Search Criteria: Research Area is "Diabetes and Obesity Research: Obesity Without Diabetes"
Additional Register Interest Strains
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002052 | B6.129P2-Apoetm1Unc/J | Level 2 |
| Mice homozygous for the Apoetm1Unc mutation show a marked increase in total plasma cholesterol levels that are unaffected by age or sex. Fatty streaks in the proximal aorta are found at 3 months of age. The lesions increase with age and progress to lesions with less lipid but more elongated cells, typical of a more advanced stage of pre-atherosclerotic lesion. Moderately increased triglyceride levels have been reported in mice with this mutation on a mixed C57BL/6 x 129 genetic background. Aged apoE-deficient mice (>17 months) have been shown to develop xanthomatous lesions in the brain consisting mostly of crystalline cholesterol clefts, lipid globules, and foam cells. Smaller xanthomas were seen in the choroid plexus and ventral fornix. Additional studies indicate that apoE-deficient mice have altered responses to stress, impaired spatial learning and memory, altered long term potentiation, and synaptic damage. | ||
| 004456 | NONcNZO10/LtJ | Level 2 |
| Onset of hyperglycemia occurs between 10-12 on a 10-11% fat (wt/wt) chow diet with greater than 85% diabetic by 18 weeks. Males exhibit increased serum triglycerides, moderate to severe liver steatosis and pancreatic islet atrophy similar to NZO/HlLt males. Serum insulin and leptin values are significantly lower than in NZO/HlLt, and are only moderately elevated above those recorded in NON/ShiLtJ males. Unlike the very obese NZO/HlLt mice, NONcNZO10/LtJ mice do not exhibit hyperphagia or hypercorticism and are much easier to breed. Although NONcNZO10/LtJ males develop only a moderate level of obesity compared to NZO/HlLt males, the interaction with known diabetogenic QTL from the NON/ShiLtJ strain produce an earlier onset and higher prevalence of chronic hyperglycemia than observed in NZO/HlLt males.
NONcNZO10/LtJ is differentially sensitive to adverse hepatic side effects of thiazolidinediones and may be useful for pharmac ogenetic analysis. This strain represents a model of polyg ..... | ||
| 003008 | B6;129S-Tnftm1Gkl/J | Level 4 |
| Mice homozygous for the Tnftm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does ..... For more information please see the full phenotype on the strain data sheet | ||
| 002423 | NON/ShiLtJ | Level 4 |
| Although closely related to NOD mice, NON mice contain a diabetes resistant MHC haplotype (H2nb1 = Kb, Anb1, Ek, Db). The name was derived from "Non-Obese Non-diabetic"; however, NON/ShiLtJ mice should not be considered "normal." They carry the retinal degeneration (Pde6b) mutation and exhibit certain tendencies toward autoimmune disease. This strain maintains a low plasma insulin level, which may account in part why certain loci from NON/ShiLt can enhance development of autoimmune type 1 diabetes in segregating hybrid mice following outcross to NOD/ShiLtJ. The NON strain-characteristic immunologic abnormalities include perivascular/periductular leukocyte infiltration into the pancreas and submandibular salivary glands, and T lymphocytopenia evident by 20 weeks of age in spleen. NON/ShiLt mice clearly harbor genes predisposing to type 2 diabetes, as evidenced by early impaired glucose tolerance in males and females, d ..... For more information please see the full phenotype on the strain data sheet | ||
| 000687 | SM/J | Level 4 |
| SM/J mice carry a number of rare polymorphic alleles and are often matched to LG/J (Stock No. 000675), A/J (Stock No. 000646) or NZB/BINJ (Stock No. 000684) for quantitative trait locus analysis. These mice are susceptible to diet-induced obesity and diet-induced atherosclerosis. SM/J mice exhibit a hyperresponsiveness to B cell mitogens (Clark et al. 1981, Engel et al. 1981). A point mutation in Neu1 is responsible for a partial deficiency of lysosomal neuraminadase and may explain the altered immune response (Rottier et al. 1998). Small in size at birth and through weaning, SM/J mice attain a normal body weight as they age. | ||
| 004545 | 129S-Npytm1Rpa/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brain or adrenal gland tissue. Beta-galactosidase activity assays and in situ hybridization demonstrate similar expression patterns for the lacZ gene and the endogenous wildtype gene. Spontaneous seizures are exhibited by some mice at age 6 to 8 weeks. Homozygous mice are susceptible to seizures induced by GABA antagonist treatment. Mutant mice have an increased sensitivity to leptin treatment which results in a greater initial reduction of food intake and weight loss when compared to wildtype mice. This mutant mouse strain may be useful in studies related to the role of neuropeptide Y in obesity. | ||
| 003580 | 129S4/SvJae-Pparatm1Gonz/J | Repository- Live |
| Mice homozygous for the Pparatm1Gonz targeted mutation are viable, fertile and appear normal in appearance and behavior. An altered response to a group of compounds (peroxisome proliferators) that induce peroxisome proliferation and hapatocarcinogenesis is observed. No peroxisome proliferation response is detected when these mice are challenged with classical peroxisome proliferators. Typically, such a response includes hepatomegaly, peroxisome proliferation and transcriptional activation of a set of target enzyme genes. Accumulation of lipid droplets observed in liver tissue suggests that Ppara is involved in maintaining the homeostasis of hepatic lipid metabolism. | ||
| 014556 | 129S6/SvEv-Apoetm4Mae/J | Repository- Live |
| The Apoetm4Mae mutant allele was created using the same targeting vector used to generate the Apoetm1Unc 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 | ||
| 003070 | ALR/LtJ | Repository- Live |
| ALS/LtJ (Stock No. 003072) and ALR/LtJ inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. ALR/LtJ mice are of particular interest to investigators studying the immunogenetics of NOD/ShiLtJ mice in that the ALR/LtJ MHC haplotype (H2gx) is a variant of the diabetogenic NOD H2g7 haplotype. The (H2gx) haplotype is identical to the H2g7 haplotype from the H2-K end of the complex through the class II and class III region distal to Hsp70. However, at the distal H2-D end of the complex, ALR/LtJ mice have a rare H2-Dgx allele. Despite the ..... For more information please see the full phenotype on the strain data sheet | ||
| 008195 | B6.129-Adipoqtm1Chan/J | Repository- Live |
| Homozygous mice are viable and fertile, with absence of targeted allele expression confirmed in adipose tissue (mRNA) and plasma (adiponectin protein). While homozygous mice have normal glucose tolerance and insulin resistance, beta-oxidation activity is significantly increased in muscle and liver. Homozygotes also have endothelial dysfunction (increased leukocyte rolling and leukocyte adhesion), are protected from DSS-induced colitis, and are more susceptible to myocardial ischemia/reperfusion. When fed a high fat diet, obese homozygotes are significantly heavier with increased insulin levels and altered insulin resistance. These adiponectin-deficient (Adipoq-/- or Adipo-/-) mice may be useful in studying obesity, diabetes, insulin resistance, metabolism, inflammation, leukocyte-endothelium interactions, and colitis. | ||
| 003124 | B6.129-Ucp1tm1Kz/J | Repository- Live |
| Mice that are homozygous for this knockout allele are viable and fertile, but exhibit sensitivity to cold temperatures. The Donating Investigator notes that homozygous offspring have increased survival rates to weaning age when maintained at 25°C to 28°C. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brown adipose tissue from homozygotes. When maintained at 20°C, homozygotes are resistant to diet induced obesity with reduced white fat depot weights, exhibit a 0.1-0.3°C higher body temperature, and a slightly lowered respiratory quotient compared to controls. Notably, when maintained at 27°C, homozygous mutant mice are no longer resistant to diet induced obesity and gain weight at a rate similar to wildtype controls. An increase in the number of brown adipocytes in the inguinal fat depots is observed in mutant mice maintained at 20°C, on either diet. Homozygotes have reduced levels of plasma fatty acids, circula ..... For more information please see the full phenotype on the strain data sheet | ||
| 005540 | B6.129S-Tnftm1Gkl/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does not affect the degree of obe ..... For more information please see the full phenotype on the strain data sheet | ||
| 003991 | B6.129S4-Itgamtm1Myd/J | Repository- Live |
| Mice that are homozygous for the Itgamtm1Myd targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No Itgam protein is detected in homozygous mutant neutrophils. Homozygous null animals have a diminished ability to clear thioglycollate-induced neutrophils, have reduced mast cell numbers in the dorsal skin and peritoneal wall/cavity, and are less susceptible to cerebral ischemia/reperfusion injury. Neutrophils from these animals are deficient at spreading, phagocytosing complement-opsonized particles, and in several Fc-mediated functions. They also exhibit impaired oxidative burst and a diminished responsiveness in LPS- and taxol-mediated gene expression. | ||
| 007083 | B6.Cg-Cav1tm1Mls/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical abnormalities. Mutant mice exhibit exercise intolerance when challenged and are slightly hyperphagic. No gene product (protein) is detected by Western blot analysis in adipose, lung and heart tissues or in cultured mouse embryonic fibroblasts (MEFs). A decrease in the level of co-expressed caveolin-2 protein is immunodetected. At age 4-5 months, mutant mice are often smaller than their wildtype littermates. By one year of age, mutant mice weigh 5 to 7 grams less than wildtype, and are resistant to diet-induced obesity. Progressive adipose pathology results in reduced white adipose tissue with abnormally small adipocytes and enlarged, hyperplastic brown adipose tissue. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Isolated aortic tissue segments have a diminished vasoconstriction ..... For more information please see the full phenotype on the strain data sheet | ||
| 006414 | B6;129S4-Mc4rtm1Lowl/J | Repository- Live |
| The mice have a loxp-flanked transcriptional blocking (loxTB) sequence that prevents normal endogenous gene transcription and translation from the endogenous locus. As such, homozygous mice are devoid of functional mRNA in all tested regions of the brain. Homozygous mice exhibit severe early-onset obesity, accompanied by hyperphagia, increased snout-anus length and hyperinsulinemia. The function of this disrupted allele can be restored by the enzymatic activity of Cre-recombinase. These mutant mice may be useful in studies of neurobiology, obesity, diabetes, hunger/appetite, and fat and energy metabolism.
When bred to a strain expressing Cre recombinase in the hypothalamus see Stock No. 006395 for example), this mutant mouse strain exhibits as intermediate phenotype in comparison to homozygous null mice. | ||
| 008752 | B6;129S4-Nhlh2tm1Irk/J | Repository- Live |
| Male mice homozygous for this targeted mutation exhibit bilateral cryptochism, hypogonadism, azoospermia, low testosterone and follicle stimulating hormone levels and lack instinctual male sexual behavior. Homozygous females are hypogondal unless raised in the presence of male mice, have estrous cycle defects, and reduced fertility. No gene product (mRNA) is detected by Northern blot analysis of embryos. Initially, homozygous male mice, 4 to 7 weeks of age, have a reduced weight compared to wildtype controls. By 12 weeks of age, homozygous males are significantly heavier than wildtype, and mutants progressively increase weight with age. Female homozygotes 5 to 6 weeks of age have normal body weight, however by 7 weeks of age they are significantly heavier than wildtype controls. The increased body weight is due to increased adipose tissue, with the exception of female homozygotes more than 52 weeks of age that exhibit increased lean body mass. Male heterozygotes and homozygotes, ..... For more information please see the full phenotype on the strain data sheet | ||
| 008154 | B6;129S4-Pparatm1Gonz/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. An altered response to a group of compounds (peroxisome proliferators) that induce peroxisome proliferation and hepatocarcinogenesis is observed. No peroxisome proliferation response is detected when these mice are challenged with classical peroxisome proliferators. Typically, such a response includes hepatomegaly, peroxisome proliferation and transcriptional activation of a set of target enzyme genes. Accumulation of lipid droplets observed in liver tissue suggests that Ppara is involved in maintaining the homeostasis of hepatic lipid metabolism. Homozygotes exhibit increased gonadal adipose tissue stores, abnormal epidermal development and delayed wound healing. This mutant mouse strain may be useful in studies of lipid metabolism, cell proliferation, diabetes, obesity, and wound healing. | ||
| 017321 | C57BL/6-Tg(Fabp4-Dgat1)2Far/J | Repository- Live |
| 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 | ||
| 009345 | C57BL/6J-Mstnlean/J | Repository- Live |
| Mice homozygous for this ENU-induced mutation, called the lean (Ln) allele of myostatin (MstnLn), are viable and fertile. The MstnLn 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 (MstnLn/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 | ||
| 007082 | CByJ.129S(B6)-Tnftm1Gkl/J | Repository- Live |
| Mice homozygous for the Tnftm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does ..... For more information please see the full phenotype on the strain data sheet | ||
| 004585 | STOCK Cav1tm1Mls/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical abnormalities. Mutant mice exhibit exercise intolerance when challenged and are slightly hyperphagic. No gene product (protein) is detected by Western blot analysis in adipose, lung and heart tissues or in cultured mouse embryonic fibroblasts (MEFs). A decrease in the level of co-expressed caveolin-2 protein is immunodetected. At age 4-5 months, mutant mice are often smaller than their wildtype littermates. By one year of age, mutant mice weigh 5 to 7 grams less than wildtype, and are resistant to diet-induced obesity. Progressive adipose pathology results in reduced white adipose tissue with abnormally small adipocytes and enlarged, hyperplastic brown adipose tissue. Homozygotes display lipid metabolism and uptake disruption with elevated serum triglycerides and free fatty acid levels, and reduced leptin levels. Isolated aortic tissue segments have a diminished vasoconstriction ..... For more information please see the full phenotype on the strain data sheet | ||
| 005965 | STOCK Tg(Pomc1-cre)16Lowl/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre activity is demonstrable in brain area neurons involved in the control of food intake (arcuate nucleus (hypothalamus) and solitary tract nucleus (hindbrain)). When bred with a mouse containing a loxP site-flanked sequence of interest, Cre-mediated recombination results in deletion of the flanked genome in tissues that normally express Pomc1. The mice may be useful in studies of obesity, food intake, hunger, endocrine and exocrine function, and for tissue specific gene targeting.
View cre expression characterization. | ||
| 017476 | 129S-Ucp1tm1Kz/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 | ||
| 013046 | 129S6/SvEv-Liastm1Mae/J | Under Development - Now Accepting Orders |
| The Liastm1Mae 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 | ||
| 010750 | 129S.129-Bbs1tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous M390R mutant animals exhibit photoreceptor degeneration and severe obesity. By week 12, homozygous mutant mice are significantly heavier than wildtype or heterozygous mice. Animals are hyperphagic and hyperleptinemic with reduced locomotor activity but no elevation of mean arterial blood pressure. Lateral ventricles in the brain are enlarged and the corpus striatum is reduced. Males lack sperm flagella and are infertile. Although a model of Bardet-Biedl syndrome (BBS, these mice do not demonstrate polycactyly or renal cysts). Expression levels are comparable to those of wildtype mice as determined by Northern blot. Homozygotes are recovered at predicted Mendelian ratios from heterozygous crosses. | ||
| 010751 | 129S.129-Bbs2tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous targeted mutant animals develop obesity that increases with age (cause unknown). They have phenotypes associated with selective cilia dysfunction, including retinopathy, renal cysts, and a deficit in olfaction. Retinal degeneration is characterized by a mislocalization of rhodopsin followed by photoreceptor apoptosis. Male sperm do not develop flagella, causing infertility. Heterozygous crosses produce fewer homozygotes than predicted by Mendelian ratios. Mice also exhibit a defect in social function. | ||
| 010752 | 129S.129-Bbs4tm1Vcs/J | Cryopreserved - Ready for recovery |
| These targeted mutation mice have phenotypes associated with a selective lack of cilia formation or function. Homozygotes weigh less than their littermates at 3 weeks of age, but for unknown reasons become obese over time. Retinal degeneration begins at birth and continues until the entire photoreceptor cell layer is ablated at about 7 months of age. Sperm never develop flagella, causing male infertility. Northern blot analysis confirms that expression of the targeted gene is eliminated in eyes, brain, kidney, ovary, liver, spleen, heart, lungs, and muscle. | ||
| 007584 | 129S4.129S7-Npy5rtm1Rpa/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile. Young mice feed and grow normally, but develop mild late-onset obesity characterized by increased body weight, food intake and adiposity. Obesity is more notable in males than in females. Their response to intracerebroventricular administration of neuropeptide Y (NPY) and related peptides is either reduced or absent. The mice also show enhanced sensitivity to kainate-induced seizures. Transcript is detected in whole brain of null mice at levels less than 10% that of wildtype mice as determined by RT-PCR. Although lacZ is incorporated in the mutant locus, it is not expressed well (or at all). | ||
| 012247 | B6.129-Aldh1a1tm1Gdu/J | Cryopreserved - Ready for recovery |
| This Aldh1a1 (aldehyde dehydrogenase family 1, subfamily A1) targeted mutant lacks exon 11 which encodes the substrate binding pocket and the tetramerization domain. Protein is not detected by Western blot analysis of liver, lung and testes. Protein is not detected by immunohistochemistry in embryonic retina. Retinoic acid synthesis is reduced in embryonic retina and adult liver. Expression is significantly reduced in the hematopoietic system, but hematopoiesis is not affected. Homozygotes are resistant to diet-induced obesity and insulin resistance and show increased energy dissipation. Approximately 63% of animals are reported to develop mild anterior subcapsular cataracts at 6-9 months of age. This strain may be useful in further characterizing the various functions of the targeted gene. | ||
| 010726 | B6.129-Bbs1tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous M390R mutant animals exhibit photoreceptor degeneration and severe obesity. By week 12, homozygous mutant mice are significantly heavier than wildtype or heterozygous mice. Animals are hyperphagic and hyperleptinemic with reduced locomotor activity but no elevation of mean arterial blood pressure. Lateral ventricles in the brain are enlarged and the corpus striatum is reduced. Males lack sperm flagella and are infertile. Although a model of Bardet-Biedl syndrome (BBS, these mice do not demonstrate polycactyly or renal cysts. Expression levels are comparable to those of wildtype mice as determined by Northern blot. Homozygotes are recovered at predicted Mendelian ratios from heterozygous crosses. | ||
| 010727 | B6.129-Bbs2tm1Vcs/J | Cryopreserved - Ready for recovery |
| Homozygous targeted mutant animals develop obesity that increases with age (cause unknown). They have phenotypes associated with selective cilia dysfunction, including retinopathy, renal cysts, and a deficit in olfaction. Retinal degeneration is characterized by a mislocalization of rhodopsin followed by photoreceptor apoptosis. Male sperm do not develop flagella, causing infertility. Heterozygous crosses produce fewer homozygotes than predicted by Mendelian ratios. Mice also exhibit a defect in social function. This strain may be useful as a model for Bardet-Biedl syndrome. | ||
| 010728 | B6.129-Bbs4tm1Vcs/J | Cryopreserved - Ready for recovery |
| These targeted mutation mice have phenotypes associated with a selective lack of cilia formation or function. Homozygotes weigh less than their littermates at 3 weeks of age, but for unknown reasons become obese over time. Retinal degeneration begins at birth and continues until the entire photoreceptor cell layer is ablated at about 7 months of age. Sperm never develop flagella, causing male infertility. Northern blot analysis confirms that expression of the targeted gene is eliminated in eyes, brain, kidney, ovary, liver, spleen, heart, lungs, and muscle. This strain may be useful as a model for some features of Bardet-Biedl syndrome. | ||
| 002627 | B6.129-Htr2ctm1Jul/J | Cryopreserved - Ready for recovery |
| Homozygous mice show spontaneous and infrequent epileptic seizures, sometimes resulting in death. They also show overeating behavior and an increase in the accumulation of white adipose tissue. | ||
| 008518 | B6.129-Leprtm1Mgmj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the LeprS1138 mutant allele (or s/s mice) are viable and partially fertile with a Tyr->Ser replacement at amino acid residue 1138 of the leptin receptor long form (LRb)-specific exon 18b. The mutation specifically disrupts LRb-STAT3 transcription factor signaling. The mutant protein, LRbS1138, is expressed normally on the cell surface and mediates other leptin signals normally, but fails to activate STAT3. Similar to homozygous db/db mice (which are devoid of all leptin signaling), homozygous s/s mice display hyperphagia, decreased energy expenditure, and decreased thyroid function resulting in profound obesity and dramatically increased serum leptin levels compared to wild-type. Unlike db/db mice, however, s/s mice are fertile and long bodied, have improved glucose tolerance (less hyperglycemic), are not protected from intimal hyperplasia following vessel injury, and do not exhibit elevated hypothalamic ex ..... For more information please see the full phenotype on the strain data sheet | ||
| 008385 | B6.129-Leprtm2Mgmj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the LeprLeu985 mutant allele (or l/l mice) are viable and fertile with a Tyr->Leu replacement at amino acid residue 985 of the leptin receptor long form (LRb)-specific exon 18b. The mutation specifically disrupts LRb-SHP2 and LRb-SOCS3 transcription factor signaling. The mutant protein, LRbL985, is expressed normally and mediates other leptin signals normally, but fails to recruit SHP2 or SOCS3. Homozygous male and female mice are neuroendocrinologically normal, but homozygous females may exhibit decreased feeding, body weight, adipocity, circulating leptin, circulating insulin, expression of orexigenic neuropeptides, protection from high-fat diet-induced obesity, and increased leptin sensitivity depending upon diet and genetic background. Homozygous LeprLeu985 mutant mice may be useful for studying the influence of LRb-SHP2 and LRb-SOCS3 signaling in the physiological and metabolic function of leptin; specifically b ..... For more information please see the full phenotype on the strain data sheet | ||
| 003870 | B6.129-Plin1tm1Chan/J | Cryopreserved - Ready for recovery |
| Homozygous null Plin mice are viable and fertile. At birth they are normal in size and do not display any gross physical or behavioral abnormalities. No transcripts are detected and Western-blot analysis of adipocyte and testes indicate no protein products are present. Although null mice consume more food than wildtype littermates, they have significantly less body fat (30-74%) and exhibit smaller white adipocytes (62%). With diminished fat stores, the mice are cold sensitive under fasting conditions. A greater muscle mass allows them to maintain a normal body weight. Hormone sensitive lipase activity is greatly increased in null mice resulting in elevated levels of basal lipolysis. Null mice are resistant to diet-induced obesity. The inheritance of the null alleles in Leprdb/db mice reverses their obesity phenotype. | ||
| 008841 | B6.129S2-Ccrn4ltm1Bjc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Nocturnin (Ccrn4l or Noc) targeted mutation are viable and fertile, with no detectable Noc protein made from the targeted gene. Homozygotes are resistant to diet-induced obesity and remain lean on high-fat diets, with lower body weight and reduced visceral fat. Unlike lean lipodystrophic mouse models, Noc-deficient mice do not have fatty livers (hepatic steatosis) and do not exhibit increased activity or reduced food intake. In addition to changes in glucose tolerance and insulin sensitivity, homozygous mice may also have deficits in lipid metabolism or lipid uptake. Nocturnin-deficient mice may be useful in studying resistance to diet-induced obesity, physiologic rhythms downstream of the circadian clockwork, and post-transcriptional regulation of genes necessary for nutrient uptake, metabolism, and storage. | ||
| 003191 | B6.129S2-Pomctm1Low/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Pomctm1Low targeted mutation are viable and fertile. Homozygous mutant mice display no overt developmental or behavioral abnormalities. The hypothalmic-pituitary-adrenal axis functions normally. Homozygotes do display significantly greater nonopioid analgesia in response to cold water swim stress compared with controls and display paradoxical naloxone-induced analgesia. Male mice show an altered growth curve during puberty resulting in increased body mass and white fat. This phenotype is present in both the homozygous mutant males and in wildtype males reared by homozygous parents. This strain is useful for looking at response to pain. | ||
| 011085 | B6.129S4-Mogat2tm1Far/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. On a high fat diet, homozygotes exhibit resistance to obesity, glucose intolerance, hypercholesterolemia and fatty liver. For example, after 16 weeks of feeding on a 60 kcal% fat diet, male mice gain 40% less weight and have a 50% lower fat mass than wild type mice. Female mice exhibit similar resistance. Heterozygotes have an intermediate phenotype. After 2 months on high fat diet, male mice have lower fasting insulin concentrations, better glucose tolerance, lower total and non-HLD cholesterol, and are resistance to hepatic steatosis. Although food consumption and dietary fat absorption are similar in wild-type and mutant mice, entry of dietary fat into the circulation occurs at a reduced rate. This mutant mouse strain may be useful in studies of obesity, fat absorption and energy homeostasis. | ||
| 005897 | B6.129S4-Ppardtm1Rev/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exon 4 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice with a cre recombinase gene under the control of a promoter of interest, exon 4 of the targeted gene is deleted in the tissue of interest, leading to premature termination of the translation product upstream of the DNA binding domain. This strain may be useful in generating tissue-specific mutants of the floxed allele for use in studies including embryo development, adipocyte physiology, fat metabolism and storage, inflammation, and cancer. | ||
| 005901 | B6.129S4-Ppardtm2Rev/J | Cryopreserved - Ready for recovery |
| Heterozygous mice are viable and fertile. All homozygous mice die in utero. Macrophages homozygous for this mutation have no transcriptional response to very low-density lipoprotein treatment. No evaluation of lacZ expression is published. The donating investigator reports homozygous mice on this background have a similar, albeit earlier, embryonic phenotype as the exon 4 deleted mutants described in other publications (Barak PNAS 2002 99:303-8, Chawla PNAS 2003 100:1268-73, and Lee Science 2003 302:453-7). Heterozygous mice or homozygous embryo-derived cells may be useful in studies of embryo development, adipocyte physiology, fat metabolism and storage, inflammation, and cancer. | ||
| 005981 | B6.129S7-Rai1tm1Jrl/J | Cryopreserved - Ready for recovery |
| Mice are albino. Heterozygous mice are viable and fertile and weigh slightly less than wildtype at 0-2 weeks of age. RT-PCR shows a blunted N-terminal product in kidney tissues that does not contain the two nuclear localization signals (NLS) or zinc finger like plant homeo domain (PHD). Heterozygous embryos have differential tissue expression of lacZ during development, faithfully recapitulating the expression pattern of Rai1. Less than 5% of heterozygous mice exhibit polydactyly. While noticeably smaller at 4-7 weeks, heterozygotes are significantly obese by 20-23 weeks. 7-18% of heterozygotes have craniofacial defects (broader and shorter nasal bone and lateral bending of the snout). The vast majority of homozygotes are embryonic lethal, with death occurring after implantation but before 15.5 days post coitum (during gastrulation and organogenesis). All homozygotes surviving to birth exhibit growth retardation and premature death with most dying before wean. Homozygous mice ha ..... For more information please see the full phenotype on the strain data sheet | ||
| 004366 | B6.129X1-Brs3tm1Jfb/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size at birth and do not display any gross physical or behavioral abnormalities. This targeted mutation is X-linked; males bearing the targeted allele display a mutant phenotype. At 15 to 16 weeks of age male mice heterozygous for the mutant allele display increased body weight as compared to wildtype littermates. This mutant mouse strain represents a model that may be useful in studies related to energy metabolism and obesity. | ||
| 003126 | B6.129X1-Grprtm1Jfb/J | Cryopreserved - Ready for recovery |
| Mice homozygous (females) or hemizygous (males) for the X-linked Grprtm1Jfb targeted mutation are viable with no gross phenotypic abnormalities observed. There is a deficiency in bombesin-induced mediation of satiety as measured by glucose intake. A modest increase in body weight is observed in older animals. At 18-20 months of age, hemizygous males (N = 8) are 44.5g ± 5.1 (mean ± std dev) and wildtype littermates (N = 8) are 38.3g ± 5.1 (L. Hampton, unpublished observation). We have recently observed head tilts and bobbing in the hemizygous males in our production colony. The donating investigator of this strain has also observed this phenotype and considers it a mutation not related to the gene. We are working to remove this phenotype, but we will continue to ship from the colony while we finish this process. | ||
| 009365 | B6.129X1-Mark2tm1Hpw/J | Cryopreserved - Ready for recovery |
| Homozygous targeted mice show and increased metabolic rate, decreased adiposity, resistance to high fat diet-induced weight gain, and insulin hypersensitivity. Western blot analysis demonstrates that expression is eliminated in brain, spleen, kidney and liver, lymph nodes, thymus, white and brown adipose tissues, large and small intestines, stomach. Homozygous pups are born slightly below predicted Mendelian ratios and show both embryonic and postnatal growth retardation as well as increased mortality as compared to wildtype animals. The age of death can range from 3 weeks to several months. Approximately 85% of homozygotes exhibit some combination of immunological disorders between the ages of 5 and 12 months. B and T cell development is normal, but CD4+ T cells lacking this protein exhibit a marked upregulation of the memory marker CD44 and produce more gamma interferon and interleukin 4 on stimulation through the T cell receptor in vitro. B cell responses to T ..... For more information please see the full phenotype on the strain data sheet | ||
| 008115 | B6.129X1-Pomctm2Ute/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. 60 to 75% of homozygotes die perinatally. Surviving homozygotes have decreased fertility and homozygous females produce milk that does not allow pups to survive past 14 days of age. No serum adrenocorticotropic hormone (ACTH) or corticosterone was detected by radioimmunoassay (RIA) of homozygotes. Serum epinephrine and aldosterone levels are reduced. Although homozygotes are born with adrenal glands or normal size, adrenal glands fail to grow postnatally and become almost undetectable with age. By 3 months of age, mice homozygous for the mutation are twice the weight of wildtype controls and increased serum leptin levels. Heterozygotes exhibit elevated serum leptin levels, but not increased weight and reduced levels of serum adrenocorticotropic hormone (ACTH), corticosterone, and aldosterone levels. Both heterozygotes and homozygote ..... For more information please see the full phenotype on the strain data sheet | ||
| 000017 | B6.C3-Avy/J | Cryopreserved - Ready for recovery |
| Homozygous (Avy/Avy) and heterozygotes (Avy/A and Avy/a) show considerable variation in appearance, ranging from clear yellow, to mottling with dark patches, to a completely agouti-like coat. The variation is strongly influenced by the agouti-locus genotype and strain genome of the dam. Homozygotes and heterozygotes tend to become obese, and the degree of obesity is correlated with the amount of yellow in the coat. Avy resembles Ay in causing greater tumor susceptibility and lower graft vs. host reactivity and higher hepatic malic enzyme activity. Homozygotes have a reduced humoral response to tetanus toxoid and decreased rates of carbon clearance as well as impaired mononuclear phagocyte function. The greater tumor susceptibility as well as several altered immune responses occur in Avy/a mice of mottled phenotype but not in those of agouti phenotype. | ||
| 006200 | B6.Cg-Tnks2tm1.1Yjc/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of activated spleen lymphocytes. While neither telomere shortening nor chromosomal abnormalities (even across multiple generations) are observed, homozygous mice have significantly decreased body weight. These mutant mice may be useful in studies of both telomerase function and telomerase-independent pathways which affect development and metabolism. | ||
| 010901 | B6.Cg-Tg(ACTA1-Il15)10941Lsq/J | Cryopreserved - Ready for recovery |
| In both mouse and human, the interleukin-15 (Il15) gene encodes two IL-15 mRNA variants that utilize different signal sequences but produce identical mature IL-15 proteins following signal peptide cleavage. The long signal peptide IL-15 (LSP-IL-15) isoform is inefficiently secreted from cells, whereas the short signal peptide (SSP)-IL-15 isoform is not secreted and localization is intracellular. Mice hemizygous for the HSA-natLSP-IL15 transgene are viable and fertile, with overexpression of the inefficiently secreted native LSP-IL-15 mRNA and protein directed to skeletal muscle tissue by the human α-skeletal actin (HSA or ACTA1) promoter. Compared to wildtype littermates, IL-15 mRNA/protein expression in skeletal muscle is approximately 300-fold/400-fold greater in hemizygous males (and approximately 100-fold/400-fold greater in hemizygous females), respectively. No overexpression of IL-15 protein is detectable in the serum of hemizygous males or females. These HS ..... For more information please see the full phenotype on the strain data sheet | ||
| 011002 | B6.Cg-Tg(ACTA1-Il15*)11650Lsq/J | Cryopreserved - Ready for recovery |
| In both mouse and human, the interleukin-15 (Il15) gene encodes two IL-15 mRNA variants that utilize different signal sequences but produce identical mature IL-15 proteins following signal peptide cleavage. The long signal peptide IL-15 (LSP-IL-15) isoform is inefficiently secreted from cells, whereas the short signal peptide (SSP)-IL-15 isoform is not secreted and localization is intracellular. Mice hemizygous for the HSA-IL2SP-IL15 transgene are viable and fertile, with overexpression of the IL2SP-IL15 mRNA and protein directed to skeletal muscle tissue by the human α-skeletal actin (HSA or ACTA1) promoter. Compared to wildtype littermates, IL-15 mRNA/protein expression in skeletal muscle is approximately 1000-fold greater in hemizygous males (and approximately 800-fold/1000-fold greater in hemizygous females, respectively). Because the native IL-15 LSP is replaced with the IL-2 signal peptide, efficient secretion of mature IL-15 leads to overexpression in the ..... For more information please see the full phenotype on the strain data sheet | ||
| 012379 | B6.Cg-Tg(Ckm-Ppara)HEDpk/J | Cryopreserved - Ready for recovery |
| This transgenic strain expresses mouse Ppara (peroxisome proliferator activated receptor alpha) cDNA carrying a C-terminal FLAG tag under the control of the mouse Ckm (creatine kinase, muscle) promoter. Expression levels in this "high expression" (HE) line are increased approximately 100-fold over endogenous levels. Highest expression is found in fast-twitch muscle and less expression occurs in heart and soleus. Hemizygotes develop glucose intolerance (as early as 6 weeks of age) and insulin resistance despite being protected from diet-induced obesity. This strain may be useful in studies of diabetes, obesity, and muscle lipotoxicity. | ||
| 008221 | B6.Cg-Tg(IGFBP1)2Miel/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the hIGFBP-1 transgene are viable and fertile with no reported gross morphological or developmental changes. The hIGFBP-1 transgene encompasses the entire human IGFBP-1 structural gene and its regulatory sequences, allowing transgene expression of IGFBP-1 to remain responsive to normal hormonal regulation. Transgenic mice overexpress hIGFBP-1, with hIGFBP-1 mRNA expression in a tissue-specific fashion more similar to the human pattern than the murine pattern. Fasting transgenic mice have elevated total serum IGFBP-1 levels that fluctuate according to nutritional status (as they do in humans), and exhibit postprandial hyperinsulinemia with preservation of normal glucocompetence and insulin sensitivity. Transgenic mice also have significantly greater hyperinsulinemic response to glucose challenge and cardiovascular abnormalities in response to carbohydrate load and vasoconstrictors. Transgenic mice exhibit fasting hyperglycemia and hyperinsulinemia and glucose intoler ..... For more information please see the full phenotype on the strain data sheet | ||
| 008222 | B6.FVB-Tg(IGFBP2)1Miel/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the IGFBP-2 transgene are viable and fertile with no reported gross morphological or developmental changes. Transgenic mice overexpress human IGFBP-2 (hIGFBP-2), with hIGFBP-2 mRNA detected in a variety of organs and tissues, including adipose tissue. Overexpression of hIGFBP-2 is associated with reduced susceptibility to obesity and improved insulin sensitivity; transgenic mice are protected from glucose intolerance and increased blood pressure with age, and are also resistant to obesity and insulin resistance on a high fat diet. The phenotype of hIGFBP-2 overexpressing mice may vary between male and female mice. These IGFBP-2 transgenic mice may be useful in studying metabolic homeostasis, adipocyte biology, and the role of insulin-like growth factor binding protein in protecting against obesity- and age-associated complications (such as hypertension and diabetes).
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alle ..... | ||
| 008156 | B6;129-Gpr83tm1.1Ayr/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. Gene product (mRNA) is not detected by quantitative RT-PCR analysis of T cells isolated from homozygous animals. Naive CD4 T cells display a marginally reduced tendency to induce forkhead box P3 (Foxp3) in response to transforming growth factor, beta 1 (TGF-beta, Tgfb1) stimulation in vitro. This strain may be useful in studies of regulatory T cell (Treg) development and function. Aged homozygous mice may show signs of obesity, supporting a proposed involvement of the gene in feeding and emotional behaviors. | ||
| 008678 | B6;129-Ubbtm1Rrk/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the targeted allele are viable and fertile. This polyubiquitin B (Ubb) mutation is characterized by a GFP-puror fusion protein "knock-in" allele that also abolishes endogenous gene function. Direct visualization of GFP fluorescence is observed in ovaries, testes, hypothalamus (arcuate nucleus) and cerebral cortex. Homozygotes have no Ubb mRNA observed in the various tissues tested, and are viable but sterile due to failure of germ cells to progress through meiotic prophase I and hypogonadism. Homozygotes also exhibit a complex metabolic phenotype initially characterized by dysfunction of neurons within the central nervous system accompanied by retarded perinatal growth that progresses to adult-onset obesity linked to selective hypothalamic neurodegeneration. Homozygotes also develop adult-onset hyperleptinemia (but normal levels of circulating glucose and insulin) as a consequence of increased fat content. These Ubb-mutant mice may be useful in studyin ..... For more information please see the full phenotype on the strain data sheet | ||
| 005689 | B6;129S1-hlb349A/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the mutation are viable and fertile. Screening of third generation mice (G3) on atherogeneic diet identified a 12 week old male (born 12/28/2002) with a weight of 30.71 grams and body fat of 22.38%. Females appear to be more severely affected than males. This mutant mouse strain may be useful in studies of obesity. | ||
| 006907 | B6;CBA-Tg(APOC3)3707Bres/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this "human apo CIII" transgene are viable and fertile. This high expressor founder line (3703) exhibits transgene expression primarily in the liver with some intestinal expression as well. Hemizygous mice have severe plasma hypertriglyceridemia and significantly increased plasma cholesterol. However, resistance to insulin-mediated glucose uptake or hyperinsulinemia are not observed. This high expressor human apo CIII transgenic strain may be useful in studying lipid metabolism, very low density lipoproteins (VLDL), hypertriglyceridemia, coronary heart disease, and/or atherosclerosis. | ||
| 000099 | C3HeB/FeJ-Avy/J | Cryopreserved - Ready for recovery |
| Homozygotes (Avy/Avy) and heterozygotes (Avy/A and Avy/a) show considerable variation in appearance, ranging from clear yellow, to mottling with dark patches, to a completely agouti-like coat. The variation is strongly influenced by the agouti-locus genotype and strain genome of the dam. Homozygotes and heterozygotes tend to become obese, and the degree of obesity is correlated with the amount of yellow in the coat. Avy resembles APy in causing greater tumor susceptibility and lower graft vs. host reactivity and higher hepatic malic enzyme activity. Homozygotes have a reduced humoral response to tetanus toxoid and decreased rates of carbon clearance as well as impaired mononuclear phagocyte function. The greater tumor susceptibility as well as several altered immune responses occur in Avy/a mice of mottled phenotype but not in those of agout ..... For more information please see the full phenotype on the strain data sheet | ||
| 009062 | C57BL/6-Magel2tm1Stw/J | Cryopreserved - Ready for recovery |
| The mouse locus 7qB4/B5 (syntenic with the Prader-Willi region at chromosome position 15q11-q13 in humans) encompasses the cluster of paternally-expressed imprinted genes Magel2, Ndn, Mkrn3, and Peg12. As maternal imprinting silences the Magel2 allele, only the paternally inherited Magel2 allele is expressed. The Magel2-lacZ knock-in allele abolishes endogenous gene function and expresses a β-galactosidase fusion protein. Under control of the upstream promoter/enhancer elements, lacZ expression is directed to the same tissues as the wildtype gene. For example, β-galactosidase expression during embryogenesis is detected in central nervous system (neural tube, forebrain, midbrain and embryonic hypothalamus), peripheral nervous system (dorsal root ganglia and peripheral neurons innervating limb and trunk muscles), and some non-neuronal tissues (genital tubercle, midgut region and placenta). Adult β-galactosidase ..... For more information please see the full phenotype on the strain data sheet | ||
| 006699 | C57BL/6J-Pcsk1N222D/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this ENU-induced "Pc1N222D" 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, Pc1N222D 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. | ||
| 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. | ||
| 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. | ||
| 007067 | D2.129P2(B6)-Apoetm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Apoetm1Unc mutation show a marked increase in total plasma cholesterol levels that are unaffected by age or sex. Fatty streaks in the proximal aorta are found at 3 months of age. The lesions increase with age and progress to lesions with less lipid but more elongated cells, typical of a more advanced stage of pre-atherosclerotic lesion. Moderately increased triglyceride levels have been reported in mice with this mutation on a mixed C57BL/6 x 129 genetic background. Aged APOE deficient mice (>17 months) have been shown to develop xanthomatous lesions in the brain consisting mostly of crystalline cholesterol clefts, lipid globules, and foam cells. Smaller xanthomas were seen in the choroid plexus and ventral fornix. Recent studies indicate that APOE deficient mice have altered responses to stress, impaired spatial learning and memory, altered long term potentiation, and synaptic damage.
In an attempt to offer alleles on well-charac ..... | ||
| 004455 | NONcNZO5/LtJ | Cryopreserved - Ready for recovery |
| A diabetes-resistant recombinant congenic developed by introgressing selected markers of resistance alleles for all but one known diabesity QTL in the parental strains NZO/HlLt and NON/Lt. The NONcNZO5/LtJ stock has been specifically constructed to exclude 5 NZO-derived and two NON-derived diabetes susceptibility QTL present in the highly diabetes-prone NONcNZO10LtJ recombinant congenic stock. NONcNZO5/LtJ males develop a comparable level of moderate obesity to that developing in the highly diabetes susceptible NONcNZO10/LtJ males, but they do not develop the extreme obesity characteristic of NZO/HlLt. Neither NONcNZO5/LtJ males nor females develop spontaneous type 2 diabetes on a 6% fat-containing diet. Serum insulin and leptin values are close to the NON/Lt parental background range and significantly lower than in NZO/HlLt. Unlike NZO/HlLt, NONcNZO5/LtJ breeds well. Unlike NZO and NONcNZO10/LtJ males, NONcNZO5LtJ males are resistant to adverse hepatic side effects of thiazolidi ..... For more information please see the full phenotype on the strain data sheet | ||
| 008777 | NZG/KgmJ | Cryopreserved - Ready for recovery |
| The New Zealand Ginger (NZG) mouse is characterized by rapid growth and a large body size as a result of excessive lean body mass. This inbred strain is not obese, diabetic or insulin resistant. Both sexes exhibit a rapid growth rate which plateaus at 60 days, however, males are heavier than females. ELISA assay indicates that mice have higher levels of circulating insulin-like growth factor I (IGF1) than C57BL/6 mice, but comparable levels of insulin and growth hormone. Mice have an unusual pattern of fat distribution compared to C57BL/6 mice with higher percentages of retroperitoneal, gonadal and inguinal fat rather than visceral fat. NZG mice have less total body fat (6%) than C57BL/6 mice (13.8%). These mice are susceptible to high fat (45%) diet-induced obesity, but not diet-induced diabetes.
Genetic analysis indicates that the yellow (ginger) coat is not the result of alleles at either agouti or the melanocortin 1 receptor (Mc1r) genes. The fur is described ..... | ||
| 006327 | STOCK Pcsk1tm1Dfs/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the targeted mutation are viable and fertile. No gene product (mRNA or protein) is detected in the homozygotes by Northern blot analysis of hypothalamic tissue or Western blot analysis of pituitary and brain tissue. Homozygote mice experience perinatal lethality, as the number of homozygotes born is less than the expected Mendelian ratio, and high postnatal lethality. By postnatal day 3, homozygotes are smaller in size than littermates. By 6 weeks of age, the surviving homozygotes are approximately 60% of wildtype body weight. Homozygotes have chronic mild diarrhea with bulky moist stools. Pituitary growth hormone transcript levels are only 25-20% of normal levels. Somatotroph cells in the anterior pituitary are reduced in size and inactive. Insulin-like growth factor 1 serum levels are significantly reduced. Transcript (mRNA) levels are greatly increased for growth hormone-releasing hormone in the hypothalamus and proopiomelanocortin in the pituitary. Ma ..... For more information please see the full phenotype on the strain data sheet | ||
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