 weeks of age.
001136	C57BL/6J-Oca2^p-un+2J/J	Cryopreserved - Ready for recovery
	Homozygotes and heterozygotes for this revertant allele are phenotypically indistinguishable from wild-type.
001506	C57BL/6J-Oca2^p-un+3J/J	Cryopreserved - Ready for recovery
	Homozygotes and heterozygotes for this revertant allele are phenotypically indistinguishable from wild-type.
001810	C57BL/6J-Oca2^p-un+4J/J	Cryopreserved - Ready for recovery
	Homozygotes and heterozygotes for this revertant allele are phenotypically indistinguishable from wild-type.
001513	C57BL/6J-Oca2^p-un+5J/J	Cryopreserved - Ready for recovery
	Homozygotes and heterozygotes for this revertant allele are phenotypically indistinguishable from wild-type.
001499	C57BL/6J-Oca2^p-un+6J/J	Cryopreserved - Ready for recovery
	Homozygotes and heterozygotes for this revertant allele are phenotypically indistinguishable from wild-type.
001033	C57BL/6J-Oca2^p-un+J/J	Cryopreserved - Ready for recovery
	Homozygotes and heterozygotes of this revertant allele are phenotypically indistinguishable from wild-type.
000028	C57BL/6J-Oca2^p-un/J	Cryopreserved - Ready for recovery
	The pink-eyed unstable (Oca2^p-un) mutation comprises a 70-kb, head-to-tail duplication of a transcribed region of the Oca2^p gene. Oca2^p-un homozygotes have a greatly diluted coat color and pink eyes; however, approximately 3.5% of Oca2^p-un/Oca2^p-un mice are mosaic for wild-type coat color (Melvold et al., 1971) because of somatic reversion of the mutation involving loss of the duplicated segment (Brilliant et al.1991, Gondo et al. 1993).
001672	C57BL/6J-Otc^spf-J/J	Cryopreserved - Ready for recovery

010747	C57BL/6J-Otog^twt-4J/Kjn	Cryopreserved - Ready for recovery
	Mice homozygous for the twisted 4 Jackson mutation have a severe head-tilt but do not circle the way other twisted mutants do. In a swim test they swim tilted to one side usually just below the surface of the water. ABR readings show that these mice are severely hearing impaired at wean age and profoundly deaf by 70 days of age. Otoconial deficiencies exist that are likely due to displacement of the otolithic membrane.
000531	C57BL/6J-Otx1^jv/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Jackson waltzer mutation run in circles and shake their heads. The lateral semicircular canal and its cristae are absent, and the sacculus and utriculus may be morphologically abnormal. However, hearing is unaffected. This pheontype is similar to that reported for the Otx1^tm1Asim targeted mutation and complementation testing with this targeted mutation showed jv to be an allele of Otx1. (Note that C57BL/6J is homozygous for ahl, the age related hearing loss 1 mutation, which on this strain background causes progressive hearing loss with onset after 10 months of age.) Homozygotes can swim.
000565	C57BL/6J-Pax3^Sp-d/J	Cryopreserved - Ready for recovery
	Mice homozygous for the splotch-delayed spontaneous mutation (Pax3^Sp-d) have a phenotype that is generally less severe than mice homozygous for the splotch mutation (Pax3^Sp, Stock No. 002469). Splotch-delayed homozygous embryos survive to birth, compared to splotch mutant embryos that die at E13 due to neural tube defects. Homozygous splotch-delayed mutant embryos display caudal rachischisis only. Heterozygous splotch-delayed have a white belly spot. Delayed splotch is a point mutation within the paired domain of Pax3. This impairs DNA binding of this domain and also, suprisingly, of the homeodomain, not directly affected in the mutant gene.
002072	C57BL/6J-Pcdh15^av-3J/J	Cryopreserved - Ready for recovery
	There have been several remutations to Ames waltzer (av) have occurred in stocks at The Jackson Laboratory. All mice homozygous for these remutations show the characteristic head-tossing, circling, and deafness characteristic of Ames waltzer. Ames wa ltzer 2J homozygous mutant mice (av^2J/av^2J) are more severely afflicted than mice homozygous for the other Jackson (J) remutations. av^2J/av^2J homozygotes become disoriented and sink in swim tests; Ames waltzer 3J homozygotes (av^3J/av^3J), like Ames waltzer-J (av^J/av^J), swim with difficulty and circle afloat. In the membranous labyrinth the fluid spaces in the Organ of Corti fail to develop. Later, hair cells and spiral ganglion cells degenerate.
004156	C57BL/6J-Pcdh15^av-5J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Pcdh15^av-5J entry.
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.
000118	C57BL/6J-Ph/J	Cryopreserved - Ready for recovery

006249	C57BL/6J-Plxna2^nmf454/J	Cryopreserved - Ready for recovery
	Due to aberrant migration of granule cells during development, mice homozygous for the nmf454 mutation have a hypercellular molecular layer of the cerebellum with many ectopic granule cells in the molecular layer.
004821	C57BL/6J-Prph2^Nmf193/J	Cryopreserved - Ready for recovery
	Carriers of Nmf193 have been found to have pan retinal photoreceptor degeneration of the outer nuclear layer. View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Nmf193 entry.
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.
000976	C57BL/6J-Rab38^cht/J	Cryopreserved - Ready for recovery
	On the C57BL/6J background Rab38^cht/Rab38^cht mice have a rich dark chocolate coat color instead of the normal black coat. This can be difficult to distinguish, but is made easier by the lightened color in the ear pinnae and tail. At birth the eyes of Rab38^cht/Rab38^cht mice are lighter in color than wild type C57BL/6J mice. The melanosomes in melanocytes cultured from newborn C57BL/6J mice are oval and intensely black while those of chocolate mice are circular and brown. The end-stage melanosomes of chocolate mice contain less TYRP1 than do wild type mice. Mutations in Tyrp1 result in increased brown rather than black pigment. Thus, Loftus et al. have hypothesized that the chocolate mutation results in decreased black pigmentation because RAB38 is important in the vesicular trafficking that moves TYRP1 from the trans-Golgi network to the end-stage melanosome. Many of the pigment diluting mutations with ..... For more information please see the full phenotype on the strain data sheet
000110	C57BL/6J-Rabggta^gm/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Rabggta^gm allele are grayish-black on a non-agouti background due to pigment dilution. Eye color is not affected. Homozygotes have reduced viability and do not breed well. These mutants have a prolonged bleeding time. Although gunmetal mice have an increased number of megakariocytes, they have about half the number platelets found in wildtype siblings. This decrease in platelet number results from a slower rate of platelet synthesis. These platelets are heterogeneous in size and are larger than normal, but have fewer dense granules per platelet and approximately half of the normal level of serotonin. The prolonged bleeding time and decreased platelet count and volume can be transferred to wildtype mice through bone marrow transplantion. Likewise bone marrow transplants from wildtype mice reversed the platelet deficiency in gunmetal recipients. Western blots of platelet extracts showed a decrease in fibrinogen, von Willebrand factor, and platel ..... For more information please see the full phenotype on the strain data sheet
005744	C57BL/6J-Reln^rl-6J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Reln^rl-6J entry.
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).
016255	C57BL/6J-Rnl16/BPgn	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 20 week old male with an increased blood urea nitrogen (BUN) of 34 mg/dL. Testing one week later confirmed the increased BUN value (34 mg/dL). This mutant mouse strain may be useful in studies of kidney function.
008793	C57BL/6J-Rnl18/Pgn	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 20 week old male with an increased blood urea nitrogen (BUN) of 36 mg/dL. Testing one week later confirmed the increased BUN value (33 mg/dL). This mutant mouse strain may be useful in studies of kidney function.
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).
008795	C57BL/6J-Rnl23/Pgn	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 20 week old male (born 3/28/2006) with an increased blood urea nitrogen (BUN) of 37 mg/dL. Testing one week later confirmed the phenotype (BUN=55 mg/dL). This mutant mouse strain may be useful in studies of kidney function and blood homeostasis.
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).
016256	C57BL/6J-Rnl25/BPgn	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 20 week old male with an increased blood urea nitrogen (BUN) of 34 mg/dL. Testing one week later confirmed the increased BUN value (35 mg/dL). This mutant mouse strain may be useful in studies of kidney function.
008412	C57BL/6J-Rnl27/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 20 week old male (born 5/17/2006) with an increased blood urea nitrogen (BUN) of 47 mg/dL. Testing one week later confirmed the increased BUN value (52 mg/dL). This mutant mouse strain may be useful in studies of kidney function.
016916	C57BL/6J-Rnl27/Pgn	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 20 week old male with an increased blood urea nitrogen (BUN). Testing one week later confirmed the increased BUN value. This mutant mouse strain may be useful in studies of kidney function.
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).
008801	C57BL/6J-Rnl32/Pgn	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 20 week old male (born 6/25/2006) with an increased blood urea nitrogen (BUN) of 37 mg/dL. Testing one week later confirmed the phenotype (BUN=35 mg/dL). This mutant mouse strain may be useful in studies of kidney function and blood homeostasis.
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).
005047	C57BL/6J-Rora^sg-3J/J	Cryopreserved - Ready for recovery
	Mice homozygous for this ENU-induced mutation are smaller than normal and, by 3.5 weeks of age on average, display splayed hind limbs and a leaning gait. They fall over on their sides and have difficulty regaining a walking position. A disorganized Purkinje cell layer and loss of granule cells has been found. For additional information on Rora^sg-3J view the web page on the Neuroscience Mutagenesis Facility web site.
005096	C57BL/6J-Rpgrip1^nmf247/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Rpgrip1^nmf247 entry.
005495	C57BL/6J-Scarb1^Hlb398/J	Cryopreserved - Ready for recovery
	Mice carrying this 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 an 8 week old male (born 2/5/2004) with a 4 hour fasted total cholesterol of 190 mg/dl and a high density lipoprotein (HDL) of 146 mg/dl, which is approximately 62% and 102%, respectively, higher than controls. Retesting one week later confirmed these results. This is a dominant mutation affecting 5 out of 6 of the F1 progeny. This mutant mouse strain may be useful in studies of hypercholesterolemia.
004102	C57BL/6J-Scn8a^4J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Scn8a^4J entry.
004105	C57BL/6J-Scn8a^5J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Scn8a^5J entry.
005482	C57BL/6J-Shar/J	Cryopreserved - Ready for recovery
	By 3 weeks of age mice carrying the dominant Shar mutation have a shiny and rough coat that has a greasy appearance.
000570	C57BL/6J-Slc45a2^uw Adamts20^bt-2J/J	Cryopreserved - Ready for recovery
	Mice homozygous for the recessive Adamts20^bt-2J 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.
000003	C57BL/6J-Slc45a2^uw/J	Cryopreserved - Ready for recovery

005135	C57BL/6J-Sls/GrsrJ	Cryopreserved - Ready for recovery

000563	C57BL/6J-Sobp^jc/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Jackson circler spontaneous mutation (Sobp^jc) show erratic circling behavior which becomes more pronounced with age. Homozygous mutant mice are very active, bobbing up and down and flexing head and trunk ventrally towards the tail and mice can swim. Mice can be identified at weaning by a characteristic flexing behavior when suspended by tail.
005449	C57BL/6J-Spnb4^qv-8J/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf379 entry.
008785	C57BL/6J-Stk39^Rnl5/Pgn	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 20 week old male (born 11/21/2002) with an increased albumin-creatinine ratio of 22 mg/g. Retesting one week later confirmed this observation with a reading of 91 mg/g. This mutant mouse strain may be useful in studies of albuminuria.
004587	C57BL/6J-Szt1/FrkJ	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Szt1 entry.
000545	C57BL/6J-T^2J/J	Cryopreserved - Ready for recovery

000068	C57BL/6J-Tyrp1^b-J/J	Cryopreserved - Ready for recovery

000708	C57BL/6J-Utp14b^jsd/J	Cryopreserved - Ready for recovery

000520	C57BL/6J-Vps33a^bf/J	Cryopreserved - Ready for recovery
	Mice homozygous for the recessive buff (Vps33a^bf) mutation on a non-agouti (a/a) background have a lightened coat color that has been described as khaki. On an agouti background, Vps33^bf homozygotes have dark ears, opaque eyes, and the belly is lighter in color than is the rest of the coat. Although no change in eye color is outwardly evident, electron microscopy shows fewer and smaller melanosomes than normal in the retinal pigment epithelium and choroid. These mutants have a platelet-storage pool defect evidenced by an increased bleeding time of 9.7 minutes on average, a reduction in the number of platelet dense granules, and slightly decreased collagen-mediated platelet aggregation, secretion of dense-granule ATP and secretion of seratonin. Hakansson and Lundin found increased activity of the lysosomal glycosidases beta- galactosidase, beta-glucuronidase, and N-acetyl-beta-hexosaminidase in kidney cell lysates. Suzuki et al. found n ..... For more information please see the full phenotype on the strain data sheet
000055	C57BL/6J-a^t-33J/J	Cryopreserved - Ready for recovery

000070	C57BL/6J-a^td/J	Cryopreserved - Ready for recovery

008264	C57BL/6J-hlb145/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 7 week old female (born 4/16/2002) with a white blood cell count of 2.7 x 103 cells/ul, which is approximately 66% lower than controls. Retesting 2 weeks later confirmed the phenotype. This mutant mouse strain may be useful in studies of leukopenia.
004517	C57BL/6J-hlb156/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 6 week old male (born 5/27/2002) with a neutrophil level of 27.4%, which is approximately 130% higher than controls. This mutant mouse strain may be useful in studies of neutrophilia.
004530	C57BL/6J-hlb15/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 9 week old female (born 4/15/2001) with a mean systolic blood pressure of 133 +/- 16 mmHg, which is approximately 22% higher than controls. This mutant mouse strain may be useful in studies of hypertension.
008508	C57BL/6J-hlb218/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 8 week old male (born 9/15/2002) with a n4 hour fasted plasma total cholesterol of 17 mg/dl and HDL cholesterol of 15 mg/dl, which is approximately 85% and 79% lower than controls, respectively. This mutant mouse strain may be useful in studies of cholesterol homeostasis.
008265	C57BL/6J-hlb233/J	Cryopreserved - Ready for recovery

007231	C57BL/6J-hlb243/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) after more than 5 weeks atherogenic diet identified a 13 week old female (born 9/04/2002) with a 4 hour fasted plasma total cholesterol of 517 mg/dl and HDL of 129 mg/dl, which is approximately 522% and 160% higher, respectively, than controls. One sibling was similarly affected. This mutant mouse strain may be useful in studies of diet-induced hypercholesterolemia.
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.
005343	C57BL/6J-hlb381/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 6 week old male (born 1/7/2004) with a platelet count of 24 x 103 cells/ul,which is approximately 98% lower than controls. One sibling was similarly affected. This mutant mouse strain may be useful in studies of neutrophilia.
005496	C57BL/6J-hlb385/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 7 week old female (born 12/13/2003) with a complete blood count (CBC) of 3.2 x 103 white blood cells (WBC)/ul, approximately 60% lower than controls. Retesting 2 weeks later confirmed the phenotype. This mutant mouse strain may be useful in studies of leukopeniia.
005580	C57BL/6J-hlb388/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) identified a fasted 8 week old male (born 12/25/2003) with a plasma HDL level of 97.6 mg/dl, which is approximately 35% higher than controls. HDL levels were 106.9 mg/dl when the mouse was retested one week later. This mutant mouse strain may be useful in studies of hypercholesterolemia.
008269	C57BL/6J-hlb414/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 9 week old male (born 2/15/2004) exhibiting a hyper-response to methacholine (MCH). Absolute Penh values are as follows: saline control 0.46(0.66), 5mg/ml MCH 0.64(0.60), 10 mg/ml MCH 0.92(1.28), 20 mg/ml MCH 4.54(12.48). Second run values are in parenthesis. This mutant mouse strain may be useful in studies of asthma and airway hyper-responsiveness (AHR).
010952	C57BL/6J-hlb444/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 an 8 week old male (born 9/15/2004) with a 4 hour fasted plasma triglyceride level of 187 mg/dl, which is increased in comparison to controls. Retesting one week later confirmed this observation with a reading of 204 mg/dl. This mutant mouse strain may be useful in studies of triglyceride and lipid homeostasis.
008280	C57BL/6J-hlb454/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 atherogenic diet identified a 9 week old male (born 9/12/2004) exhibiting a hyper-response to methacholine (MCH). Absolute Penh values are as follows: 5mg/ml MCH 0.1.37(0.98), 10 mg/ml MCH 2.01(1.94), 20 mg/ml MCH 11.47(5.28). Second run values are in parenthesis. Two siblings were similarly affected. This phenotype has been validated by an invasive resistance evaluation using a flexivent protocol. This mutant mouse strain may be useful in studies of asthma and airway hyper-responsiveness (AHR).
008497	C57BL/6J-hlb459/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 11 week old male (born 11/8/2004) with a heart rate of 805 bpm. Repeat testing one week later confirmed the phenotype (822 bpm). This mutant mouse strain may be useful in studies of tachycardia.
008266	C57BL/6J-hlb495/J	Cryopreserved - Ready for recovery

008261	C57BL/6J-hlb497/J	Cryopreserved - Ready for recovery

008267	C57BL/6J-hlb520/J	Cryopreserved - Ready for recovery

008268	C57BL/6J-hlb521/J	Cryopreserved - Ready for recovery

008270	C57BL/6J-hlb52/J	Cryopreserved - Ready for recovery

010955	C57BL/6J-hlb541/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 male with an increased percentage of fat in comparison to controls. This mutant mouse strain may be useful in studies of obesity.
010956	C57BL/6J-hlb560/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) identified a mouse with elevated plasma triglycerides. This mutant mouse strain may be useful in studies of cardiovascular research and metabolism.
008498	C57BL/6J-hlb575/J	Cryopreserved - Ready for recovery
	Mice with this mutation exhibit an increased percentage of body fat on a standard laboratory chow diet.
008640	C57BL/6J-hlb583/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the mutation are viable and fertile. Screening of third generation mice (G3) on standard chow identified a male with an increased percentage of fat. This mutant mouse strain may be useful in studies of obesity.
005330	C57BL/6J-hpbk/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the humpback mutation appear normal at wean age, but by 5 weeks of age can be distinguished by thoracic kyphosis and scrawniness. Both phenotypes progress with age, and sudden death is common in adults. Histology reveals myopathy. Homozygotes females are not able to deliver pups and homozygous males develop phimosis so do not breed.
006948	C57BL/6J-hstp/J	Cryopreserved - Ready for recovery
	Mice homozygous for the high stepper mutation display an abnormal gait in which they pull their rear legs up to the body as they walk. They also draw the rear legs to the belly when picked up by the tail. Electroretinogram recordings are abnormal for all homozygotes on a pure C57BL/6J background or on a (C57BL/6J x CAST/EiJ)F2 background. Histology of the eye shows rosettes and misplaced ganglion cells by approximately 2 weeks of age.
004814	C57BL/6J-nmf127/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf127 entry.
005006	C57BL/6J-nmf131/J	Cryopreserved - Ready for recovery
	Homozygosity for the nm131 mutation can cause retinal dysplasia, retinal degeneration, vitreal fibroplasia, and, less commonly, cataracts or microphthalmia. This mutation has low penetrance. View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf131 entry.
004816	C57BL/6J-nmf161/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf161 entry.
004818	C57BL/6J-nmf172/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf172 entry.
005009	C57BL/6J-nmf195/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf195 entry.
004823	C57BL/6J-nmf205/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf205 entry.
004830	C57BL/6J-nmf206/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf206 entry.
004831	C57BL/6J-nmf219/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf219 entry.
005101	C57BL/6J-nmf268/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf268 entry.
005298	C57BL/6J-nmf313/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf313 entry.
005329	C57BL/6J-nmf318/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf318 entry.
005448	C57BL/6J-nmf347/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf347 entry.
005741	C57BL/6J-nmf356/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf356 entry.
005467	C57BL/6J-nmf370/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf370 entry.
005451	C57BL/6J-nmf391/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf391 entry.
004085	C57BL/6J-nmf4/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf4 entry.
004107	C57BL/6J-nmf9/J	Cryopreserved - Ready for recovery
	View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf9 entry.
006107	C57BL/6J-rslk^2J/GrsrJ	Cryopreserved - Ready for recovery
	Homozygotes have white spotting and a diluted gray coat color.
000108	C57BL/6J-sea/J	Cryopreserved - Ready for recovery
	Mice homozygous for the sepia (sea) mutation have a pigment dilution that is similar to but not as severe as that of beige (Lyst^bg) mutants. On a nonagouti background sea/sea mice have lighter colored coat, ears and tail relative to their heterozygous and wildtype siblings, but do not have a detectable dilution in eye pigment at birth (Sweet and Lane, 1977). Unlike other coat color dilution mutations (including beige, reduced pigmentation, pallid, and pale ear) sepia mice do not have a diminution in NK cell activity (Orn et al., 1982).
001009	C57BL/6J-tp^3J/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 (ru) mutation but the eye color is not affected and the belly fur is lighter in color with yellow at the margins. tp/tp 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.)
005962	C57BL/6J-uwl/GrsrJ	Cryopreserved - Ready for recovery
	At birth homozygotes have unpigmented eyes and a very light skin color. The eyes become ruby colored as the mouse matures, but the skin color remains light. The coat is a very light cream color, which is a more severe dilution than that of the original underwhite mutation.
006362	C57BL/6J-Tg(CMV-Cox8a/EYFP)17J/J	Cryopreserved - Ready for recovery

005967	C57BL/6J-Tg(Mt1-Tnfsf4)1Pgn/Pgn	Cryopreserved - Ready for recovery
	Transgenic mice are susceptible to high fat diet-induced atherosclerosis as compared to C57BL/6 controls. Wang (Wang X, et al., Nat Genet, 2005) characterizes Tg(Mt1-Tnfsf4)2Pgn, however, Tg(Mt1-Tnfsf4)1Pgn has a similar phenotype (personal communication).
005968	C57BL/6J-Tg(Mt1-Tnfsf4)2Pgn/Pgn	Cryopreserved - Ready for recovery

006921	C57BL/6J-Tg(RP23-31I19)45Dn	Cryopreserved - Ready for recovery

007044	C57BL/6J-Tg(RP23-59K6)38Dn	Cryopreserved - Ready for recovery

008027	C57BL/6J-Tg(RP24-229O13)53Dn	Cryopreserved - Ready for recovery

008028	C57BL/6J-Tg(RP24-229O13)54Dn/J	Cryopreserved - Ready for recovery

003927	C57BL/6J-Tg(Sry-EGFP)92Ei/EiJ	Cryopreserved - Ready for recovery
	Tg(Sry-EGFP)92Ei has been shown to drive expression of GFP in pre-Sertoli and pre-granulosa cells of the genital ridge, with expression stronger in homozygotes than hemizygotes. Gonadal expression is not found in germ cells or vascular endothelial cells, but is restricted to a subset of somatic cells. Expression in the genital ridge begins in the center and moves out to the poles, with a bias toward the caudal pole. GFP expression is also found in tyrosine hydroxylase-expressing neurons of the substantia nigra of the midbrain and the medial mammillary bodies of the hypothalamus in males, but not females, with lower levels of expression observed sparsely throughout the cortex. Strongest expression in the male brain is in the pars compacta and, at the cellular level, both cytoplasmic and nuclear localization are found.
008245	C57BL/6J-Tg(Th-SNCA)5Eric/J	Cryopreserved - Ready for recovery
	These hwα-SYN-5 mice express wildtype human alpha-synuclein (hα-SYN) under the control of the rat tyrosine hydroxylase promoter. Expression of hα-SYN is detected in cell bodies, axons, and terminals of the nigrostriatal system (mRNA expression in midbrain, eye, and adrenal gland, with high levels of protein expression in the cell bodies of dopaminergic neurons in the midbrain and striatum). Hemizygous mice exhibit several Parkinson's disease-related characteristics including increased density of the dopamine transporter, impairments of the ubiquitin-proteasome system, and age-related progressive loss of locomotor activity and substantia nigra pars compacta dopaminergic neurons. The Parkinson's disease-related phenotype of these hwα-SYN-5 mice is intermediate between that of the C57BL/6J wild-type controls and the severely affected hm²α-SYN-39 strain (see Stock No. 008239). As such, these h ..... For more information please see the full phenotype on the strain data sheet
003650	C57BL/6J-Tg(Zp3-cre)82Knw/KnwJ	Cryopreserved - Ready for recovery
	This is a transgenic line in which cre expression is controlled by the regulatory sequences from the mouse zona pellucida 3 (Zp3) gene. This promoter normally directs expression exclusively in the growing oocyte prior to the completion of the first meiotic division. This strain is useful for deleting a floxed sequence specifically in the female germ line. The Donating Investigator suggests to accomplish this, females homozygous or heterozygous for the floxed allele, as well as hemizygous for the Zp3cre allele are crossed with wild type males. Progeny will carry the deleted-floxed allele.
008278	C57BL/6J-Tg(tetO-Clock)1Jt/J	Cryopreserved - Ready for recovery
	Homozygous transgenic mice are viable and fertile. These animals express the wildtype Clock gene under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoters, transgene expression can be conditionally regulated in the appropriate tissue of the bitransgenic offspring with the tetracycline analog, doxycycline. Transgenic expression of the Clock gene in the suprachiasmatic nucleus and brain of mice regulates the period length of circadian locomotor rhythms. This wild-type transgene shortens the period of circadian locomotor rhythms in mice, whereas overexpression of the Clock^delta19 mutant transgene (Stock No. 008277) lengthens the period. These effects ca ..... For more information please see the full phenotype on the strain data sheet
007599	C57BL/KaLawRij-Sharpin^cpdm/RijSunJ	Cryopreserved - Ready for recovery
	Mice homozygous for this spontaneous mutation develop a severe, chronic, inflammatory skin disease beginning at 3-5 weeks of age. Mice appear runted and life span is shortened. In addition to dermatitis, homozygotes exhibit multi-organ inflammation with eosinophilia, defective TH1 cytokine production, splenomegaly, absent Peyer's patches (adult), diminished serum immunoglobulins, and an absence of B cell follicles, follicular dendritic cells, and germinal centers in secondary lymph organs. This mutant mouse strain may be useful in studies related to eosinophilic dermatitis, inflammation, and secondary lymphoid organ deveopment.
000144	C57BLKS-sch/J	Cryopreserved - Ready for recovery

008625	C57BLKS/J-Cacna2d2^du-2J/LetJ	Cryopreserved - Ready for recovery
	Mice homozygous for ducky-2J mutation exhibit ataxia and paroxysomal dyskinesia, however, they lack the "ducky" gait found in mice homozygous for the ducky allele (du) . EEG recordings reveal infrequent bilateral spike wave discharges accompanied by behavioral arrest. Absence seizures are increased in comparison to ducky mice (personal communication). This strain may be useful for studies of epilepsy and voltage-dependent calcium channels.
008337	CBA/Ca-Tg(H2-K-HLA-G,B2M)1Alm/CmwJ	Cryopreserved - Ready for recovery
	HLA-G transgenic (HLA-Gtg) mice are viable, fertile, and harbor two co-injected transgenes; H-2K^b/HLA-G and hβ₂m. It was found that co-injecting the hβ₂m transgene greatly facilitated expression of the whole HLA-G molecule, implying that endogenous mouse β₂m cannot substitute for its human homolog. In addition, the CBA/Ca genetic background has a spontaneous deletion of the genes that encode the structurally/functionally homologous mouse Qa-2 protein, thus experimental results obtained using these HLA-Gtg mice may be attributed directly to transgene expression. Expression of HLA-G expression is observed in pre-implantation embryos and a variety of tissues; expression in the reproductive organs (uterus, ovary, and testes), lung, and liver is much more similar to mouse expression of Qa-2 than to K_b (despite the presence of the H-2K_b promoter and downstream coding sequence), while HLA-G expression in spleen, ..... For more information please see the full phenotype on the strain data sheet
000813	CBA/J-Atp7a^Mo-pew/J	Cryopreserved - Ready for recovery
	The Atp7 genes encode Cu2⁺ ATPases. Atp7a is the mouse ortholog of the human ATP7A gene, which is mutated in children with Menke's syndrome. The range of defects in both Menke's syndrome and in mice having mutations of Atp7a--the mottled series of mutants--are due to deficiencies in a number of copper-requiring enzymes, in turn attributed to an intracellular copper transport defect. Thus, it is likely that the Atp7a gene product functions as a copper transport protein. (For brief review and references, see Levinson et al., 1994.) Atp7a^Mo-pew, the mottled-pewter mutation, has the mildest effect of the known mutations at this locus. The sole phenotype noted in hemizygous males and homozygous females is their pale, silvery gray coat color. The coats of affected mice of both sexes are initially agouti; males become pewter by about 4 weeks and females at 5-6 weeks of age. Heterozygous females have normal, agouti coats throug ..... For more information please see the full phenotype on the strain data sheet
001006	CBA/J-Tyr^c-10J/J	Cryopreserved - Ready for recovery

003398	CBA/J-dal/GrsrJ	Cryopreserved - Ready for recovery
	Dark-like dal is a recessive mutation causing a darkened coat color, smaller size, gonad abnormalities, and dark staining urine. dal maps to Chromosome 7 and a previously described mutation named dark da maps to the same chromosomal region. Dark-like may be a remutation to dark da.However a test for allelism is not possible because dark is thought to be extinct. Mice homozygous for the dal mutation are easily recognized by 14 days of age by their darkened coats and smaller size. Some homozygotes appear, both phenotypically and pathologically (dense bones), to have skeletal abnormalities however X-rays appear normal. At 7 months of age females had no follicles and many corpora lutea and males mild testicular degeneration with increased Leydig cells. Serum assays for Albumin, BUN, Creatine, Bilirubin, and iron showed no significant differences from controls.
004416	D2(B6Ei)-twit/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for this recessive mutation are recognizable by 2.5 - 3 weeks of age by their smaller body size, gaunt torso, frailty, and constant quivering which is most obvious from the nose to the abdominal-thoracic area. Mutants also show poor ability to hold onto an edge with either their fore- or hindlimbs. Adult mutants may chatter excessively. Some homozygous mutants die before weaning; others survive through adulthood but they are unreliable breeders. twithas been mapped between the flanking markers D14Mit44 and D14Mit175 in the B band of Chr 14 at 22.9 Mb and 27.9 Mb, respectively.
004423	DBA/1LacJ-Lrp4^mdig/GrsrJ	Cryopreserved - Ready for recovery
	Homozygotes have variable brachydactyly and syndactyly of all four feet and incomplete polydactyly can occur in the front feet.
004518	DBA/2J-Agtpbp1^pcd-5J/GrsrJ	Cryopreserved - Ready for recovery

001594	DBA/2J-Dtnbp1^sdy/J	Cryopreserved - Ready for recovery
	The autosomal recessive mutation sandy (sdy) takes its name from the lightened coat color first identified on the DBA/2J background. As early as 7-8 days of age the pinnae, feet, tail and fur are lighter in color than those of wildtype littermates and the lack of eye pigment is a defining trait at birth. The eye color does not darken with age unlike muted (mu) homozygotes. On the agouti C3H background, sandy homozygotes look like muted homozygotes, but on the non-agouti C57BL/6J or DBA/2J backgrounds, sandy homozygotes look like pallid (Pldn^pa) homozygotes. The reduced pigmentation is linked to a storage pool deficiency. Sandy homozygotes have a prolonged bleeding time, in excess of 15 minutes, yet have normal platelet counts and normal sized platelets. Electron microscopy detects very few, if any, dense granules present in individual platelets of sandy homozygotes. Those that are detected are of normal size. Platelet serotonin levels are 7% that ..... For more information please see the full phenotype on the strain data sheet
000548	DBA/2J-Grid2^ho-4J/J	Cryopreserved - Ready for recovery

004641	DBA/2J-Grxcr1^pi-2J/J	Cryopreserved - Ready for recovery
	Mice homozygous for the pirouette 2 Jackson mutation display bi-directional circling and head bobbing and are completely deaf by ABR assessment. Consistent with a vestibular defect, they fail to swim at the surface of water, but instead roll underwater and sink before rescue.
000963	DBA/2J-Myo5a^d+17J/Myo5a^d/J	Cryopreserved - Ready for recovery

001789	DBA/2J-ge/J	Cryopreserved - Ready for recovery

002337	DBA/2J-pdw/J	Cryopreserved - Ready for recovery
	Mice homozygous for the recessive proportional dwarf (pdw) mutation can be identified by 25 days of age, having shortened limbs, tail, head, and body. Abnormalities were not detected in growth plates and skeletal mineralization patterns. Some pre-wean mortality has been reported. Both female and male homozygotes are fertile. (Sweet et al., 1992.)
006057	DBA/2J-sky/J	Cryopreserved - Ready for recovery
	Mice homozygous for the severe kyphosis mutation have open eyelids at birth, a progressive S-shaped kyphosis of the lumbar region of the spine, and a resultant shortened trunk and higher tail position. Small granulomas in muscle and brown fat are also found. Death usually occurs between 3 and 6 months of age and homozygotes do not breed.
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
006655	FVB-Tg(ACTA1-PABPN1*A17)1Drub/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 until roughly four months of age. At four months, hemizygotes develop a time-dependent progressive muscle weakness (measured by grip strength, wire maneuver and vertical gripping tests), which leads to late onset locomoter defects around nine months of age. At nine months mice can not lift their own body weight. They drag their pelvis when walking and show reluctance to walk. There is no difference in body weight or mortality up to 15 months of age compared to controls. Hemizygotes develop KCl-insoluble inclusions containing PABPN1 in the nuclei of skeletal muscle fibers with tubulo-filamentous ultrastructures. The proportion of myocte nuclei with aggregates increases with age. Significantly elevated numbers of TUNEL-positive myocyte nuclei can be found at six and 12 months. TUNEL staining is widely used as a cell-death marker in muscle disease ..... For more information please see the full phenotype on the strain data sheet
006405	FVB-Tg(Ckmm-cre)5Khn/J	Cryopreserved - Ready for recovery
	Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice have the Cre recombinase gene driven by the muscle creatine kinase (MCK or Ckm) promoter. Cre activity is observed in skeletal and cardiac muscle. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in skeletal and cardiac muscle deletion of the flanked genome.
010515	FVB-Tg(GAS7)63.2Lus/J	Cryopreserved - Ready for recovery
	These transgenic mice express the human growth arrest-specific 7, GAS7, under the direction of the endogenous human gene promoter. Transgene expression is detected in kidney, lung, heart, brain, adipose, liver, but not spleen. The transgene inserted on the X chromosome in tandem. Hemizygous male transgenic mice exhibit decreased fat/lean ratio with lower body weight; decreased gonadal fat pad weight and total fat pad weight; decreased triglycerides, unesterified cholesterol and glucose; and increased total cholesterol and HDL levels. Hemizygous female transgenic mice do not exhibit the decreased fat/lean ratio, but do have decreased mesenteric fat pad weight and reduced unesterified cholesterol. Hemizygous male animals exhibit normal body weight at weaning. This mutant mouse strain may be useful in studies of obesity and lipid metabolism.
010676	FVB-Tg(GFAP-CRYAB)141.6Mes/J	Cryopreserved - Ready for recovery
	These Cryab^Tg transgenic mice express the hamster Cryab, alpha B crystalline gene under the control of the human GFAP, glial fibrillary acidic protein, promoter. Transgene expression is astrocyte specific. Mice that are hemizygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of Alexander disease, astrocyte biology and neurodegeneration. When bred to mice that overexpresses GFAP and carry a targeted mutation of the crystallin, alpha B, gene, the lethal phenotype of the double mutant is partially rescued.
009638	FVB-Tg(GFAP-luc,GAPDH-rluc)172.9Mes/J	Cryopreserved - Ready for recovery
	These Dual-glo transgenic mice express both firefly luciferase (luc) under the control of the human GFAP (glial fibrillary acidic protein) promoter and Renilla luciferase under the control of the 0.5kb human GAPDH (glyceraldehyde-3-phosphate dehydrogenase) promoter. GFAP-fLuc transgene expression is highest in brain, with lower levels detected in heart and no detectable expression in kidney, muscle, lung and liver. The firefly luciferase protein co-localizes with GFAP in astrocytes after kainic acid induced injury. GAPDH-RLuc transgene expression is highest in brain and heart, with lower levels detected in kidney, muscle, lung and liver. Interindividual variability in firefly luciferase expression is reduced with normalization of the GFAP-fLuc signal to the GAPDH-RLuc signal. Retinal expression of luciferase is increased due to photoreceptor degeneration for mice on the FVB background and the homozygous presence of the retinal degeneration 1, Pde6b^rd1 ..... For more information please see the full phenotype on the strain data sheet
010947	FVB-Tg(Gstm5-EGFP)1Ilis/J	Cryopreserved - Ready for recovery
	Mice harboring the Gstm5-EGFP transgene are viable and fertile, normal in size and do not display any gross physical or behavioral abnormalities. The mouse glutathione S-transferase, mu 5 (Gstm5) promoter directs expression of enhanced green fluorescent protein (EGFP) to testis. Expression is not detected in liver, brain or kidney. Expression of EGFP does not completely parallel GSTM5. EGFP is widely distributed throughout the cytoplasm of spermatocytes, round spermatids and spermatozoa, but not spermatogonia, Sertoli cells or other cells, and is present from the pachytene spermatocytes to mature spermatozoa.
006125	FVB-Tg(H2-D-Il15)3304Clgr/J	Cryopreserved - Ready for recovery
	Mice hemizygous for this transgene are viable and fertile. The transgene was designed to optimize the overexpression of secreted, mature interleukin-15. Transgenic IL-15 expression has a similar tissue distribution as the endogenous gene, but at a significantly higher level. IL-15 protein is detectable in the serum from most mutant, but not from wildtype, mice. Mutant mice develop a progressive alopecia by as early as 5-6 weeks of age, with skin lesions appearing over time. While all transgenic mice exhibit early polyclonal/benign expansion of natural killer and memory CD8⁺ T lymphocytes (T/NK), two distinct phenotypes emerge over time: approximately 70% of the transgenic mice will exhibit polyclonal T/NK progression in multiple tissues, while the remaining 30% are characterized by T/NK clonal expansion in multiple tissues and acute lymphoblastic leukemia (T/NK ALL). Both T/NK phenotypes are fatal within the first year of life. Mice harboring this transgene may be useful in ..... For more information please see the full phenotype on the strain data sheet
006822	FVB-Tg(KRT14-MAP2K1/Esr1)12Pkha/J	Cryopreserved - Ready for recovery
	Mice hemizygous for this "K14-Mek1:ER" transgene are viable and fertile, with expression of the Mek1:ER fusion protein (a constitutively active mutant region from human mitogen activated protein kinase-kinase 1 (Mek1^R4F; containing an amino-terminal deletion of aa 32-51 and the S218E/S222D substitutions) fused at its carboxy terminal with the G525R mutant murine estrogen receptor ligand binding domain (ER^TM)) directed to epidermis by the human keratin 14 promoter. Because of the ER^TM region of the fusion protein, Mek1:ER is restricted to the cytoplasm and the biochemical activity of the Mek1:ER fusion gene can be induced following tamoxifen administration. For example, induction of this constitutively active form of human Map2k1 (Mek1^R4F) promotes the undifferentiated, proliferative phenotypic characteristics observed in epidermal neoplasia in as few as 5 days (including hyperplasia, increased levels of phosphorylated ERK1/2, increased mitot ..... For more information please see the full phenotype on the strain data sheet
005705	FVB-Tg(KRT14-Vegfa)3Dtm/J	Cryopreserved - Ready for recovery
	Mice hemizygous for the transgene are viable and fertile. Transgene expression is demonstrated in the basal keratinocyte layer of the epidermis and outer root sheath keratinocytes of hair follicles. Homozygous mice spontaneously develop severe psoriasis-like lesions between 3-6 months of age, where hemizygous mice do not. Transgenic mice have increased density of tortuous cutaneous blood capillaries with elevated expression of select VEGF receptors, most prominently in neonates. Dermal mast cell localization and capillary hyperpermeability are also increased. Postcapillary venules exhibit significantly enhanced leukocyte rolling and adhesion. Transgenic expression promotes lymphangiogenesis associated not only with delayed-type hypersensitivity induced psoriasis-like skin inflammation but also with cutaneous tissue repair after wounding. Further, transgenic mice have accelerated chemically induced skin carcinogenesis with tumor associated lymphangiogenesis and angiogenesis. Elevated me ..... For more information please see the full phenotype on the strain data sheet
008784	FVB-Tg(Lactb)74.2Lus/J	Cryopreserved - Ready for recovery
	Mice hemizygous for the mouse Lactb (lactamase, beta) transgene are viable, fertile, normal in size and do not display any gross behavioral abnormalities. The transgene encompasses the entire mouse structural gene and its regulatory sequences. Transgenic mice have a higher fat-mass-to-lean-mass (FMLM) ratio compared to wild-type littermates when fed a 6% fat diet. Over time the FMLM ratio difference between transgenic and wild-type animals increases. This mutant mouse strain may be useful in studies of metabolic syndrome and obesity.
008680	FVB-Tg(MECP2)3Hzo/J	Cryopreserved - Ready for recovery
	As hemizygotes, these human methyl CpG binding protein 2 transgenic mice express the gene at ~3-5 fold wildtype levels in the brain. Mice show progressive neurobehavioral abnormalities consisting of forepaw clasping, aggressiveness, kyphosis, hypoactivity characterized by a freezing-like behavior, and premature death (a proportion die at ~3 weeks of age). The transgene is inserted on the X chromosome. Males have a more severe phenotype, whereas females have a variable and milder phenotype. This strain may be useful in studies of X-linked neurobehavioral disorders, including MECP2 triplication syndrome, mental retardation, and autism.
010587	FVB-Tg(Myh6-MEF2A)1Jmol/J	Cryopreserved - Ready for recovery
	Expression of the full-length human MEF2A (myocyte enhancer factor 2A) cDNA is driven by the mouse cardiac-specific alpha myosin heavy chain promoter in this transgenic strain. Mice develop a dilated cardiomyopathy.
010581	FVB-Tg(Myh6-Map2k1*)1Jmol/J	Cryopreserved - Ready for recovery
	The mouse Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha) promoter drives expression of Ser217/221Glu mutant mitogen-activated protein kinase kinase 1 (Map2k1). These mice develop a mild concentric cardiac ventricular hypertrophy. No premature lethality or cardiac dilation is observed in hemizygotes.
010582	FVB-Tg(Myh6-Map2k3*)1Jmol/J	Cryopreserved - Ready for recovery
	The mouse Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha) promoter drives expression of Ser189/193Ala mutant mitogen-activated protein kinase kinase 3 (Map2k3). These mice develop a progressive, severe hypertrophic cardiomyopathy detected at two months of age. Histological staining reveals interstitial cell fibrosis and a significant increase in myocyte cross-sectional area by 4 months of age.
010584	FVB-Tg(Myh6-Map2k7)1Jmol/J	Cryopreserved - Ready for recovery
	Mouse Map2k7 cDNA expression is driven by the alpha myosin heavy chain (Myh6) promoter in this transgenic strain. Expression is increased three to four fold in the hearts of these mice. Animals develop a mild compensated cardiac hypertrophy (10-15% increase over wildtype).
010585	FVB-Tg(Myh6-Mapk1)1Jmol/J	Cryopreserved - Ready for recovery
	Rat Mapk1 cDNA expression is driven by the alpha myosin heavy chain (Myh6) cardiac-specific promoter in this transgenic strain. No visible phenotype has been observed.
010583	FVB-Tg(Myh6-Mapk14*)1Jmol/J	Cryopreserved - Ready for recovery
	The mouse Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha) promoter drives expression of TGY->AGF mutant mitogen-activated protein kinase 14 (Mapk14). These mice develop severe hypertrophic cardiomyopathy. At two months of age, transgenic mice show a significant increase in heart-to-body weight ratios that progresses with age.
010586	FVB-Tg(Myh6-Mef2c)2Jmol/J	Cryopreserved - Ready for recovery
	Expression of the full-length mouse Mef2c (myocyte enhancer factor 2C) cDNA is driven by the cardiac-specific alpha myosin heavy chain promoter in this transgenic strain. A 1.6-fold increase in expression is observed in the heart by Western blotting. Mice develop a dilated cardiomyopathy and large atrial clots, consistent with a heart failure phenotype and poor ventricular function.
009438	FVB-Tg(Myh6-SOD2,Tyr)3Pne/J	Cryopreserved - Ready for recovery
	These transgenic mice overexpress the human superoxide dismutase 2, mitochondrial (SOD2) under the control of the mouse myosin, heavy polypeptide 6, cardiac muscle, alpha, Myh6, promoter. This transgenic insert was co-injected with the tyrosinase coat color marker, TyBS, which confers dark grey pigmentation on an albino background. 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 reports that homozygotes are viable but have not been tested for fertility. Transgene expression is specific to the heart as detected by Western blot analysis. Expression is localized to mitochondria. SOD activity increased by 20-fold in heart and cardiac catalase activity is increased 2-fold. Exogenous reactive oxygen species (ROS) are reduced in cardiomyocytes isolated from transgenic mice. This mutant mouse strain may be useful in studies of diabetic cardiom ..... For more information please see the full phenotype on the strain data sheet
011037	FVB-Tg(Myh6-cre)2182Mds/J	Cryopreserved - Ready for recovery
	The cardiac-specific murine alpha myosin-heavy chain (Myh6, myosin, heavy polypeptide 6, cardiac muscle, alpha) promoter drives expression of cre in this transgenic strain. Breeding this mouse with another carrying loxP-flanked sequences results in the deletion of the flanked sequences in the offspring. The promoter induces greater than 90% recombination in cardiac muscle cells. No recombination is observed in liver, lung, skeletal muscle (quadriceps), and spleen, or in extraneous cell types in the heart.
010588	FVB-Tg(Myh6/NFAT-luc)1Jmol/J	Cryopreserved - Ready for recovery
	The mouse alpha myosin heavy chain cardiac promoter drives expression of nuclear factor of activated T cell (NFAT) binding sites and a luciferase reporter to detect calcineurin-NFAT signaling. In the adult heart, NFAT-luciferase activity is upregulated in association with cardiac hypertrophy induced by pressure-overload and following myocardial infarction-induced heart failure.
012684	FVB-Tg(Myh6/tetO-POSTN)22.1Jmol/J	Cryopreserved - Ready for recovery
	These transgenic mice express human POSTN (periostin, osteoblast specific factor) cDNA under the control of an inducible mouse Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha) minimal promoter. When bred with transgenic mice expressing a tetracycline transactivator or reverse transactivator protein, cardiac myocyte-specific expression of the human cDNA can be controlled in the offspring by withdrawal or administration of a tetracycline analog. Constitutive expression of the cDNA produces no phenotypic abnormalities or enhancements at baseline. This strain may be useful in studies of the transgene and its role in cardiac function.
010580	FVB-Tg(Myh6/tetO-PRKCA*)1Jmk/J	Cryopreserved - Ready for recovery
	These transgenic mice express a dominant negative form of rabbit PRKCA (protein kinase C, alpha) under the control of an inducible mouse Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha) minimal promoter. When bred with transgenic mice expressing a tetracycline transactivator or reverse transactivator protein, cardiac-specific expression of the rabbit cDNA can be controlled in the offspring by withdrawal or administration of a tetracycline analog. When crossed with a transcriptional transactivator (tTA) line in the absence of doxycycline, the mice develop a mild cardiomyopathy.
008073	FVB-Tg(PDGFB-Adra2b)13Hag/J	Cryopreserved - Ready for recovery
	Mice that carry this transgene are viable and normal in size and express the mouse alpha 2b adrenergic receptor in cerebellum, brainstem, hippocampus and cortex. Expression in whole brain is 1.8 fold higher than the endogenous protein. Transgene expression in the kidney, heart, aorta, and liver tissues was not observed. By 8-9 weeks, transgenic mice exhibit elevated systolic blood pressure. Heart rate is similar to wild-type. This mutant mouse strain may be useful in studies of hypertension.
008878	FVB-Tg(Pbsn-Ar*E231G)7353Ng/J	Cryopreserved - Ready for recovery
	These transgenic mice express a mutant mouse androgen receptor (Ar), E231G, under the control of the minimal -426/+28 rat probasin promoter. The E231G mutant androgen receptor has an N-terminal domain mutation that increases ligand-independent basal activity and responsiveness to coactivators. The transgene expression is detected specifically in the epithelial compartment of the ventral prostate by RT-PCR analysis; the majority of expression is detected in the ventral prostate, with lower expression in the dorsolateral prostate. At 12 weeks of age, hemizygous transgenic male mice develop epithelial hyperplasia and dysplasia in the ventral prostate lobes, that progresses (by approximately 50 weeks of age) to primary prostate tumors with associated lymphocytic invasion and metastatic deposits in lungs. Histological analysis reveals lesions consistent with mouse prostatic intraepithelial neoplasia (PIN). Female mice that are homozygous for the transgene are viable, normal in s ..... For more information please see the full phenotype on the strain data sheet
008874	FVB-Tg(Pbsn-IGF1*)5305Ng/J	Cryopreserved - Ready for recovery
	These transgenic mice express an isoform of the human insulin-like growth factor 1 (somatomedin C) under the control of the minimal -426/+28 rat probasin promoter. The expressed des(1-3) IGF-1 isoform (IGF-1^des) has decreased interaction with IGF binding proteins due to a 3-amino acid deletion in the N terminus of the mature protein. The transgene is detected in the dorsolateral and ventral prostate lobes by RT-PCR analysis. Hemizygous transgenic male mice develop spontaneous atypical prostate hyperplasia, but the lesions do not progress to neoplasia within 1 year. Histological analysis reveals lesions consistent with mouse prostatic intraepithelial neoplasia (PIN) with increased abnormal acini. Female mice that are homozygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of prostate tumorigenesis. When bred to C57BL/6-Tg(TRAMP)8247Ng/J mice ( ..... For more information please see the full phenotype on the strain data sheet
005625	FVB-Tg(Pcp2-tTA)3Horr/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Cerebellar Purkinje cell-specific tTA expression has been confirmed using PCR. Constitutive expression of tTA in Purkinje cells makes this strain suitable for creating bitransgenic mice that can, by withdrawing tetracycline (or its derivative doxycycline), inducibly express a gene of interest in Purkinje cells when the gene of interest is under the direction of a tetracycline-responsive element (TRE; tetO).
008326	FVB-Tg(Pomc-rtTA)1Rck/J	Cryopreserved - Ready for recovery
	The mouse pro-opiomelanocortin-alpha (Pomc) promoter drives expression of a modified reverse tetracycline regulatable transactivator (rtTA2^S-M2_{F86Y A209T}) in this Tet-On transgenic strain. When these mice are mated to a second transgenic strain carrying a target gene regulated by the tetO responsive elements, expression of the target gene is turned on in POMC-expressing neurons by the tetracycline analog doxycycline (dox). Dox can be administered orally in the food or water. Hemizygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
008537	FVB-Tg(Tek-cre)2352Rwng/J	Cryopreserved - Ready for recovery
	These transgenic mice express the Cre recombinase under the control of the mouse Tek, endothelial-specific receptor tyrosine kinase (also known as Tie2), promoter. Cre recombinase expression is detected in most endothelial cells and blood islands of the extraembryonic mesoderm by embryonic day (ED)7.5 and in the dorsal aorta by ED8.5. Especially high levels of expression are seen in head vasculature by ED9. When crossed with reporter strains (expressing beta-galactosidase or alkaline phosphatase), recombination is detected in all blood vessels and some blood cells examined at ED11.5, which indicates that Cre activity occurs in early vascular progenitor cells, endothelial cells and some hematopoietic cells. Mice homozygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This strain represents an effective tool for generating endothelial cell specific-targeted conditional mutations.
012662	FVB-Tg(Ttr-Igf1)1Sykr/J	Cryopreserved - Ready for recovery
	These "HIT" transgenic mice overexpress rat IGF1 specifically in the liver, with normal tissue IGF-I but have increased serum IGF-I levels. Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator reports that there is no difference between the phenotype exhibited by homozygotes compared to hemizygotes.
005021	FVB-Tg(ZP2)2Dean/J	Cryopreserved - Ready for recovery
	These transgenic mice express the human zona pellucida 2 (ZP2) protein. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygotes die shortly after birth. Transgene expression (mRNA and protein) is oocyte specific. This transgene rescues the homozygous null Zp2 infertility phenotype (see Stock No. 004129). This mutant mouse strain represents a model that may be useful in studies of reproduction and fertility.
013156	FVB-Tg(tetO-CDK5R1*)1Vln/J	Cryopreserved - Ready for recovery
	These tetO-CDK5R1* mice express a truncated human cyclin-dependent kinase 5, regulatory subunit 1 (CDKR1 or p35) cDNA sequence, also referred to as p25, under the control of a tetracycline operator (tetO; also called tetracycline-responsive element (TRE, TetRE) or tet-operator). The N-terminal truncated isoform of p35 is p25. Unlike p35, which is membrane bound in postmitotic neurons in the brain, p25 is non-tethered and expression is seen in all cellular compartments of neuronal somata and dendrites. Mice that are hemizygous for this transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred with another mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), CDK5R1 expression can be regulated with the tetracycline analog doxycycline (dox) in the resulting double mutant offspring. For example, when bred to a strain expressing ..... For more information please see the full phenotype on the strain data sheet
010578	FVB-Tg(tetO-Dusp6)1Jmol/J	Cryopreserved - Ready for recovery
	A tetracycline-responsive element (TRE; tetO) and mouse alpha myosin heavy chain minimal promoter regulate expression of Myc-tagged mouse Dusp6. When these transgenic mice are bred to Myh6-tTA transgenic animals, in the offspring, Dusp6 expression is upregulated in the heart. Transgene expression can be abated in the double transgenic animals with doxycycline administration.
008685	FVB-Tg(tetO-Kdr*)4377.5Rwng/J	Cryopreserved - Ready for recovery
	These transgenic mice express a truncated mouse Kdr (kinase insert domain protein receptor) gene under the control of a tetracycline-responsive promoter element (TRE or tetO). The truncated gene encodes amino acids 1 through 828, which includes the cytoplasmic tyrosine kinase domain, and has a hemaglutin (HA) tag fused at the C terminus. When bred with a transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), a bitransgenic animal can be produced that has tissue-specific expression of Kdr that can be regulated with the tetracycline analog, doxycycline. For example, when bred to a strain expressing tTA in liver (see Stock No. 003563) and a targeted mutation of Kdr (see Stock No. 002938) , this mutant mouse strain may be useful in studies of liver organogenesis. ..... For more information please see the full phenotype on the strain data sheet
008695	FVB-Tg(tetO-MET)23Rwng/J	Cryopreserved - Ready for recovery
	These transgenic mice express the human MET (met proto-oncogene (hepatocyte growth factor receptor)) gene under the control of a tetracycline-responsive promoter element (TRE or tetO). When bred with another transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), a bitransgenic animal can be produced that has tissue-specific expression of MET that can be regulated with the tetracycline analog, doxycycline. When bred to mice carrying the transgene LAP-tTA, (see Stock No. 003563 for example), the resulting bi-transgenic mice have inducible overexpression of MET in hepatocytes and represent an effective tool for studying hepatocellular carcinoma.
012385	FVB-Tg(tetO-Ppargc1b)7Dpk/J	Cryopreserved - Ready for recovery
	These transgenic mice express Ppargc1b (peroxisome proliferative activated receptor, gamma, coactivator 1 beta) regulated by the tetracycline operator (tetO; also called tetracycline-responsive element (TRE, TetRE) or tet-operator). When mated to a mutant strain expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), tissue Ppargc1b expression may be regulated with the tetracycline analog doxycycline (dox) in the double mutant offspring. This "high expressor" strain may be useful in studies further characterizing the signaling role of the transgene as it pertains to physiology and disease, particularly mitochondrial function.
006439	FVB-Tg(tetO/CMV-KRAS*G12C)9.1Msmi/J	Cryopreserved - Ready for recovery
	Hemizygous mice are viable and fertile. These Ki-ras^G12C transgenic mice express the human KRAS^G12C mutation under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoters, transgene expression in the appropriate tissues of the bitransgenic offspring can be regulated with the tetracycline analog, doxycycline. When crossed with mice containing a lung-specific rtTA protein (e.g. Stock Nos. 006222, 006232, 006242 or 006225), treatment with doxycycline results in the formation of benign hyperp ..... For more information please see the full phenotype on the strain data sheet
006402	FVB/N-Adrb3^tm1Lowl/J	Cryopreserved - Ready for recovery
	Homozygous mice are viable and fertile. No gene product (mRNA) is detected by Northern blot analysis from homozygous brown or white adipose tissue. Homozygous mice have modest increases in fat stores (female more than male). In contrast to control animals, homozygous mice are unresponsive to beta-3 adrenergic receptor (beta3-AR) agonist treatment (no effect on adenylate cyclase activity, lipolysis, or gastro-intestinal motility). These mutant mice may be useful in studies of energy balance, obesity, fat metabolism, cholesterol homeostasis, diabetes, and pharmacological screening of beta3-AR agonists for potential drug treatment.
013574	FVB/N-Tg(149m19)M141Kunst/J	Cryopreserved - Ready for recovery
	These transgenic mice contain the 149m19, line M141, BAC transgene. Expression of the Serf1, Smn1, Naip2 and Naip5 genes is detected by RT-PCR. Smn1 expression is also detected by Western Blot. The phenotype of FVB-Tg(Sod1G86R)M1Jwg/J (Stock No. 005110) mice is partially rescued when crossed to these 149m19, line M141, mice. The phenotype of mice carrying the Tg(SOD1G93A)1Gur transgene on the FVB/NJ background is not rescued by crossing to these 149m19, line M141, mice (onset and survival is the same as transgenic strain). 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 verified homozygosity.
008200	FVB/N-Tg(CAG-EGFP,-ALPP)2.6Ggc/J	Cryopreserved - Ready for recovery
	Mice harboring the piGAP transgene are viable and fertile, with expression of the eGFP-F-IRES-hPLAP dicistronic gene blocked by an upstream loxP-flanked STOP-polyA sequence. When bred to mice that express Cre recombinase, the resulting offspring will have the STOP-polyA sequence deleted in the cre-expressing tissue(s), permitting dicistronic expression of eGFP-F-IRES-hPLAP. When transgene expression is induced in neurons, human Placental Alkaline Phosphatase (PLAP or ALPP) outlines axonal and dendritic projections and can be visualized by a simple histochemical reaction in fixed cells. Likewise, in vivo fluorescence of farnesylated Enhanced Green Fluorescent Protein (eGFP-F; optimized to target expression to the cytoplasmic side of the plasma membrane) labels axons, and dendrites throughout their length. Because both proteins localize alongside the neuronal surface, concomitant detection of cell body, neurites, and presynaptic and postsynaptic sites may be o ..... For more information please see the full phenotype on the strain data sheet
009354	FVB/N-Tg(Dazl-EGFP)10Rarp/J	Cryopreserved - Ready for recovery
	Mice harboring the Dazl-eGFP transgene are viable and fertile, with the mouse Dazl (deleted in azoospermia-like) promoter/enhancer regions directing expression of enhanced green fluorescent protein (EGFP) primarily to adult mouse testis. Specifically, robust EGFP expression (both transcript and fluorescence) is observed in adult mouse testis in a developmentally-regulated, stage-specific expression pattern during spermatogenesis. Much lower EGFP transcript and fluorescence is observed in adult ovaries. Very low levels of EGFP transcript expression (but not fluorescence) is reported in fetal and newborn gonads of both sexes. These Dazl-eGFP transgenic mice may be useful for gametogenesis studies, including pachytene spermatocytes.
002059	FVB/N-Tg(HIV-1)316Morr/J	Cryopreserved - Ready for recovery

002259	FVB/N-Tg(HIV-1)333Morr/J	Cryopreserved - Ready for recovery

002060	FVB/N-Tg(HIV-luc)326Morr/J	Cryopreserved - Ready for recovery

011032	FVB/N-Tg(Hoxc13)61B1Awg/J	Cryopreserved - Ready for recovery
	Mice hemizygous for the transgene mice are viable, fertile and overexpress HOXC13. At birth, transgenic mice can be identified by a short tail (reduced number of verterbrae), taut skin, kinky whiskers and small size. By 4.5 months, mice exhibit retarded coat hair growth, followed by progressive alopecia and a hyperproliferative disorder resembling ichthyosis. Both cellular and squamous epidermal layers appear thickened, irregular and disorganized. Hair follicles are enlarged, and, in older mice, many follicles degenerate into cyst-like structures.
007800	FVB/N-Tg(Ins1-luc)VUPwrs/J	Cryopreserved - Ready for recovery
	Mice hemizygous for this MIP-luc transgene are viable and fertile, with luciferase (luc) expression under control of the mouse insulin I promoter (MIP or Ins1). After injection of the luciferin substrate, luc expression can be visualized using bioluminescence imaging (BLI). Mice from founder line VU (MIP-Luc-VU) exhibit strong and consistent luc bioluminescence emanating exclusively from β cells of the pancreatic islet, and luc-expressing beta cells can be visualized through the skin. MIP-Luc-VU pancreatic islets have normal islet architecture and insulin secretion both in vivo and in vitro, with luciferase intensity reporting the number of islets. In transplantation settings and models of increased/decreased beta cell mass, bioluminescence is proportional to beta cell mass (incorporating some aspects of islet function, with signal up-regulation in hyperglycemic states). These MIP-Luc-VU mice may be useful as a source of luciferase-expressing β cel ..... For more information please see the full phenotype on the strain data sheet
012459	FVB/N-Tg(Myh6*/tetO-Capn1)L2Gwd/J	Cryopreserved - Ready for recovery
	Mice hemizygous for the MHCmin^TetO-Capn1 transgene are viable and fertile, normal in size and do not display any gross physical or behavioral abnormalities. Expression of Capn1 is regulated by a tetracycline operator (tetO), driven by an enhanced α-MHC promoter which limits calpain 1 expression in heart. When mated to a mutant strain expressing tetracycline-controlled transactivator protein (tTA), expression of calpain 1 protein may be regulated with tetracycline or its analog doxycycline (dox) in the double mutant offspring. Calpain 1 is necessary for proteolytic processing and subsequent proteasomal degradation of a subset of myocardial proteins whose abnormal accumulation produces autophagosomes and cardiomyocyte degradation. Calpain 1 is pathologically activated in myocardial ischemia and may be responsible for features of myocardial stunning. In overexpression systems, calpain 1 is lethal and leads to cardiac disease, while this s ..... For more information please see the full phenotype on the strain data sheet
008716	FVB/N-Tg(Myh6-AIP/PLN*)46Jded/J	Cryopreserved - Ready for recovery
	SR-AIP transgenic mice carry the α-MHC-AIP₄-SR transgene. Hemizygous SR-AIP mice are viable and fertile, with expression of AIP₄ (a tetramer of the CaMKII autocamtide inhibitory peptide AIP) directed to the sarcoplasmic reticulum (SR) of the heart by the murine alpha-myosin heavy chain (α-MHC or Myh6) promoter and a truncated phospholamban (PLB) transmembrane domain (harboring two loss-of-function mutations to prevent direct SERCA inhibition by the fusion protein). FLAG epitope expression may be used to identify presence of the fusion protein. The SR-targeted AIP concatemer peptide binds CaMKII, preventing phosphorylation of PLB and subsequent activation of SERCA, thereby increasing diastolic intracellular calcium. Whole heart function and diastolic relaxation are slightly impaired, and pregnancy leads to earlier onset of cardiac hypertrophy. These SR-AIP transgenic mice may be useful in studying sarcoplasmic reticulum-targeted CaMKII inhibitio ..... For more information please see the full phenotype on the strain data sheet
012461	FVB/N-Tg(Myh6-Cast)1Gwd/J	Cryopreserved - Ready for recovery
	Mice hemizygous for the Myh6-Cast allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Expression of Cast is regulated by an α-myosin heavy chain (Myh6) promoter, which results in the overexpression of calpastatain, a highly specific global inhibitor of calpain 1 and calpain 2, in the heart. Overexpression of calpastatin causes diminished ubiquitination of myocardial proteins resulting in a progressive dilated cardiomyopathy characterized by accumulation of intracellular protein aggregates, formation of autophagosomes, and degeneration of sarcomeres. These Myh6-Cast mice may be useful for assessing the consequences of cardiomyocyte-specific calpain inhibition in normal, ischemic, and failing hearts, and the contribution of endogenous calpains to myocardial protein turnover.
008202	FVB/N-Tg(NPHS2-rtTA2*M2)1Jbk/J	Cryopreserved - Ready for recovery
	These mice express an optimized reverse tetracycline-controlled transactivator (rtTA2-M2) protein under the control of the human NPHS2 promoter, which directs expression to podocytes within kidney glomeruli. When mated to a second strain carrying a gene under the regulatory control of a tetracycline-responsive promoter element (TRE or tetO), expression of the gene in podocytes is induced with administration of the tetracycline analog, doxycycline (dox). These podocin-rtTA mice provide a Tet-On tool that allows dox-inducible expression of genes in podocytes, and may be useful in studying the role of podocyte nephrobiology in renal disorders.
003140	FVB/N-Tg(PAI1-lacZ)1Jjb/J	Cryopreserved - Ready for recovery
	Transgenic mice carry a beta-galactosidase reporter gene driven by human plasminogen activator inhibitor type I (PAI1) promotor. Transgene expression detected in two independent lines was observed only in kidney from embryonic day 13 to adult, and was seen primarily in proximal tubule cells of the outer medulla. Transgene expression and activity was unchanged in response to TGFbeta and remained restricted to kidney.
005942	FVB/N-Tg(Pf4-tTA/VP16)42Kra/J	Cryopreserved - Ready for recovery
	Transgenic mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Transgenic tetracycline-controlled transactivator protein (tTA) expression is limited to megakaryocytes by the rat chemokine (C-X-C motif) ligand 4 (Cxcl4; formerly called platelet factor four (Pf4)) promoter. When bred to mice carrying a gene of interest coupled to a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene is induced specifically in megakaryocytes. Administration of tetracycline/doxycycline sequesters the transgenic protein, and prevents expression of the TRE-regulated target gene. This mouse originally was designed to be bred with Tg(tetO-Aurkb,lacZ)41Kra (see Stock No. 005941); a transgenic mouse with a bidirectional tetO promoter controlling a mitotic regulator gene (aurora kinase B) and a beta-galactosidase reporter. Megakaryocytes and platelet cells from th ..... For more information please see the full phenotype on the strain data sheet
006875	FVB/N-Tg(Tagln-rtTA)E1Jwst/J	Cryopreserved - Ready for recovery
	Transgenic SM22-rtTA mice are viable and fertile. These mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the murine SM22-alpha (SM22α or transgelin) promoter. When hemizygotes are mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene in the bitransgenic offspring is inducible in smooth muscle cells with administration of the tetracycline analog, doxycycline. These SM22-rtTA mice provide a "Tet-On" tool that allows the inducible expression of genes in smooth muscle cells.
007247	FVB/N-Tg(YAC353G6)W7Hay/J	Cryopreserved - Ready for recovery
	These transgenic mice express the human huntingtin protein containing a 133 CAG repeat expansion and a mutation in exon 13 conferring resistance to caspase-6 cleavage to the gene product. Expected caspase-6 cleaved fragments are not detected in brain lysates by Western blot analysis. Transgenic mice have brain weight and striatal volume similar to wild-type controls and do not exhibit neuronal loss at 12 months of age when compared to transgenic mice that express human huntingtin protein containing a 128 CAG repeat (FVB-Tg(YAC128)53Hay/J Stock No. 004938). These transgenic mice have activity levels and motor function similar to wild-type controls, and are resistant to neuron excitotoxicity. Immunohistochemical analysis of striatal brain sections reveals delayed nuclear localization of mutant huntingtin protein in these transgenic mice at nine months of age. Between nine and 12 months of age, an increase of nuclear huntingtin i ..... For more information please see the full phenotype on the strain data sheet
005941	FVB/N-Tg(tetO-Aurkb,lacZ)41Kra/J	Cryopreserved - Ready for recovery
	Hemizygous and homozygous transgenic mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Expression of the bicistronic transgene is directed by a tetracycline-responsive regulatory element (TRE; tetO). When transgenic mice are bred with another transgenic strain expressing the tetracycline-controlled transactivator protein (tTA) under the regulation of a tissue-specific promoter, both aurora kinase B (Aurkb) and lacZ cistrons are inducibly expressed in the appropriate tissue in the bitransgenic offspring. This mouse was originally designed to be bred with Tg(Pf4-tTA)42Kra transgenic mice, which express tTA from a megakaryocyte-specific promoter. Megakaryocytes and platelet cells derived from the bitransgenic offspring show inducible and reversible beta-galactosidase expression. Further, megakaryocytes inducibly express Aurkb mRNA (but not protein) with a modest effect on megakaryocyte ploidy and no effect on platelet quant ..... For more information please see the full phenotype on the strain data sheet
006202	FVB/N-Tg(tetO-BCR/ABL1)2Dgt/J	Cryopreserved - Ready for recovery
	Hemizygotes are viable, fertile, normal in size, and do not display any behavioral abnormalities. Transgene expression is directed by the tetracycline-responsive element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoters , BCR-ABL1 fusion protein expression can be regulated in the appropriate tissue of the bitransgenic offspring with the tetracycline analog, doxycycline. These mice originally were designed to be bred with transgenic mice harboring a Tal1-tTA transgene (see Stock No. 006209), creating double transgenic offspring as a model for studies of the Philadelphia chromosome and inducible chronic myeloid leukemia. When bred to a strain expressing tTA in the epithelial cells of secretory organs and skin (see Stock ..... For more information please see the full phenotype on the strain data sheet
003315	FVB/N-Tg(tetORo1-lacZ)3Conk/J	Cryopreserved - Ready for recovery
	Transgenic mice express both Ro1 (Receptor Activated Solely by a Synthetic Ligand (RASSL), opioid, #1) and lacZ under the regulation of tetracycline responsive elements (TRE; tetO)(see Strain Development for more information). When Ro1 is expressed in the heart (by crossing it with strain FVB.Cg-Tg(Myh6-tTA)6Smbf/J - Stock No. 003170), administration of the drug spiradoline produces a dramatic decrease in heart rate. Since Ro1 and lacZ are co-integrated and under tetracycline/doxycycline control, X-gal staining can be used to identify cells in which the tet-inducible system is working. Ro1 activates G_i-signaling in response to spiradoline, and can be used to study the effect of G_i-signaling in many tissues. In the heart, Ro1-mediated activation of G_i-signaling slows heart rate, but in other tissues it is predicted to control diverse physiological events, such as cell proliferation, se ..... For more information please see the full phenotype on the strain data sheet
006109	FVB/NJ-Tg(GART)2Eri/DnJ	Cryopreserved - Ready for recovery
	This transgene drives minimal human GART mRNA expression and no protein was detected. Auditory startle response may be decreased at 5 months of age, but ABR studies did not detect a hearing deficit.
006110	FVB/NJ-Tg(GART)3Eri/DnJ	Cryopreserved - Ready for recovery
	This transgene drives minimal human GART mRNA expression and no protein was detected. Auditory startle response may be decreased at 5 months of age, but ABR studies did not detect a hearing deficit.
008279	FVB/NJ-Tg(RP24-173I23)1Sun/Sun	Cryopreserved - Ready for recovery
	Carriers are phenotypically normal and males and females are fertile. One copy of this Sharpin-containing transgene is adequate to rescue the chronic proliferative dermatitis (cpdm) homozygous phenotype.
003896	MRL/MpJ Fas^lpr-Foxq1^sa-J/J	Cryopreserved - Ready for recovery
	MRL/MpJ, and one of its ancestral strains LG/J, display heightened wound healing relative to a panel of other inbred strains. At 4 weeks post-injury, 2mm ear punch wounds healed to 0-0.4mm in MRL/MpJ mice but were still 1.2-1.6mm in C57BL/6 mice. At 15 days post-injury C57BL/6 showed a maximal closure of 30% reduction in ear hole size while MRL showed 85% reduction. The process of healing in MRL/MpJ mice was faster, more complete, showed increased swelling, angiogenesis, fibroblast migration, extracellular matrix deposition, and decreased scarring and fibrosis. Additionally, hair follicles and accompanying sebaceous glands were regenerated to a much greater degree. The other ancestral strains of MRL/MpJ (C3H, C57BL/6, and AKR) do not display this enhanced healing. Bone marrow transplantation showed that the MRL/MpJ healing phenotype did not readily transfer with bone marrow and did remain in the irradiated host tissues. Enhanced healing of cardiac wounds has also been reported in MRL/M ..... For more information please see the full phenotype on the strain data sheet
013252	MRL/MpJ-Npr2^cn-3J/GrsrJ	Cryopreserved - Ready for recovery

013782	MRL/MpJ-aphl/GrsrJ	Cryopreserved - Ready for recovery
	Homozygotes can be identified as early as 7 to 8 days of age when the first coat comes in. The hair growth is sparse and grows in stripes with bald areas between. The areas around the eyes often develop a mild, crusty growth and rash. All four hair types are present. Of two homozygotes tested both display a low cone response by electroretinograph.
005739	NOD-Tg(H2-Ea-Ins2)1Wehi/WehiJ	Cryopreserved - Ready for recovery
	Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. RT/PCR indicates transgene expression in the spleen and thymus. Blood glucose levels of transgenic and non-transgenic littermates are identical. 90-98 % of the transgenic islets of females and males are insulitis free. Transgenic mice do not develop spontaneous diabetes and are resistant to cyclophosphamide-induced diabetes. Sialitis is not statistically different between transgenic and littermate controls (French MB, Diabetes 1997 46:34-9). Transgenic bone marrow transplanted into 4-week-old irradiated NOD female�s almost entirely prevented diabetes compared to control NOD to irradiated NOD transplants, which have an overall diabetes incidence similar to untreated controls. Thymoma incidence was similar in both irradiated groups.(Steptoe RJ, J Clin Invest 2003 111:1357-63) This model may be helpful for looking at antigen speci ..... For more information please see the full phenotype on the strain data sheet
005522	NOD-Tg(Ins2*Y16A)1Ell/GseJ	Cryopreserved - Ready for recovery
	Expression has been reported in the pancreatic islets and thymus of NOD mice carrying the Tg(Ins2Y16A)1Ell mutation. Approximately 75% of line B female transgenic mice become diabetic in the presence of native insulin genes by 35 weeks of age. NOD female transgenic mice lacking both Ins1* and Ins2 fail to produce insulin autoantibodies, and there is no diabetes or insulitis at 26 weeks of age, but sialitis is present. Donating investigator reports male transgenics lacking both Ins1 and Ins2 develop metabolic diabetes before 10 weeks of age. In contrast, transgenic female mice in the presence of Ins1 and lacking Ins2 develop diabetes in 75% of the animals by 25 weeks of age (Nakayama et al, 2004, 2005). Donating investigator reports line B transgenics have lower expression levels than line F and that male transgenics lacking both Ins1 and Ins2 develop metabolic diabetes before 10 weeks of age. NOD-Tg(Ins2*Y16A)1Ell/GseJ is usefu ..... For more information please see the full phenotype on the strain data sheet
005523	NOD-Tg(Ins2*Y16A)3Ell/GseJ	Cryopreserved - Ready for recovery
	Expression has been reported in the pancreatic islets and thymus of NOD mice carrying the Tg(Ins2Y16A)3Ell mutation. Approximately 15% of line F female transgenic mice become diabetic in the presence of native insulin genes by 35 weeks of age. NOD female transgenic mice lacking both Ins1* and Ins2 fail to produce insulin autoantibodies, and there is no diabetes or insulitis at 26 weeks of age, but sialitis is present. In contrast, transgenic mice in the presence of Ins1 and lacking Ins2 develop diabetes in 75% of the animals by 25 weeks of age (Nakayama et al, 2004, 2005). NOD-Tg(Ins2*Y16A)3Ell/GseJ is useful to study insulin-reactive autoimmunity.
006436	NOD.Cg-(Gpi1-D7Mit346)^C57BL/6J Tg(TcraAI4)1Dvs/DvsJ	Cryopreserved - Ready for recovery

006437	NOD.Cg-(Gpi1-D7Mit346)^C57BL/6J Tg(TcrbAI4)1Dvs/DvsJ	Cryopreserved - Ready for recovery

003843	NOD.Cg-Prkdc^scid Tg(Ins2-GAD2)1Lt/LtJ	Cryopreserved - Ready for recovery
	NOD.Cg-Prkdc^scid Tg(Ins2-GAD2)1Lt/LtJ transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgenic mice are homozygous for Prkdc^scid and are free of potential insulitic lymphocytes resulting in diabetes resistance. Similar to the NOD/Lt-Tg(Ins2-GAD2)1Lt (Stock No. 003074) the transgene inserted into Chromosome Y, thus only males are transgenic (Bridgett et al, Diabetes 1998 47:1848-56). This model provides a tool for studying the role of GAD2 as a islet autoantigen in the NOD mouse model of Type 1 diabetes.
003844	NOD.Cg-Prkdc^scid Tg(Ins2-GAD2)2Lt/LtJ	Cryopreserved - Ready for recovery
	NOD.Cg-Prkdc^scid Tg(Ins2-GAD2)2Lt/LtJ transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgenic mice are homozygous for Prkdc^scid and are free of potential insulitic lymphocytes resulting in diabetes resistance. Delayed diabetes onset is observed when splenic lymphocytes from 5 week old pre-diabetic NOD females are adoptively transferred into NOD transgenic mice homozygote for Prkdc^scid when compared to adoptive transfers into control NOD females. Similar to the NOD/ShiLt(Cg)-Tg(Ins2-GAD2)2Lt/J (Stock No. 005870) homozygous transgenic mice are developmentally lethal due to the transgene insertion site (Bridgett et al, Diabetes 1998 47:1848-56). This model provides a tool for studying the role of GAD2 as an islet autoantigen in the NOD mouse model of Type 1 diabetes.
005524	NOD.Cg-Tg(Ins2Y16A)1Ell Ins1^tm1Jja Ins2^tm1Jja*/GseJ	Cryopreserved - Ready for recovery
	Transgenic mice reportedly express the mutant Ins2Y16A protein in the pancreatic islets and thymus. The donating investigator reports approximately 75% of female transgenic mice (founder line B) become diabetic in the presence of native insulin genes by 35 weeks of age. In contrast, NOD female transgenic mice lacking both Ins1* and Ins2 fail to produce insulin autoantibodies, and neither diabetes nor insulitis develops by 26 weeks of age. Sialitis does occur, however. Line B transgenics have lower expression levels than line F (see Stock No. 005525), and 50% of the line B male transgenics lacking both Ins1 and Ins2 develop metabolic diabetes, with little to no insulitis, before 10 weeks of age. This strain is useful to study insulin-reactive autoimmunity.
005525	NOD.Cg-Tg(Ins2Y16A)3Ell Ins1^tm1Jja Ins2^tm1Jja*/GseJ	Cryopreserved - Ready for recovery
	Expression has been reported in the pancreatic islets and thymus of NOD mice carrying the Tg(Ins2Y16A)3Ell mutation. Approximately 15% of line F female transgenic mice become diabetic in the presence of native insulin genes by 35 weeks of age. NOD female transgenic mice lacking both Ins1* and Ins2 fail to produce insulin autoantibodies, and there is no diabetes or insulitis at 26 weeks of age, but sialitis is present. In contrast, transgenic mice in the presence of Ins1 and lacking Ins2 develop diabetes in 75% of the animals by 25 weeks of age (Nakayama et al, 2004, 2005). This stock is useful to study insulin-reactive autoimmunity.
005734	NOD/Lt-Tg(Ins2-rtTA)1Ach/AchJ	Cryopreserved - Ready for recovery
	Tg(Ins2-rtTA)2Ach encodes the reverse tetracycline regulatable transactivator (rtTA) regulated by the rat insulin promoter (Ins2, commonly designated RIP), and is expressed in the pancreatic beta cells. Hemizygous transgenic mice are viable, fertile, normal in size, display normal NOD diabetes onset, but do not display any other gross physical or behavioral abnormalities. When NOD/Lt-Tg(Ins2-rtTA)2Ach/AchJ mice are mated to a second transgenic strain carrying a target gene regulated by the tetO responsive elements, expression of the target gene is turned on by the tetracycline analog, doxycycline (dox). Dox can be administered orally in the food or water. This strain provides a Tet-On tool that permits the inducible expression of genes in the pancreatic beta cells during various stages of diabetes development (As reported by donating investigator, data unpublished). This transgenic strain is likely to have characteristics similar to Stock No. For more information please see the full phenotype on the strain data sheet
005870	NOD/ShiLt(Cg)-Tg(Ins2-GAD2)2Lt/J	Cryopreserved - Ready for recovery
	This transgene expresses human glutamic acid decarboxylase 2 cDNA under the control of the rat insulin 2 promoter. FISH analysis and pseudo-giemsa metaphase spead analysis establish the insertion site of this transgene on proximal Chr 15 near the centromere. Expression of the transgene in the islets has been confirmed by RT-PCR and Western blot analysis. Southern blot analysis confirm 4-5 copies of the transgene are present. Homozygotes are developmentally lethal. Transgene positive animals are significantly protected from diabetes onset (females- 14%, Males- 15% at 50 weeks) compared to NOD/ShiLt controls (Females- 100%, Males-50% by 50 weeks). Insulitis in 9 week old females is not significantly different between transgenics and controls. This model provides a tool for studying at the role of autoantigens, specifically GAD2, in diabetes.
005082	NOD/ShiLt-Tg(ACTB-Ica1/EGFP)18Mdos/MdosJ	Cryopreserved - Ready for recovery
	ACTB-Ica1/EGFP (commonly referred to as Ica69/EGFP) Line 18 transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Tissue fluorescence is strongest in the heart, intermediate in the exocrine pancreas and kidney and weak in the liver. Tissue fluorescence is observed in isolated transgenic islets. No fluorescence was observed in the brain, thymocytes or spleen cells. NOD transgenic females exhibit reduced diabetes incidence (45%) by 40 weeks of age and more rapid insulitis onset (50%, severe infiltration) at 12 weeks of age compared with NOD controls (80% diabetic by 40 wk and 20% insulitis-positive at 12 weeks). Intra-islet lymphocytes expressing interferon gamma were 50 times more frequent in sections from transgenic Line 18 than in wild-type controls, while IL4 stained cells were barely detectable in either. NOD-Tg(ACTB-Ica1/EGFP)18Mdos/MdosJ can be used as a tool to study the constant over expression of Ica1 in NOD m ..... For more information please see the full phenotype on the strain data sheet
005328	NOD/ShiLt-Tg(Cd4-DsRed)4Lt/J	Cryopreserved - Ready for recovery
	The donating investigator reports that hemizygous transgenic mice are viable, fertile and normal in size. FACS analysis of splenic lymphocytes shows transgenic expression in 36% of CD4⁺ and 6% of CD8⁺ T cells and minimal expression (background levels) in B cells and macrophages. When compared to wild-type NOD/ShiLt mice, the diabetes incidence is lower (50%) and diabetes onset is delayed. Adoptive transfer experiments with splenocytes and bone marrow from hemizygous CD4-DsRed transgenic mice does not confer diabetes protection on NOD inbred mice, suggesting that the agent of protection is not dependent on hematopoietic cells. No homozygous transgenic mice have been identified in litters produced from hemizygote intercrosses, suggesting that homozygotes are not viable. This strain is useful for tracking resting and activated T cells in vivo and in vitro.
005334	NOD/ShiLt-Tg(Cd4-EGFP)1Lt/J	Cryopreserved - Ready for recovery
	Homozygous transgenic mice are viable, fertile, normal in size and do not exhibit any gross physical or behavioral abnormalities. The donating investigator reports uniform transgenic expression, about 81% of inactivated or resting CD8⁺ T cells and CD4⁺ T cells, with minimal expression in B cells (2.3%) and macrophages (1.5%). Over a three day period following activation in vitro with anti-CD3, gating on live populations of CD4⁺ and CD8⁺ subsets show continued GFP expression in both. However, there is a greater diminution of GFP fluorescence in the activated CD8⁺ T population by day three in vitro. Diabetes onset is similar to wild-type NOD/ShiLt mice. These CD4-GFP transgenic mice may be useful for fluorescent monitoring of T cells both in vivo and in vitro.
012310	NOD/ShiLt-Tg(GFAP-Cd274)5Mdos/J	Cryopreserved - Ready for recovery
	NOD/ShiLt-Tg(GFAP-Cd274)5Mdos/J mice, commonly referred to as GFAP-tg, express Cd274 (B7-H1), under the control of glial fibrillary acidic protein promoter (GFAP). Hemizygous and homozygous mice are viable and fertile. Rt-PCR indicates B7-H1 transgenic expression appears in neuronal tissues, including the brain and sciatic nerve, pancreas, colon, salivary gland and purified or cultured peri-islet Schwann cells (pSC). Protein expression does not correlate with transcription profiles as protein expression was only found to be elevated in the pSC and brains of transgenic mice when compared to wildtype mice. At 4-weeks of age, transgenic and non-transgenic mice exhibit no difference in glucose and insulin sensitivity tests. By 8-weeks of age, there was enhanced loss of pSC in transgenic females; which followed elevated GFAP autoreactivity. Insulitis is enhanced and more invasive in the transgenic female when compared to wildtype controls (Males not reported). By ..... For more information please see the full phenotype on the strain data sheet
006778	NOD/ShiLt-Tg(GFAP-Cd80)9Mdos/MdosJ	Cryopreserved - Ready for recovery
	Gfap-Cd80 (GFAP-B7-1) transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator reports that transgenic mice are protected from diabetes development.
010632	NOD/ShiLt-Tg(INS-NP)6171Mvh/J	Cryopreserved - Ready for recovery
	Transgenic mice were created with the Lymphocytic choriomeningitis virus (LCMV) nucleoprotein(NP) under the control of the human insulin promoter (HIP). RT-PCR analysis indicates that transgenic mice express LCMV-nucleoprotein in the pancreas and thymus. Naive transgenic female mice exhibit slightly accelerated diabetes onset (95% diabetic by 35 weeks of age) when compared to wildtype controls (80% diabetic by 35 weeks of age), with no significant difference in overall diabetes incidence by 40 weeks of age. Immunohistochemistry of pancreas at one-week post LCMV infection shows an early infiltration of CD8 T cells in transgenic mice. Within 2 weeks of infection with LCMV HIP-NP mice exhibit rapid onset of diabetes compared to 6-8 months in infected B6.RIP-NP (Stock No. 004826) mice. LCMV infected transgenic mice exhibit upregulation of CXCR3 and CXCR10. This model provides a novel autoantigen expressed in pancreatic islet cells. LCMV infected transgenic mice provide an inducible syste ..... For more information please see the full phenotype on the strain data sheet
006777	NOD/ShiLt-Tg(Ins2-Cd274)2Mdos/MdosJ	Cryopreserved - Ready for recovery
	Ins2-Cd274 (Rip-B7H1) transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator indicates transgenic mice over express Cd274 in pancreatic beta cells and reports accelerated diabetes in Ins2-Cd274 transgenic mice compared to wildtype cohorts. This strain is useful to study the role of Cd274 in autoimmunity and peripheral tolerance.
005733	NOD/ShiLt-Tg(Ins2-Fas*I246N)1Ach/AchJ	Cryopreserved - Ready for recovery
	Diabetes onset is significantly delayed in Rip-Fas^cg transgenic mice (45% diabetic by 30 weeks of age) compared to wildtype cohorts (90% diabetic by 30 weeks of age). Adoptive transfer studies using splenocytes from diabetic NOD/Lt mice into Rip-Fas^cg transgenic mice indicate the transgenic mice become diabetic later than wildtype controls. This transgenic strain is useful in studies looking at the effects of Fas on pancreatic islets.
002033	NOD/ShiLt-Tg(Ins2-TAg)1Lt/J	Cryopreserved - Ready for recovery
	Homozygous NOD/Lt-Tg(RipTag)1Lt mice develop pancreatic beta cell adenomas. They are able to produce 2-3 litters before the insulin secreted from the adenoma makes them too hypoglycemic.
003855	NOD/ShiLt-Tg(Ins2-cre)5Lt/LtJ	Cryopreserved - Ready for recovery
	This strain expresses Cre recombinase under the control of the rat insulin II promoter. Hemizygous mice carrying this transgene are phenotypically normal and overexpresss cre specifically in pancreatic beta cells. Homozygous transgenic mice experience delayed onset diabetes compared to wildtype controls. This transgenic strain is used in combination with mice carrying floxed targeted mutations to create various pancreatic beta cell-specific gene knockouts using the Cre/loxP system.
006604	NOD/ShiLtDvs-Tg(HLA-A/H2-D/B2M)1Dvs/J	Cryopreserved - Ready for recovery
	This transgenic NOD mouse model, commonly referred to as NOD.HHD, develops significantly accelerated diabetes onset compared to NOD/ShiLtDvs (NOD) inbred mice. When transgenic mice are bred to NOD-B2m-deficient mice (e.g. Stock No. 002309), which completely lack CD8⁺ T cells, CD8⁺ T cells are restored in the double mutant mice, but at significantly lower levels than in NOD inbred mice. FACS analysis indicates that the transgenic NOD-B2m-deficient mice express only the HLA-A2.1/H2-D^b chimeric class I molecule. In contrast to NOD.B2m^tm1Unc females, which are diabetes free, 55% of the transgenic NOD B2m-deficient females develop diabetes by 30 weeks of age. Insulitis scores determined by histological examination are similar between the NOD double mutant mice and NOD/ShiLtDvs inbred mice, and cultured pancreatic islets from transgenic NOD B2m-deficient mice an ..... For more information please see the full phenotype on the strain data sheet
004226	NOD/ShiLtDvs-Tg(Ins2-E3*309)5Dvs/DvsJ	Cryopreserved - Ready for recovery

004227	NOD/ShiLtDvs-Tg(Ins2-E3*704)2Dvs/DvsJ	Cryopreserved - Ready for recovery

004990	NOD/ShiLtDvs-Tg(Ins2-E3*734)4Dvs/DvsJ	Cryopreserved - Ready for recovery

004939	NOD/ShiLtJ-Lepr^db-5J/LtJ	Cryopreserved - Ready for recovery
	Coisogenic, NOD/ShiLtJ-Lepr^db-5J/LtJ (NOD- Lepr^db-5J) homozygous mice develop juvenile onset obesity and type II diabetes coupled with suppression of spontaneous type I diabetes in which the NOD/ShiLtJ (NOD/ShiLt) strain is known. RT-PCR confirms the expression of the leptin receptor long isoform (Rb) in the hypothalamus. NOD/ShiLt mice homozygous for this mutation are viable and retain some fertility although the stock is maintained by heterozygous matings. By five weeks of age, homozygous mice are hyperphagic, eating twice the amount of mouse chow as lean controls and develop hyperglycemia not requiring insulin therapy for long tem survival (39+ weeks of age). Lean littermate mice (wild-type or heterozygotes) develop spontaneous type 1 diabetes in an age dependent (post-adolescent) manner. In contrast, Lepr^db-5J homozygotes of both sexes develop hyperglycemia within one to two weeks of weaning. This is a type II diabetes based u ..... For more information please see the full phenotype on the strain data sheet
004774	NOD/ShiLtJ-wly/J	Cryopreserved - Ready for recovery
	Mice develop curly hair by 4 weeks of age; whiskers are normal (straight). Giant hair follicles in anagen and a paucity of subdermal fat were found in histology of the skin at 5 weeks of age.
005309	NODCaj.Cg-Ighm^tm1Cgn Tg(Igh-VB1-8/Igh-6)2Mjsk/FswJ	Cryopreserved - Ready for recovery
	Transgenic mice carrying the Ighm^tm1Cgn allele are viable, fertile, and normal in size and restores the B220+ B-cells. The number of B-cells is reduced and the ratio of CD4 to CD8 is normal. Although only a fraction of the transgenic mice have an increased amount of insulitis, it is significantly more severe, especially in males. No diabetes was observed in NODCaj.Cg-Ighm^tm1Cgn Tg(Igh-VB1-8/Igh-6)2Mjsk/FswJ mice by 50 weeks of age. This model serves as a control for the membrane bound, non-secreted, NODCaj.Cg-Ighm^tm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk/FswJ (Stock No. 005306).
005306	NODCaj.Cg-Ighm^tm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk/FswJ	Cryopreserved - Ready for recovery
	Transgenic mice carrying the Ighm^tm1Cgn allele are viable, fertile, and normal in size and restores the B220+ B-cells to normal. The number of B-cells is normal and the ratio of CD4 to CD8 is normal. Although only a fraction of the transgenic mice have an increased amount of insulitis, it is more severe, especially in males. Diabetes incidence is partially restored in NODCaj.Cg-Ighm^tm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk/Fsw with approximately, 11% females and 0% males becoming diabetic by 50 weeks of age compared to approximately 2% Ighm^tm1Cgn female controls and 0% Ighm^tm1Cgn male controls by 50 weeks of age or 90% female NOD controls and 70% male NOD controls by 30 weeks of age. T- cell depleted spleen cells from Ighm^tm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk mice stimulated with lipopolysaccharide (LPS) respond normally. NODCaj.Cg-Ighm^tm1Cgn Tg(Igh-VB1-8/Igh-6m )2Mjsk/Fsw like NOD.129S2(B6)-<> ..... For more information please see the full phenotype on the strain data sheet
001504	NOR2/LtDn-Vsx2^or-2J/J	Cryopreserved - Ready for recovery

005415	RHJ/LeJ-stpm/GrsrJ	Cryopreserved - Ready for recovery
	The phenotype of this mutation can be identified by a curly coat, which is different from the smooth coat of control littermates. At 3 weeks of age, mice homozygous for this new mutation have very curly coats and slightly curved vibrissae. In several weeks time the curly coat disappears but the hair retains a rough texture, and the vibrissae then appear normal. Heterozygous mice have normal smooth coats and straight whiskers.
001910	SJL/J-Crm^2J/J	Cryopreserved - Ready for recovery

005004	ZRDCT Rax^ey1/ChUmdJ	Cryopreserved - Ready for recovery
	Ninety percent of mice homozygous for Rax^ey1 are anophthalmic and 10% are microphthalmic. Anophthalmic mice have orbits and eyelids but lack eyes and optic tracts (Chase et al. 1941). Microphthalmic mice have one or two small eyes, and may have an optic nerve (Chase et al. 1941). The phenotype is first distinguished at approximately embryonic day ten. Optic vesicles develop, however, they are reduced in size and contact poorly with surface ectoderm (Chase et al. 1941). A normal eyed control strain, ZRDCT Rax⁺/ChUmdJ (Stock No. 005005) was developed in parallel with ZRDCT Rax^ey1. Rax^ey1 mice exhibit an abnormal hypothalmus (Silver 1977) and altered circadian rhythm (Laemle et al. 1998). This strain serves as a model for human anophthalmia.
007027	C57BL/6-Tg(Thy1-APPSwDutIowa)BWevn/Mmjax	Transferred

003905	BALB/cAnBomUrd-Phex^Hyp-Duk/J	Under Development for Cryo
	This mutant offers a model for X-linked dominant hypophosphatemic rickets. The serum phosphorus (2.95 mg/dL) in hemizygous males is lower than that found in hypophosphatemia, hypophosphatemia 2 Jackson, or gyro hemizygous males. The skeletal defects include shortened long bones and craniofacial defects and hemizygous males have cochlear degeneration and a heightened auditory brainstem response threshold, higher than that in other Phex mutants. The heightened ABR threshold is dependent upon a modifier that is absent in BALB/cByJ. Consistent with vestibular dysfunction, approximately half of the hemizygous males and some of the heterozygous females display circling behavior, and in hemizygous males head bobbing or unstable gait have also been noted. Hemizygous males are mildly growth retarded, with a squared and shortened body, and shortened hind limbs and tail. While some heterozygous females display circling and growth retardation, not all do and they are more difficult to d ..... For more information please see the full phenotype on the strain data sheet
017340	129S-Maoa^tm1Shih/J	Under Development - Now Accepting Orders

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
014556	129S6/SvEv-Apoe^tm4Mae/J	Under Development - Now Accepting Orders
	The Apoe^tm4Mae mutant allele was created using the same targeting vector used to generate the Apoe^tm1Unc mutant allele. Both alleles are functionally identical; replacing part of exon 3 and intron 3 with a neomycin resistance cassette and abolishing apoE expression. Mice homozygous for the apoE mutation (apoE-deficient mice) are viable and fertile, with defective lipoprotein metabolism. Compared to wildtype mice, apoE-deficient mice exhibit increased plasma cholesterol and triglyceride levels, along with spontaneous development of atherosclerotic plaques in the aortic root and aortic arch. Several strain-specific differences are reported between apoE-deficient mice coisogenic on a 129S6/SvEv genetic background (129S6-apoE^-/-) and apoE-deficient mice congenic on a C57BL/6 genetic background (B6-apoE^-/- ; see Stock No. 002052). Compared to B6-apoE^-/- mice, 129S6-a ..... For more information please see the full phenotype on the strain data sheet
013046	129S6/SvEv-Lias^tm1Mae/J	Under Development - Now Accepting Orders
	The Lias^tm1Mae mutant allele has the exons 4-6 of the of the lipoic acid synthetase (Lias) gene deleted. The deleted region encodes the functionally conserved Cys motifs of the enzyme responsible for converting octanoic acid to α-lipoic acid (also called 1,2-dithiolane-3-pentanoic acid, thioctic acid, ALA, or LA) via insertion of a sulfur atom into the hydrocarbon chain of octanoic acid. Lias mRNA expression in heterozygous mice is approximately half of wildtype levels. Lias homozygous mice die in utero shortly after implantation. When heterozygous dams are fed an exogenous racemic α-lipoic acid diet (equal amounts of left- and right-handed enantiomers of the chiral α-lipoic acid molecule), embryonic lethality of homozygous embryos is not rescued. Heterozygous mice are viable and fertile, with a mild reduction of plasma antioxidant capacity. Inducing stress conditions (such as inflammation, hypercholesterolemia and hyperglycemia) is exp ..... For more information please see the full phenotype on the strain data sheet
016096	B6.Cg-Tg(Zap70*M413A)2Weis/J	Under Development - Now Accepting Orders
	Mice hemizygous for the BAC Zap70M413A* transgene are viable and fertile. These mice express a mutated form of mouse zeta-chain (TCR) associated protein kinase (Zap70M413A), involving the gatekeeper methionine residue of the ATP-binding domain. Expression is directed by the endogenous Zap70* promoter/enhancer regions on the BAC transgene. Zap70 is a tyrosine kinase required for thymic development of peripheral T cells from double positive CD4⁺CD8⁺ T cells. These Zap70 (AS) mice overexpress the mouse Zap70M413A mutant protein which causes a conformational change in the ATP-binding domain. The increased size of the binding domain allows Zap70* inhibition by 3-MB-PP1, a bulky analog of the kinase inhibitor PP1. These mice may be useful for studying selective reversible Zap70 inhibition and its effect on T cell receptor signaling.
016926	BTBR T⁺ tf-Fbxl3^Ovtm/J	Under Development - Now Accepting Orders
	Ovtm ENU-induced mutants contain an A to G transition at nucleotide in exon 5 of the F-box and leucine-rich repeat protein 3 (Fbxl3) gene that defines an amino acid change from isoleucine to threonine at residue 364. While homozygous males are viable, fertile, and normal in size, homozygous females are viable and normal in size, but are often infertile. FBXL3 is part of the SKP1-CUL1-F-box-protein (SCF) ubiquitin protein ligase complex which mediates phosphorylation-dependent ubiquitination. Homozygotes have a long circadian period of ~26 hours. These mice may be useful for studying circadian rhythm modulation.
016929	C57BL/6-Cd1d1^tm1.1Aben/J	Under Development - Now Accepting Orders
	These mice carry a floxed allele of the Cd1d1 (CD1d1 antigen) gene. When bred to mice expressing Cre recombinase under the control of a chosen promoter, exons 2-6 are deleted in the tissue of interest, blocking expression of Cd1d1. As the homologous Cd1d2 gene has a frameshift mutation preventing expression of a functional protein, blocking expression of Cd1d1 results in the complete absence of CD1D proteins at the cell surface. Homozygous floxed mice are viable and fertile and do not display any gross physical or behavioral abnormalities. When crossed with Cd4-Cre mice, progeny reportedly show an 8-fold reduction in natural killer T (NKT) cell numbers on average in a manner commensurate with the levels of CD1D protein downregulation achieved among cortical thymocytes. This result is consistent with the requirement for Cd1d1 expression by CD4+ CD8+ double positive (DP) thymocytes for NKT cell development. When these floxed mice are ..... For more information please see the full phenotype on the strain data sheet
017311	C57BL/6-Irf5^tm1Ppr/J	Under Development - Now Accepting Orders
	These mice possess loxP sites on either side of exon 2 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 these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 deleted in the cre-expressing tissue(s). When bred to a strain with Cre recombinase expression in dendritic cells and B cells, this mutant mouse strain may be useful in studies of innate immunity and autoimmunity.
012444	C57BL/6-Lrrk2^tm1Mjfa/J	Under Development - Now Accepting Orders
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Exon 41, which encodes the kinase domain, is deleted. Homozygotes exhibit increased mean process length and branching in primary neurons from the hippocampus and midbrain. Heterozygotes and wildtype controls exhibit similar neuritic outgrowth.
017285	C57BL/6-Prkd2^tm1.1Daca/J	Under Development - Now Accepting Orders
	These mutant mice carry two point mutations, S707A and S711A (alanine substitution for serine), in the catalytic domain activation loop region, which are phosphorylated by protein kinase C and activate PKD catalytic activity, of the endogenous gene. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Although protein expression levels are not changed, total PRKD1 and PRKD2 activity is impaired (residual level of activity detected) in homozygotes, as measured by immunoprecipitation assay of thymocytes. Phorbol-ester-activated mutant protein produced in splenocytes or thymocytes from homozygotes does not effectively autophosphorylate on Ser⁸⁷³. Homozygotes exhibit normal T cell development and maturation and baseline Ig serum levels, but have a diminished antigen-specific IgM response. Mutant homozygous mice immunized with with NP-OVA have reduced antigen-specific IgM and ..... For more information please see the full phenotype on the strain data sheet
016941	C57BL/6-Trdc^tm1Mal/J	Under Development - Now Accepting Orders
	Tcrd-H2BEGFP mutant mice contain an internal ribosome entry site (IRES), and a human histone H2B fused to an enhanced green fluorescent protein (EGFP) downstream of the internal stop codon of the T-cell receptor delta, constant region (Trdc) gene. Homozygotes are viable, fertile, and normal in size. EGFP expression is evident in all CD3ε⁺ TCRγδ⁺ intraepithelial lymphocytes (IELs) in the small intestines, and TCRγδ cells in the spleen and lymph nodes. These mice have a lower number of thymic but not peripheral γδ T cells. These mice may be useful for visualizing and studying the development of adult thymic γδ T cells and the biology of γδ T cells in the periphery. The donating investigator reports that for visualizing γδ T cells in secondary lymphoid organs or other tissues containing a large excess of αβ T cells over γδ T cells, the use of F ..... For more information please see the full phenotype on the strain data sheet
014564	C57BL/6-Tg(CMV-Tsc2*)1Arbi/KlanJ	Under Development - Now Accepting Orders
	These Delta RG transgenic mice express a dominant negative mutant mouse Tsc2 (tuberous sclerosis 2) gene that lacks the sequence encoding the rabaptin-5 and rap1GAP motifs. Expression is directed by the CMV, cytomegalovirus, promoter. Transgenic mice develop skin and brain hamartomas with aggregates of granular cells at the surface cerebellum (subpial) and collagenous fibrovascular proliferations containing abundant mast cells in the skin. Hemizygotes exhibit higher anxiety, spending less time in the open arms of an elevated plus maze when compared to wildtype mice. Mild learning and memory defects are alos observed. Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities.
017321	C57BL/6-Tg(Fabp4-Dgat1)2Far/J	Under Development - Now Accepting Orders
	These transgenic mice express mouse Dgat1 (diacylglycerol O-acyltransferase 1), FLAG epitope amino-terminal tagged, under the control of the white adipose tissue specific mouse Fabp4 (fatty acid binding protein 4, adipocyte) promoter. In this founder line 2 (high expressing line) Dgat1 protein and mRNA levels are increased two fold in white apidose tissue and increased ~6?8.5 fold in peritoneal macrophages. Transgenic mice have adipocytes that are larger in size and mass than wildtype controls and elevated triglyceride levels in the reproductive fat pads. On either a chow or high fat diet, transgenic mice have a greater mean total fat pad weight than controls. When fed a high fat diet for 4 weeks, transgenic mice exhibit hyperphagy, higher body weight, elevated serum free fatty acid levels and lower serum triglyceride levels when compared to wildtype controls. Serum glucose and insulin levels, and liver and skeletal muscle triglyceride levels of transgenic and ..... For more information please see the full phenotype on the strain data sheet
016617	C57BL/6-Tg(Nr4a1-EGFP/cre)820Khog/J	Under Development - Now Accepting Orders
	Mice hemizygous for the Nur77-GFPCre BAC transgene (Nur77^GFP BAC transgenic mice) are viable and fertile with normal lymphoid and myeloid development. Nur77-GFPCre BAC transgenic mice express an enhanced green fluorescent protein/codon-optimized "humanized" Cre recombinase fusion protein (eGFP-hCre) under control of the Nr4a1 (Nur77) promoter/enhancer regions within the BAC transgene. Nur77-GFPCre BAC transgenic mice from founder line B6-820 exhibit GFP expression patterns consistent with endogenous Nur77. Specifically, GFP is highly expressed in a subset of myeloid lineage cells of the spleen (but not lymph node), while low levels of GFP are observed in T and B lymphocytes. GFP is up-regulated by antigen receptor stimulation in Nur77-GFPCre BAC transgenic mice, but unlike the CD69 marker of T cell activation, GFP is not induced by inflammatory stimuli. Furthermore, the level of GFP expressed during acute activation reflects the strength of T cell receptor (TCR) stim ..... For more information please see the full phenotype on the strain data sheet
016608	C57BL/6-Tg(Prnp-TARDBP)3cPtrc/J	Under Development - Now Accepting Orders
	TDP-43_PrP transgenic mice express a full length wild type human TAR DNA binding protein (TARDBP or TDP-43) cDNA under control of the prion protein (Prnp) promoter. Hemizygotes are viable, fertile, and normal in size. TDP-43 is a ubiquinated protein localized to the nucleus of cells. Accumulations of TDP-43 are involved in the development of Amyotrophic lateral sclerosis (ALS). These mice express wildtype human TDP-43 primarily in the nuclei of neurons throughout much of the gray matter of the spinal cord and brain, including the hippocampus, striatum, brainstem and cortex. Homozygotes and hemizygous express TDP-43 in brain at 2.5 and 1.9-fold endogenous TDP-43 levels, respectively. Endogenous TDP-43 is down-regulated in response to transgene overexpression. Beginning at 14 days of age, homozygous TDP-43_PrP are smaller than hemizygous littermates. By 21 days of age homozygotes develop body tremors, have difficulty walking, and devel ..... For more information please see the full phenotype on the strain data sheet
016131	C57BL/6J-Sec61a1^m1Gek/J	Under Development - Now Accepting Orders
	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
017537	C57BL/6J-Tmem173^gt/J	Under Development - Now Accepting Orders
	These Tmem173^gt chemically-induced (ENU) mutant mice carry a missense mutation in exon 6 of the transmembrane protein 173 (Tmem173 or Sting) gene, which results in an isoleucine-to-asparagine change in amino acid 199, in the C-terminal of the protein. No gene product (protein) is detected by Western blot analysis of bone marrow-derived macrophages from homozygotes. Thioglycolate-elicited peritoneal macrophages isolated from homozygotes do not produce type I interferons (IFN-β) in response to cyclic dinucleotides (c-di-GMP) or Listeria monocytogenes infection. Mice homozygous for the mutation are viable and fertile.
012686	C57BL/6N-Tg(Ppp1r2-cre)4127Nkza/J	Under Development - Now Accepting Orders
	Hemizygous Ppp1r2-cre mice are viable and fertile, harboring a BAC transgene encoding a Cre-recombinase gene under the control of the protein phosphatase 1, regulatory (inhibitor) subunit 2 (Ppp1r2) gene. The Ppp1r2-cre transgene contains a cre-recombinase (fused to a nuclear localization signal (nls)) upstream of the initial methionine codon of the Pppl1r2 gene, and a downstream bovine growth hormone-derived polyadenylation (polyA) signal.When Ppp1r2-cre mice are bred with mice containing loxP-flanked sequence, Cre-mediated recombination will result in deletion of the floxed sequences in the Cre-expressing GABAergic neurons of the offspring. These mice may be useful for studying the development and function of corticolimbic GABAergic interneurons.
016936	C57BL/6N-Tg(Thy1-SNCA)12Youy/J	Under Development - Now Accepting Orders
	mThy1-hSNCA transgenic mice have the mouse thymus cell antigen 1 (Thy-1) promoter directing expression of the human α-synuclein (SNCA) gene. Hemizygotes are viable, fertile, and normal in size. These mice express ~23 copies of the transgene; expression is relatively high in the cerebral cortex and hippocampus, and relatively low in the kidneys. The formation of alpha-syn aggregates is a key step in the pathogenesis of Parkinson's disease. These aggregates cause formation of fibrillar aggregates causing various forms of cytotoxicity, including impairment of proteasomal and lysosomal activities, disruption of ER-Golgi traffic and microtubule-based transport, and dysfunction of mitochondria. These mice may be useful for studying the Parkinson's disease pathogenesis and neurodegeneration elicited by the toxic effects of aggregation and somatic accumulation of SNCA.
016618	FVB-Tg(Ckm-IGF1R*K1003R)1Dlr/J	Under Development - Now Accepting Orders
	MKR transgenic mice have the murine creatine kinase, muscle (Ckm) promoter directing expression of the human insulin-like growth factor I receptor (IGF-1R) gene containing the K1003R mutation. Homozygous MKR mice are viable and fertile. IGF-1R is a tyrosine kinase transmembrane receptor dimer which mediated cell signaling through IGF binding and promotes cell survival and cell proliferation. The K1003R mutation inactivates the ATP binding site of the receptor. These transgenic mice have ~12 copies of the transgene, and exhibit a 10 fold increase in expression in skeletal muscle

JAX® Mice Strains

JAX^® Mice Strains