Search Criteria: Research Area is "Metabolism Research: Lipid Metabolism"
| 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. | ||
| 002207 | B6.129S7-Ldlrtm1Her/J | Level 2 |
| Mice homozygous for the Ldlrtm1Her mutation have an elevated serum cholesterol level of 200-400 mg/dl and they have very high levels (>2,000 mg/dl) when fed a high fat diet. Normal serum cholesterol in the mouse is 80-100 mg/dl. | ||
| 014634 | 129(B6)-Nr1h2tm1Djm/J | Repository- Live |
| In this strain a neomycin (neo) resistance cassette replaces exons 5-6 of the nuclear receptor subfamily 1, group H, member 2 (Nr1h2) gene, abolishing gene function. Homozygous are viable, fertile, and normal in size. Also known as liver X receptor beta (Lxrβ), Nr1h2 binds to retinoid X receptors (RXRα, RXRβ, RXRγ; NR2B1, NR2B2, and NR2B3) and is activated by oxysterols to regulate the expression of genes involved in cholesterol metabolism. . Homozygous Lxrβ-/- mice lose their ability to appropriately regulate cholesterol, lipid, and carbohydrate metabolism, and have defects in immune function. These defects are more severe when combined with the knockout of Lxrα (available as Stock No. 013762). These mice may be useful for studying lipid and cholesterol metabolism, and regulation of the immune response. | ||
| 013762 | 129-Nr1h3tm1Djm/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 | ||
| 012755 | 129-Sirt3tm1.1Fwa/J | Repository- Live |
| The targeted mutation deletes exon 2-3 of the mouse sirtuin (silent information regulator 2 (Sir2)) homolog 3, Sirt3, gene, abolishing gene function. Homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Sirt3-/- mice exhibit hyperacetylation of mitochondrial enzymes, including glutamate dehydrogenase (GDH) and long-chain acyl co-enzyme A dehydrogenase (LCAD), leading to a decrease in the modulation of mitochondrial metabolism and fatty acid oxidation. They show reduced ATP production, cold intolerance, and hypoglycemia. These mice may be useful in studying the role of fatty acid oxidation in diabetes, cardiovascular disease, steatosis, fasting, cold exposure, and life span. | ||
| 008286 | 129S6.129P2(B6)-Nos3tm1Unc/J | Repository- Live |
| Homozygous mutant mice 129S6/SvEvTac background are viable, fertile, normal in size and do not exhibit any gross physical or behavioral abnormalities. On the C57BL/6 congenic background homozygous mutants mice exhibit elevated blood pressure that is about 20 mmHg higher than that seen in normal wildtype siblings. They also show a decreased heart rate. Female homozygotes are smaller in body weight than normal wildtype siblings. Hyperglycemic-euglycemic clamp studies demonstrate that homozygotes exhibit insulin resistance at the level of the liver and peripheral tissues. This mutant mouse strain may be useful in studies of wound healing, hypertension and other cardiovascular defects, insulin resistance, hyperlipidemia and lung development. 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. This is the case for the strain ..... | ||
| 008355 | B6.129(Cg)-Slc6a4tm1Kpl/J | Repository- Live |
| Mice that are homozygous for the serotonin transporter targeted mutation (SERT-/- or 5-HTT-/-) are viable and fertile with a superficially unremarkable behavioral phenotype through early adulthood. Serotonin uptake is completely absent in homozygous mice. SERT-deficiency is pleiotropic (many different phenotypic traits). Homozygotes and, to a lesser extent, heterozygotes exhibit diminished responses to serotonin receptor agonists and other classes of drugs (including MDMA, SSRIs, 8-OH-DPAT, and DOI). SERT-mutant mice are also reported to have increased anxiety-like behaviors, altered neuroendocrine and sympathoadrenal responses to even minor stress, diminished aggression, altered emotional learning, substantially increased rapid eye movement (REM) sleep time, reduced brain excitability, increased body temperature, increased colonic motility, reduced spinal reflex to injury, reduced bladder response to stretching, blood pressure responses, diminished bone and muscl ..... For more information please see the full phenotype on the strain data sheet | ||
| 006952 | B6.129-Akt2tm1.1Mbb Ldlrtm1Her/J | Repository- Live |
| Independently, homozygous Akt2 mutant mice develop insulin resistance and diabetes, while LDLR homozygotes are predisposed to atherosclerosis. Double mutant mice that are heterozygous for the Akt2 allele and homozygous for the LDLR mutation are viable and fertile. These double mutant mice may be useful in studies of diabetes, metabolism, hyperglycemia, and atherosclerosis. | ||
| 009106 | B6.129-Cyp27a1tm1Elt/J | Repository- Live |
| These mice harbor a targeted mutation of the Cyp27a1 (cytochrome P450, family 27, subfamily a, polypeptide 1) locus that abolishes endogenous gene expression. Homozygous mice (also called Cyp27a1-/-, cyp27-/-, or sterol 27-hydroxylase-deficient mice) are viable and fertile, with no RNA or protein expression from the targeted gene detected in liver tissue. Both formation of bile acids and excretion of fecal bile acids are decreased in homozygous mice. Compensatory up-regulation of hepatic enzymes that convert cholesterol to bile acids (bile acid synthesis) is also observed. Cyp27a1-/- mice exhibit a dramatic increase in cytochrome P450 3A (Cyp3a11) which catalyzes side-chain hydroxylations of bile acid intermediates subsequently facilitating their excretion in the bile and urine. Homozygous mice also have increased expression of other nuclear xenobiotic receptor PXR (pregnane X receptor) target genes. | ||
| 008597 | B6.129-Ppargc1atm1Brsp/J | Repository- Live |
| Mice that are homozygous for this targeted mutation are fertile, normal in size and do not display any gross physical or behavioral abnormalities. Approximately half of homozygotes exhibit postnatal lethality. The Donating Investigator reports maintaining homozygous pups at a higher temperature (77°F) increases their survival. No gene product (mRNA or protein) is detected by RNA hybridization, real-time PCR analysis of skeletal muscle or liver, or Western blot analysis of brown fat. Histological examination of the brown fat from homozygotes reveals abnormal accumulation of large lipid droplets. Examination of brain tissue shows spongiform lesions and gliosis. When fed a high fat diet homozygotes have increased insulin sensitivity, glucose tolerance and reduced body weight. After 24 hours of fasting, homozygotes develop mild hypoglycemia. Mutants have impaired mitochondrial function and gluconeogenesis and are hypermetabolic as well as hyperactive. Homozygotes are unable to survive ..... For more information please see the full phenotype on the strain data sheet | ||
| 008227 | B6.129S4-Ppargtm3Yba/J | Repository- Live |
| These mice express tTA (tetracycline regulated transactivator) from the endogenous Pparg locus. A fusion transcript (including the 5' portion of Pparg, IRES and tTA (AF1-IRES-tTA)) and a wild-type Pparg transcript are detected by Northem blot analysis of epididymal fat pads from heterozygotes. Mice that are heterozygous for this targeted mutation exhibit a similar but milder phenotype than that observed in Pparg-Ldi mice (129-Ppargtm2Yba/J, Stock No. 008079). Heterozygotes exhibit mild lipodystrophy with pale, unilocular brown adipocytes, hypertrophy of brown fat, reduced subcutaneous fat, gonadal fat pads smaller than wild-type and mild hepatomegaly. Mutant mice develop insulin resistance and dyslipidemia. Treatment with doxycycline prevents this phenotype. Mice that are homozygous for the targeted mutation are not viable. This mutant mouse strain may be useful in studies of lipodystrophy. | ||
| 012564 | B6.129S5-Dhcr24tm1Fein/SbpaJ | Repository- Live |
| Homozygous mice on the C57BL/6 genetic background die within the first postnatal day with features of lethal restrictive dermopathy; including taut, wrinkle-free, shiny skin, severe defects in epidermal maturation/epidermal barrier function (impaired epidermal development), and increased presence of hyperproliferative immature keratinocytes (defective keratinocyte differentiation). The increased transepidermal water loss/increased epidermal water content is associated with increased aquaporin-3 (AQP3) expression throughout the epidermis. Mice heterozygous for this allele are viable and fertile, with no overt phenotype. As the Dhcr24 protein functions to catalyze the last step of cholesterol biosynthesis (the conversion of desmosterol to cholesterol), homozygous disruption of this locus results in desmosterolosis: almost no cholesterol in plasma and tissues with ~99% of total sterols in the form of desmosterol. lacZ expression from the mutant allele is not characterized.
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| 010537 | B6.129S6-Mlxipltm1Kuy/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. Mutant mice exhibit increased glucose and insulin levels, decreased free fatty acids, reduced epididymal and brown fat weight, and reductions in liver glycolysis and lipogenic enzymes. Mice fed diets high in sucrose or fructose died within one week most likely as a result of inhibited glycolysis. On a high starch diet, mice developed moderate insulin resistance and increased liver weight. This mutant mouse strain may be useful in studies of lipogenesis and glucose metabolism. | ||
| 014633 | B6.129S6-Nr1h2tm1Djm/J | Repository- Live |
| In this strain a neomycin (neo) resistance cassette replaces exons 5-6 of the nuclear receptor subfamily 1, group H, member 2 (Nr1h2) gene, abolishing gene function. Homozygotes are viable, fertile, and normal in size. Also known as liver X receptor beta (Lxrβ), Nr1h2 binds to retinoid X receptors (RXRα, RXRβ, RXRγ; NR2B1, NR2B2, and NR2B3) and is activated by oxysterols to regulate the expression of genes involved in cholesterol metabolism. Homozygous Lxrβ-/- mice lose their ability to appropriately regulate cholesterol, lipid, and carbohydrate metabolism, and have defects in immune function. These defects are more severe when combined with the knockout of Lxrα (available as Stock No. 013761). These mice may be useful for studying lipid and cholesterol metabolism, and regulation of the immune response. | ||
| 013761 | B6.129S6-Nr1h3tm1Djm/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 | ||
| 010502 | B6.129S6-Ptrftm1Pfp/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile, however, they exhibit a lean body mass and a reduced metabolic capacity. No gene product is detected by Western blot analysis. Mice lack caveolae in lung epithelium, intestinal smooth muscle, skeletal muscle and in the corresponding endothelial cells. In addition, homozygotes have increased triglyceride, insulin and free fatty acid levels and exhibit both impaired glucose tolerance and insulin resistance. This mutant mouse strain may be useful in studies of lipodystrophies and metabolic dysfunction | ||
| 016238 | B6.129S6-Rbp7tm1Vgl/J | Repository- Live |
| Mice that are homozygous for this knockout 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 heart tissue extracts from homozygous mice. Homozygous lactating females have reduced levels of total retinyl ester in milk, with the largest reduction in retinyl palmitate levels. Total retinol levels in heart tissue are reduced in homozygotes at weaning, but not in homozygotes aged 11 or 17 weeks. Decreased levels of retinol and retinyl ester are detected in the mammary glands of homozygous females 11 weeks of age. At 17 weeks of age, only total retinol levels remain diminished. Postprandial retinoid turnover is not changed in mutant mice. Homozygotes fed a high fat diet have reduced hepatic steatosis, lower hepatic triglyceride levels, and decreased serum free fatty acids and efflux from adipose tissue compared to wildtype controls. On a ..... For more information please see the full phenotype on the strain data sheet | ||
| 006883 | B6.129S7-Ldlrtm1Her Sod2tm1Leb/J | Repository- Live |
| Independently, mice that are homozygous for this MnSOD mutation (Sod2tm1Leb) allele exhibit postnatal lethality and exhibit anemia, degeneration of neurons in the basal ganglia and brainstem, progressive motor disturbances, and myocardial injury. Individual LDLR homozygous mutants are predisposed to atherosclerosis. When mutant mice are homozygous for both alleles, they die in utero. Mice heterozygous for the Sod2 mutation and homozygous for the LDLR are viable and fertile. The mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, and hypercholesterolemia, and oxidative stress. | ||
| 007214 | B6.129X1(FVB)-Nr1h4tm1Gonz/J | Repository- Live |
| Mice that are homozygous for the targeted Nr1h4 allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Nr1h4 protein product is detected in liver tissue although an aberrant transcript appears to be generated. Homozygous mice display a proatherogenic serum lipoprotein profile characterized by elevated levels of serum and hepatic cholesterol and triglycerides. Serum bile acids are also elevated. When fed a diet supplemented with 1% cholic acid, severe wasting, hypothermia and increased mortality is observed. Wildtype mice fed a similar diet display no ill effects. Levels of fecal bile excretion are reduced in homozygotes. This mutant mouse strain represents a model that may be useful in studies related to bile acid and lipid homeostasis. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an ..... | ||
| 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 | ||
| 014648 | B6.Cg-Gt(ROSA)26Sortm37(H1/tetO-RNAi:Taz)Arte/ZkhuJ | Repository- Live |
| These mutant mice have a tetracycline inducible Taz specific short hair pin RNA (shRNA) driven by the endogenous mouse Gt(ROSA)26Sor promoter.
Expression of the shRNA is controlled by the transcription of the H1 RNA polymerase III promoter, which is coupled to a tet-operator (tetO) sequence. Expression of the shRNA is blocked by codon-optimized version of the tet repressor itetR, which is part of the allelic construct found in this mouse. Doxycycline (dox--a tetracycline analog) treatment decreases the affinity of the itetR for the tetO sequence, allowing transcription of the shRNA.
Dox-induced Taz gene silencing is detected in heart (to ~3.7% of wildtype), skeletal muscle (to ~11.2%), liver (to ~8.9%) and brain (to ~3.4%) by RT-PCR analysis. Gene product (mRNA) in transgenic mice without dox induction is reduced by 35% of wildtype control levels. Withdrawal of dox at 4 weeks partially reverses the reduction of Taz expression. Protein product ..... For more information please see the full phenotype on the strain data sheet | ||
| 014635 | B6;129S-Nr1h2tm1Djm/J | Repository- Live |
| In this strain, maintained on a mixed C57BL/6 x 129S6 background, a neomycin (neo) resistance cassette replaces exons 5-6 of the nuclear receptor subfamily 1, group H, member 2 (Nr1h2) gene, abolishing gene function. Homozygous are viable, fertile, and normal in size. Also known as liver X receptor beta (Lxrβ), Nr1h2 binds to retinoid X receptors (RXRα, RXRβ, RXRγ; NR2B1, NR2B2, and NR2B3) and is activated by oxysterols to regulate the expression of genes involved in cholesterol metabolism. Homozygous Lxrβ-/- mice lose their ability to appropriately regulate cholesterol, lipid, and carbohydrate metabolism, and have defects in immune function. These defects are more severe when combined with the knockout of Lxrα (available as Stock No. 013763). These mice may be useful for studying lipid and cholesterol metabolism, and the regulation of the immune r ..... For more information please see the full phenotype on the strain data sheet | ||
| 003379 | B6;129S2-Scarb1tm1Kri/J | Repository- Live |
| The class B, type I scavenger receptor (Srb1 or Scarb1) is a cell surface HDL receptor that can recognize the apolipoproteins on the surface of the HDL particle. It plays a key role in determining the levels of plasma lipoprotein cholesterol (primarily HDL) and the accumulation of cholesterol stores in the adrenal gland.In this strain plasma cholesterol (primarily HDL) concentrations increase by 31% in heterozygotes and 125% in homozygotes, as compared to wild type controls. Also, cholesterol levels in adrenal tissue in heterozygous and homozygous mutants decrease by 42% and 72% respectively, relative to wild type controls. The plasma concentration of Apoa-I, the major protein in HDL, is unchanged in mutant animals, relative to wild type controls.Homozygous females are infertile; homozygous males are fertile. Please note that the donating investigator reports that the number of homozygotes resulting from a cross between heterozygotes is significantly lower than what the expected Mendel ..... 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. | ||
| 013763 | B6;129S6-Nr1h3tm1Djm/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 | ||
| 005993 | B6;129S6-Pcsk9tm1Jdh/J | Repository- Live |
| Homozygous mice are viable and fertile with no behavioral abnormalities. No expression of the endogenous RNA or protein is observed in liver. Homozygotes have reduced plasma cholesterol levels; apolipoprotein B (apoB)-containing low-density liproprotein (LDL) is nearly undetectable and apolipoprotein E (apoE)-containing high density liproprotein (HDL) levels are reduced 30%. Homozygotes show increased hepatic LDL-receptor (LDLR) protein (but not RNA) expression. Homogygous mice also have accelerated clearance of circulating cholesterol. Lovastatin addition to the diet of homozygous mice results in further increased hepatic LDLR and LDL clearance from the blood. Heterozygous mice have intermediate plasma cholesterol and LDL clearance. This mouse may be useful in studies of lipid homeostasis, cholesterol metabolism, apolipoprotein function, and statin treatment for hypercholesterolemia. | ||
| 002077 | B6;129S7-Ldlrtm1Her/J | Repository- Live |
| Mice homozygous for the Ldlrtm1Her mutation have an elevated serum cholesterol level of 200-400 mg/dl and they have very high levels (>2,000 mg/dl) when fed a high fat diet. Normal serum cholesterol in the mouse is 80-100 mg/dl. | ||
| 012604 | B6;129S7-Lrp1tm2Her/J | Repository- Live |
| These LRPflox/flox mutant mice possess a floxed Neo cassette and a single loxP sites downstream of exon 2 of the targeted low-density lipoprotein (LDL) receptor-related protein (LRP) 1 gene, Lrp1. 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, the resulting offspring will have exons 1 and 2 deleted in the cre-expressing tissue, resulting in inactivation of Lrp1 gene function. This strain may be useful for studying physiological role of LRP in the uptake of cholesterol-rich lipoproteins from circulation and in maintenance of plasma lipid homeostasis. | ||
| 005956 | B6;D1Lac-Scd1ab-2J/J | Repository- Live |
| The overall appearance of mice homozygous for either the Scd1ab-J allele or the Scd1ab-2J allele (Stock No. 002304 or 005956) includes slightly hunched posture, dry, scaly skin, thin fur sometimes detectable by 7 days of age, and small eyes with encrusted eyelids stuck shut. They have hypoplasia of the sebaceous glands and other hair follicle abnormalities that result in scarring alopecia. These mice have a paucity of adipose tissue, thin subcutis, and a distinctive odor. Hepatic cholesterol ester and triglyceride synthesis has been shown to be deficient in Scd1ab-J homozygotes and could not be restored through diet. Early studies of skin lipids in the original asebia mutant (Scd1ab) revealed a deficiency in wax esters, wax diesters, and sterols esterified with very long-chain fatty acids along with an in ..... For more information please see the full phenotype on the strain data sheet | ||
| 010803 | B6;FVB-Tg(Adipoq-cre)1Evdr/J | Repository- Live |
| Mice hemizygous for this Adipoq-Cre BAC transgene are viable and fertile, with expression of a Cre recombinase directed to adipose tissue by the promoter/regulatory regions of the mouse adiponectin (Adipoq) locus on the BAC transgene. Transcription/translation from the BAC Adipoq locus is disabled, and Cre recombinase expression levels are similar to that of endogenous Adipoq expression. These mice express Cre recombinase effectively in white adipose tissue (WAT) and brown adipose tissue (BAT), but not in macrophages (including adipose-tissue resident macrophages, alveolar macrophages, or thioglycollate-stimulated peritoneal macrophages). The donating investigator reports highly efficient Cre recombinase activity, with no ectopic expression. The phenotype of homozygous mice was not determined by the donating investigator. These Adipoq-Cre BAC transgenic mice may be useful in generating conditional mutations for studying adipose tissue function and storage, obesity, ..... For more information please see the full phenotype on the strain data sheet | ||
| 008850 | B6;SJL-Tg(Mt1-LDLR)93-4Reh/AgnJ | Repository- Live |
| Mice hemizygous for this MMT-I-hLDLR transgene (hLDLRTg mice) are viable and fertile, with human low density lipoprotein receptor (hLDLR) expression controlled by the mouse metallothionein 1 gene (Mt1) promoter sequences. The donating investigator reports that homozygous mice are not viable. Expression of hLDLR mRNA is highest in liver, moderate in kidney, small intestine, and heart, and lowest in brain and pancreas. Treatment with cadmium sulfate (CdSO4) stimulates transcription from the metallothionein promoter and results in higher levels of hLDLR expression. This overexpression of functional LDLR in transgenic mice results in greatly increased clearance of LDLR ligands (LDL, apoprotein B-100 and apoprotein E) from plasma when compared to wild-type mice. These hLDLRTg mice may be useful for studying the role of apolipoproteins and their receptors, lipid transport and lipoprotein metabolism in a wide variety of disease (including atherosclerosis, Alzheimer's disease, and hepat ..... For more information please see the full phenotype on the strain data sheet | ||
| 008340 | BKS.Cg-Leprdb Nos3tm1Unc/RhrsJ | Repository- Live |
| These double mutant mice harbor both the Leprdb spontaneous mutation and the Nos3 (eNOS) targeted mutation and are congenic on C57BLKS/J genetic background. Mice homozygous for both mutations (called eNOS-/- C57BLKS/J db/db, eNOS-/- db/db, or db/db/eNOS-/- double mutant mice) are viable with development of type II diabetes and diabetic nephropathy. The eNOS-/- C57BLKS/J db/db mice develop type II diabetes with significant obesity and hypertension: while both mutations are associated with insulin resistance, the mutated leptin receptor in db/db mice chiefly accounts for the observed hyperglycemia and defective leptin signaling (leading to persistent hyperphagia and obesity), and the eNOS-deficiency accounts for the moderate systemic hypertension. In addition, eNOS-/- C57BLKS/J db/db mice exhibit rapid onset and progression of pathologic ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 012845 | CBy.129S7(B6)-Ldlrtm1Her/J | Repository- Live |
| In the BALB.LDLR-/- strain, a neomycin (neo) selection cassette is inserted in exon 4 of the low density lipoprotein receptor (Ldlr) gene, abolishing endogenous gene function. Homozygous mice are viable, fertile, appear normal in size, and do not display any gross physical or behavioral abnormalities. On a 4% diet, BALB.LDLR-/- mice have increased cholesterol (~200 mg/dl), increased triglycerides (~170mg/dl), and increased blood glucose (122 mg/dl) as compared with wildtype (WT). When moved onto a 21% fat diet these mice have cholesterol levels of 572 mg/dl, triglyceride levels of 180mg/dl, and blood glucose levels of 141 mg/dl. They exhibit renal injury, tubulointerstitial injury, and an increase in interstitial macrophages, and an increase in blood urea nitrogen when challenged with hyperlipidemia and hyperglycemia. When injected with Streptozotocin these mice also exhibit atherosclerotic lesions, aortic sinus lesions, and aortic fatty streak lesions ..... For more information please see the full phenotype on the strain data sheet | ||
| 007068 | D2.129S7(B6)-Ldlrtm1Her/J | Repository- Live |
| Mice homozygous for the Ldlrtm1Her mutation have an elevated serum cholesterol level of 200-400 mg/dl and they have very high levels (>2,000 mg/dl) when fed a high fat diet. Normal serum cholesterol in the mouse is 80-100 mg/dl. This mutant mouse strain may be useful in studies of lipid and leptin homeostasis, hyperglycemia, hypercholesterolemia, atherosclerosis, and the effects of diet on skin and coat. 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. This is the case for the strain above. 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. | ||
| 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 | ||
| 006873 | STOCK Cebpbtm1Vpo/J | Repository- Live |
| Significant numbers of mice homozygous for this C/EBP-beta mutationon this mixed genetic background die perinatally due to hypoglycemia and a failure to mobilize glycogen. Homozygous males that survive to adulthood are fertile, but females are sterile, and display altered mammary duct formation. Macrophages isolated from homozygous mutant mice have impaired bactericidal activity. Surviving homozygotes exhibit fasting hypoglycemia, with reduced plasma insulin, plasma lipids, and free fatty acids (FFAs), and impaired hepatic glucose production. Further, they have a blunted response to glucagon and adrenaline primarily due to altered levels of hepatic cAMP production and reduced protein kinase A activity. Homozygous mice are resistant to obesity and have increased carbon dioxide production from increased metabolism in the brown adipose tissue and muscle. On a high-fat diet, homozygotes are protected from obesity and fatty liver due to reduced hepatic expression of lipogenic genes. Homozyg ..... For more information please see the full phenotype on the strain data sheet | ||
| 006365 | 129-Cckartm1Kpn Cckbrtm1Kpn/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for both of the targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The donating investigator reports that the double mutants have a combined phenotype.
No CCKBR receptor function was detected in competition binding assay of brain (cerebral plasma) membranes. When compared to wildtype, gastric pH in homozygotes is higher, pH 5.2, after overnight fast. Histological analysis reveals diminished parietal cell, enterochromaffin-like cell and antral comatostatin-producing D cell densities. An increase in the number of gastrin-producing G cells is observed. There is an increased number of H+, K+ -ATPase immunoreactive negative cells and abnormal distribution of parietal cells in oxyntic glands. Circulating gastrin levels are 10-fold higher in homozygotes. No CCKAR receptor function was detected in competition binding assay of pancreatic membranes. Homozygotes do not exhibit decreased ..... For more information please see the full phenotype on the strain data sheet | ||
| 006367 | 129-Cckartm1Kpn/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No receptor function was detected in competition binding assay of pancreatic membranes. Mice homozygous for the targeted mutation do not exhibit decreased food intake due to peritoneal injection of cholecystokinin. Baseline food and water intake and body weight is normal in mutant mice. These mutant mice have larger gallbladder volumes and are more likely to develop spontaneous gallstones than wildtype controls. Gastric function is impaired due to diminished intestinal lipid feedback response. Small-intestine transit time is increased in mutant mice. When fed a lithogenic diet, mutant mice have an increase in biliary cholesterol secretion rates, when compared to the wildtype. Although the total number of olfactory-gonadotropin-releasing hormone-1 neuroendocrine (GnRH-1)neurons is the same in embryonic day 14.5 aged mutant and wildtype ..... For more information please see the full phenotype on the strain data sheet | ||
| 005213 | 129-Slc10a2tm1Pda/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. Male pups tend to be smaller in size than female pups prior to weaning. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of the distal small intestine. Ileal brush border membrane vesicles isolated from homozygotes do not exhibit sodium ion dependent taurocholate uptake, indicating a loss of sodium bile acid cotransporter activity. Total plasma cholesterol levels are slightly higher than normal. Total bile acid pool size is reduced approximately 80% in homozygous mutants, although intestinal lipid absorption is reduced by only about 10%. Bile acid functional turnover rate (daily fecal bile acid excretion/pool size) is elevated 150 fold in male mutants and 75 fold in female mutants. Fecal bile acid excretion is increased 24 fold in male mutants and 11 fold in female mutants. Bile acid composition is ab ..... For more information please see the full phenotype on the strain data sheet | ||
| 008079 | 129S-Ppargtm2Yba/J | Cryopreserved - Ready for recovery |
| These mice express tTA (tetracycline regulated transactivator) and a tetO-driven Flag-tagged Pparg from the endogenous Pparg locus. A fusion transcript (including the 5' portion of Pparg, IRES and tTA (AF1-IRES-tTA)), a Flag-Pparg transcript and a wildtype transcript are detected by Northem blot analysis of white adipose tissue from heterozygotes. The fusion transcript of AF1-IRES-tTA is also detected in brown adipose tissue. Expression of tTA is detected in adipose tissue by Western blot analysis. No Flag-PPARG1 protein was detected in adipose tissue. Weak expression of tTA and the Flag-Pparg transcript is observed in placenta and liver. Endogenous PPARG2 protein is reduced in adipose tissues of heterozygotes. Heterozygotes exhibit "buffalo humps" (swollen interscapular fat pads swollen by hypertrophy and unilocular lipid deposition in mutant brown adipocytes), absence of subcutaneous adipocytes, reduced gonadal white adipose tissue, irregularly residual a ..... For more information please see the full phenotype on the strain data sheet | ||
| 007005 | 129S-Scg5tm1Led/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)). | ||
| 005066 | 129S-Slc27a2tm1Kds/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 PCR or Western blot analysis. Very long-chain acyl-CoA synthetase (VLCS) enzyme activity is reduced 4-fold in liver and 9-fold in kidney. Liver microsomes and peroxisomes fractions exhibit only a residual (30% of wildtype) VLCS activity level. The very long chain fatty acid (VLCFA) beta-oxidation rate in isolated fibroblasts is reduced by approximately 40% of wildtype activity level. This mutant mouse strain may be useful in studies of X-linked adrenoleukodystrophy and/or fatty acid metabolism. | ||
| 007070 | AK.129S7(B6)-Ldlrtm1Her/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Ldlrtm1Her mutation have an elevated serum cholesterol level of 200-400 mg/dl and they have very high levels (>2,000 mg/dl) when fed a high fat diet. Normal serum cholesterol in the mouse is 80-100 mg/dl. This mutant mouse strain may be useful in studies of lipid and leptin homeostasis, hyperglycemia, hypercholesterolemia, atherosclerosis, and the effects of diet on skin and coat. 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. This is the case for the strain above. 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. | ||
| 008884 | B6.129(Cg)-Pnliptm1Dyh/J | Cryopreserved - Ready for recovery |
| These mice harbor a null mutation of the Pnlip (pancreatic lipase [also called pancreatic triglyceride lipase or PTL]) gene. Homozygous (PTL-/-) mice are viable and fertile, with no protein expression from the targeted allele observed in pancreatic tissue extracts. Homozygotes exhibit mildly delayed triglyceride (also called triacylglycerol or TAG) absorption after low fat diet feeding, but significantly delayed TAG absorption on a high fat/high cholesterol diet. Homozygous mice have a significant decrease in the rate/amount of cholesterol absorption; attributed to PTL-deficiency delaying dietary fat absorption to the distal small intestine (ileum) where intestinal cholesterol uptake is less efficient. Because PLT-/- mice retain endogenous Cel (carboxyl ester lipase [also called cholesterol esterase]) expression, pancreatic extracts from PTL-/- mice retain robust TAG hydrolytic activity (albeit at lower levels than wildtype mice). This TAG hydrolytic ..... For more information please see the full phenotype on the strain data sheet | ||
| 008763 | B6.129-Abcg8tm1Elk/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. Female homozygotes are infertile, and male homozygotes exhibit rare infertility, if not maintained on a plant sterol free diet or with drug treatment to block uptake of plant sterols. No gene product (mRNA) is detected by Northern blot and RT-PCR analysis of total hepatic RNA from homozygous animals. Homozygotes have increased plasma and tissue levels of sitosterol and campesterol (plant sterols) with impaired cholesterol secretion in bile. Expression of Abcg5 (ATP-binding cassette, sub-family G (WHITE), member 5) is unchanged in homozygotes. Liver cholesterol levels in homozygotes is decreased by approximately 50%. Serum cholesterol levels are decreased by 52% in homozygotes and 26% in heterozygotes. Heterozygotes exhibit an intermediate phenotype with decreased biliary sterol secretion but do not become sitosterolemic. This ..... For more information please see the full phenotype on the strain data sheet | ||
| 002246 | B6.129-Apoetm1Unc Ldlrtm1Her/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Apoetm1Unc and Ldlrtm1Hertargeted mutations on a normal chow diet show cholesterol levels corresponding to those seen in the Apoetm1Unc targeted mutant strain. The lipoprotein pattern in homozygous mice also resembles that seen in the Apoetm1Unc targeted mutant strain (VLDL & chylomicron remnants). The double targeted mice have a marked increase in both APOB48 and APOB100. In addition, APOAIV is increased. | ||
| 005951 | B6.129-Dgat2tm1Far/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation have a perinatal lethal phenotype, most fail to survive past 6 hours after birth due to dehydration, skin barrier abnormalities, hypothermia and energy deficiencies. Reduced levels of gene product (mRNA) are detected by RT-PCR analysis of brown adipose tissue and livers of neonate homozygous mutants. Growth retardation is observed in homozygous embryos after embryonic day 12.5. Newborn homozygotes are hypoglycemic and lipopenic, exhibiting reduced plasma triglyceride, free fatty acid and glucose levels and have almost no white fat tissue. Within a few hours of birth, the skin of homozygotes becomes dry and cracked. Homozygous mutants rapidly lose weight due to dehydration caused by impaired permeability barrier function. Histological analysis of skin tissue from homozygotes reveals abnormally thin epidermis and compact orthohyperkeratosis of the stratum corneum. Homozygotes surviving between 8 and 24 hours develop tail necrosis. Hetero ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 006607 | B6.129-Pctptm1Bor/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. Protein product from the targeted gene is not detected in the liver cytosol of 8-day-old homozygous pups. The lipid content and composition of bile and lung surfactant secretions are normal in homozygous targeted mice. Plasma cholesterol and phospholipid levels are not affected in chow-fed homozygous targeted mutation mice, but there is an increase in the accumulation of small alpha-migrating high density lipoprotein (HDL) particles. Biliary concentrations of phospholipids, cholesterol, and bile salts are reduced in homozygous mutants as compared to wildtype mice when fed a high fat, high cholesterol, cholate-containing lithogenic diet. There is a greater hepatic accumulation of phospholipid and cholesterol in the targeted mutant animals. On the high fat diet, HDL particles are of normal size, but plasma cholesterol and phospholipid concentrations are inc ..... 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. | ||
| 006201 | B6.129-Scd1tm1Ntam/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable and fertile. Transcripts from the targeted gene are absent in homozygous liver, eyelid, skin, and white adipose tissues. In addition, the endogenous protein and enzyme activity are absent from homozygous liver tissue. Homozygous mice exhibit cutaneous abnormalities and narrow eye fissure with atrophic sebaceous and meibomian glands. Mutant mice also have reduced body adiposity, increased insulin sensitivity, increased basal and insulin-mediated glucose uptake, and are resistant to diet-induced weight gain. Homozygotes have altered hepatic glycerophospholipid profiles. Homozygous mice are not recommended for breeding as skin lesion severity may prohibit colony success. These mutant mice may be useful in studies of monounsaturated fatty acid synthesis, cholesterol homeostasis, skin disease, obesity, and diabetes. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background differ ..... | ||
| 006879 | B6.129-Scd2tm1Myz/J | Cryopreserved - Ready for recovery |
| While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die within 24 hours of birth. Brain tissues from homozygous mice show no expression from the targeted gene. Homozygotes exhibit neonatal lethality with 100% penetrance on this genetic background (less penetrant on 129SvEv genetic background) likely due to severe skin permeability barrier abnormalities. Null mice also have abnormal epidermal morphology and abnormal lipid homeostasis in the skin and liver. These mutant mice may be useful in studying monounsaturated fatty acid synthesis, lipid biosynthesis and metabolism, cholesterol homeostasis, and skin disease, as well as obesity and diabetes. | ||
| 007453 | B6.129P2(Cg)-Dhcr7tm1Gst/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Dhcr7Ex8 allele lack the exon 8 coding sequence and flanking splice acceptor site of the targeted gene, resulting in the truncated DHCR7 mutation most frequently observed in Smith-Lemli-Opitz/RSH Syndrome (SLOS) patients (IVS8-1G > C). Although a truncated product is transcribed from the targeted gene, no mRNA containing the deleted 3'-coding region is detected in homozygous liver or brain tissue. Homozygous mice exhibit the same biochemical defects as observed with SLOS patients, including markedly reduced tissue cholesterol and total sterol levels, and 30- to 40-fold elevated concentrations of 7-dehydrocholesterol. Newborn homozygotes have difficulty breathing, do not suckle, and die soon after birth with immature lungs, enlarged bladder, and, frequently, cleft palate. These Dhcr7Ex8 mutant mice may be useful in studying Smith-Lemli-Opitz/RSH Syndrome (SLOS; a birth-defect mental-retardation syndrome) or other metabolic disorders invol ..... For more information please see the full phenotype on the strain data sheet | ||
| 008235 | B6.129P2-Abcg5tm1Plo/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this adenosine triphosphate-binding cassette (ABC) half-transporter G5 mutant allele (Abcg5-/-) are viable and severely subfertile; the donating investigator reports that males have significantly reduced fertility and females are almost non-fertile. No gene product (mRNA) from the mutant allele is detected in homozygous liver extracts. The expression of beta-galactosidase (lacZ) from the targeted gene is not characterized to date (July 2008). Abcg5-deficient mice exhibit sitosterolemia (high plasma plant sterol concentrations) and macrothrombocytopenia (enlarged platelets caused by defective megakaryocyte development) associated with a near 70% reduction in total number of platelets. Specifically, when allowed ad libitum access to PicoLab Rodent Diet 5053 chow, homozygous mice exhibit strongly elevated plasma levels of β-sitosterol (37-fold) and campesterol (7.7-fold); with further increased levels upon addition of the synthetic ..... For more information please see the full phenotype on the strain data sheet | ||
| 006620 | B6.129P2-Scp2tm1Usee/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. No protein product from the targeted gene is detected in liver tissue. Northern blot experiments show a low-intensity signal from a non-functional truncated transcript, however. Histologically, greater numbers of peroxisomes are observed in the livers of these mice. Liver function appears normal based on liver enzyme levels, but cholesterol and triglyceride storage pools are depleted. Hepatic gene expression is altered. Higher expression levels of liver fatty acid binding protein and multiple peroxisomal beta-oxidation enzymes are observed. Whereas plasma insulin and cholesterol concentrations are normal, triglycerides are slightly higher and free fatty acid and glucose concentrations are moderately lower in homozygous mice. Food intake is significantly higher in homozygotes as compared to control animals. A prononounced accumulation of phytanic acid is o ..... For more information please see the full phenotype on the strain data sheet | ||
| 005429 | B6.129S-Gpamtm1Rcol/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, and do not display any gross behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis. Enzyme activity levels in liver tissue are negligible. Residual activity is due to the inactivated microsomal isoform. Homozygotes exhibit reduced body weight. Female homozygotes weigh 20% less than wildtype controls at age 10 months. Male homozygotes do not exhibit as significant a weight reduction. Gonadal fat pad mass is reduced. Liver triacylglycerol and plasma lipid levels are reduced by 37% and 15% respectively. Very low density lipoprotein (VLDL) triacylglycerol level and secretion are decreased. Hepatic triacylglycerol fatty acid and phospholipid fatty acid compositions are abnormal with diminished palmitate content. F2 mice on a 50% C57BL/6J and 50% 129SvEv genetic background were used in all of the experiments described in the primary reference. This mutant mouse strain may be useful in stu ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 005517 | B6.129S4-Cyb5r4tm1Hfb/HfbJ | Cryopreserved - Ready for recovery |
| Mice heterozygous for the targeted mutation are viable and fertile, glucose tolerant, have normal blood sugar levels, serum lipid profiles and white adipose tissue mass. No protein from the targeted gene was detected by Western Blot analysis of mice homozygous for the allele. Homozygous mice consume more food, have decreased adipose tissue mass and are hyperlipidemic compared to wildtype controls post-weaning. At 4 weeks of age glucose levels are normal but insulin levels are 40% of wildtype controls. At 7 weeks of age clinical diabetes is present in both male and female of homozygous mice. Histological evaluation of pancreas from 21 week old homozygote animals revealed a significant reduction in the number of islets and decreased cytoplasmic to nuclear ratio in the islet cells and there was no insulitis nor phagocytosis of necrotic beta cell fragments. While there is a progressive loss of beta cells in aging homozygous mice, there is no loss of alpha, delta or PP cells. Electron m ..... | ||
| 003824 | B6.129S4-Dgat1tm1Far/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Dgat1tm1Far targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities however, homozygous mutant females exhibit a complete absence of milk production, necessitating the use of foster mothers. Dgat1 mRNA is undetectable by Northern blot analysis, and DGAT enzyme activity in a variety of tissues is either absent or shows only residual levels. Surprisingly, in DGAT deficient mice triglyceride levels and fasting serum triglycerides levels are similar to wildtype controls. Although homozygotes do not differ in body weight compared to age- and sex-matched controls, total fat pad weight is reduced. Tissue triglyceride levels are reduced 30-40% in white adipose tissue and muscle. Liver triglyceride levels tend to be lower in chow-fed DGAT-deficient mice, but high-fat feeding leads to significantly lower liver triglycerides. Changes in tissue triglyceride levels are associated with in ..... For more information please see the full phenotype on the strain data sheet | ||
| 006503 | B6.129S4-Lpltm1Ijg/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exon 1 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 used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. These mice may be useful for cardiovascular studies (such as lipid metabolism and fat storage) and obesity research.
For example, when crossed to a strain expressing Cre recombinase in cardiac muscle cells (see Stock No. 011038), this mutant mouse strain may be useful in studies of cardiac lipid metabolism. | ||
| 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. | ||
| 004185 | B6.129S4-Soat2tm1Far/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for this targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Southern blot analysis and RT-PCR indicated the targeted gene was disrupted. These mice lack cholesterol ester synthesis in liver and intestine and are resistant to diet-induced hypercholesterolemia and cholesterol gallstone formation. In homozygous mice fed regular diet, acyl CoA: cholesterol acyltransferase (ACAT) enzyme activity was reduced by 92% in intestine, and by 99% in liver. Homozygous mice fed high-fat/high cholesterol diet had low ACAT activity. Although ACAT2 deficient mice absorb less cholesterol than wild-type mice when fed a high fat/ high cholesterol diet, histological examination indicated enterocytes in the mutant mice were normal. This mutant mouse strain represents a model that may be useful in studies related to human resistance to diet-induced hypercholesterolemia and cholesterol gallstone formation. | ||
| 003823 | B6.129S4-Ttpatm1Far/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Ttpa gene are viable, normal in size and do not display any gross physical abnormalities. The Ttpa protein product is required for the maintenance of proper alpha-tocopherol levels, the major form of vitamin E in plasma and tissues. The absence of Ttpa protein product in homozygous-null animals results in a corresponding 95% reduction in alpha-tocopherol. Low levels of alpha-tocopherol render female mice infertile, a condition that can be addressed with vitamin E supplements. Male fertility is unimpaired. These mice provide a viable model for studying vitamin E deficiency. | ||
| 005934 | B6.129S4-Ucp2tm1Lowl/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable and fertile and do not express full length mRNA in heart, kidney, spleen, white adipose tissue, and pancreatic islets. In splenic mitochondria, endogenous protein was undetectable. When grown under high glucose conditions, cultured pancreatic islet cells from homozygous mice have increased insulin secretion and ATP levels compared to wildtype. Homozygous mice have 18% lower blood glucose levels. Whether fasting or fed, homozygotes have approximately 3-fold greater serum insulin due to increased insulin secretion. Similarly, glucose-stimulated insulin secretion is significantly increased. High fat diet-fed mice or palmitate-treated islets maintain pancreatic glucose responsiveness in vivo and in vitro compared to wildtype. Mitochondria isolated from the dopaminergic mesencephalic nigral cells of homozygous mice have increased reactive oxygen species but lesser mitochondria number and increased sensitivity to MPTP, mimicking Parkinson's disease. <> ..... For more information please see the full phenotype on the strain data sheet | ||
| 009082 | B6.129S6-Ostatm1Pda/J | Cryopreserved - Ready for recovery |
| Homozygous (Osta-/-) mice are viable and fertile, with no mRNA or protein expression from the targeted allele. Homozygotes exhibit a small growth deficit that is ameliorated after weaning, partial impairment of intestinal bile acid absorption (impaired basolateral transport of bile acids out of the ileal epithelial cell), altered regulation of bile acid synthesis, a significantly reduced bile acid pool, intestinal lengthening and intestinal hypertrophy. Homozygous mice also have reduced hepatic Cyp7a1 expression that is inversely correlated with ileal expression of fibroblast growth factor 15 (FGF15). These mutant mice may be useful in studying cholesterol metabolism, intestinal drug absorption, intestinal bile acid absorption, bile acid synthesis, and cholesterol and bile acid homeostasis.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which ..... | ||
| 007682 | B6.129X1-Apobtm1.1Zc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this apoB38.9 allele (apoB38.9/38.9) are viable with impaired fertility, bearing a premature stop codon at residue 1767 of the targeted gene. As a result, homozygous plasma shows a truncated apoB38.9 as the sole apoB protein. Plasma from heterozygous (apoB+/38.9) mice have reduced apoB100 and apoB48 compared to wildtype, with apoB38.9 representing 20% of total circulating apoB. This apoB38.9 truncation affects both apoB100 and apoB48 metabolism in mice, and mimics human Familial Hypobetalipoproteinemia (FHBL). Homozygous and, to a lesser extent, heterozygous mice exhibit symptoms of FHBL due to impaired lipoprotein export system/VLDL secretion, including elevated hepatic triglyceride (TG), cholesterol and free fatty acids (FFA), with decreased plasma TG and cholesterol. Because plasma and liver lipid profiles range from mild to severe in populations of heterozygous apoB38.9 mice on a mixed (C57BL/6J;129X1/SvJ) genetic background, apoB+/38 ..... 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. | ||
| 009662 | B6.129X1-Ppargc1atm1Dpk/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable and fertile. During the generation of this allele, a 3' homologous recombination and insertion occurred with a duplication of exon 3 between exons 5 and 6. The exon 3 insertion, which was confirmed by RT-PCR, results in a mutant transcript that encodes a truncated protein due to a stop codon at amino acid 255. Normal gene product (mRNA) containing an exon 5?6 border is not detected. If the truncated protein gene product is stable, it could theoretically have some activity, given that it would contain nuclear receptor-interacting domains and the amino-terminal activation domain. Total body weights for homozygotes are reduced 15-20% for the first week after birth, but become normal by 3 weeks of age. By 18 weeks of age, homozygotes have heavier body weights and increased percent body fat than wildtype controls. Heart and slow twitch skeletal muscle (gastrocnemius, soleus) weights are lower in homozygotes than controls. Electr ..... For more information please see the full phenotype on the strain data sheet | ||
| 006580 | B6.Cg-Ins2Akita Ldlrtm1Her/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Akita spontaneous mutation die postnatally, typically by 12 weeks of age. Independently, heterozygous Akita mutant mice are a model of insulin dependent diabetes mellitus (IDDM) with severe hyperglycemia (see the datasheet for Stock No. 003548 for additional information). LDLR-null homozygotes have elevated serum cholesterol levels (200-400 mg/dl) which can escalate to very high levels (> 2000 mg/dl) when the mice are fed a high fat diet. LDLR-deficient mice also are predisposed to develop atherosclerosis. These double mutant mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, hypercholesterolemia, and diabetes-related macrovascular complications. | ||
| 006877 | B6.Cg-Ldlrtm1Her Tg(H2-K-AKR1B1)1Tj/J | Cryopreserved - Ready for recovery |
| Independently, mice hemizygous for this "huAR" transgene express human aldose reductase as a model for increased oxidative stress, while LDLR homozygotes are predisposed to atherosclerosis and hypercholesterolemia. The donating investigators report that the H2-Kd promoter functions on this H2-Kb genetic background without any loss of transgene expression. When mutant mice are hemizygous for the transgene and homozygous for the targeted allele, they may be useful in studies of diabetes, metabolism, atherosclerosis, hypercholesterolemia, and oxidative stress. | ||
| 006906 | B6.Cg-Lepob Ldlrtm1Her/J | Cryopreserved - Ready for recovery |
| Independently, the C57BL/6-Lepob homozygotes (Stock No. 000632) model the increasingly prevalent metabolic disorder seen in humans (hyperglycemia, hyperinsulinemia, and hyperlipidemia), while LDLR-deficient mice (Stock No. 002207) are predisposed to atherosclerosis. When mutant mice are homozygous for both mutant alleles, they exhibit exacerbated hyperlipidemia and extensive atherosclerotic lesions in the aorta. The mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, and hypercholesterolemia. | ||
| 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. | ||
| 012389 | B6.Cg-Tg(Myh6-Ppara)404-3Dpk/J | Cryopreserved - Ready for recovery |
| The mouse Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha) cardiac muscle-specific promoter drives expression of FLAG-tagged Ppara (peroxisome proliferator activated receptor alpha) in this transgenic strain. Expression of Ppara is increased approximately 135-fold as compared to wildtype in this line (404-3). Hearts of hemizygotes depend on fatty acid for the generation of energy to a significantly greater extent than do hearts of non-transgenic mice and have a substrate utilization profile similar to that of the diabetic heart. Cardiac dysfunction is exhibited by 2 months of age with no imposed stress. This strain may be useful in studies of metabolic alterations associated with diabetic cardiomyopathy. | ||
| 012382 | B6.Cg-Tg(Myh6-Ppara)404-4Dpk/J | Cryopreserved - Ready for recovery |
| The mouse Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha) cardiac muscle-specific promoter drives expression of FLAG-tagged Ppara (peroxisome proliferator activated receptor alpha) in this transgenic strain. Expression of Ppara is increased approximately 15-fold as compared to wildtype in this line (404-4). Hearts of hemizygotes depend on fatty acid for the generation of energy to a significantly greater extent than do hearts of non-transgenic mice and have a substrate utilization profile similar to that of the diabetic heart. Cardiac dysfunction is exhibited by 4-5 months of age with no imposed stress, or after being placed on a high fat diet. This strain may be useful in studies of metabolic alterations associated with diabetic cardiomyopathy and other forms of lipotoxic cardiomyopathy. | ||
| 002245 | B6;129-Apoetm1Unc Ldlrtm1Her/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Apoetm1Unc and Ldlrtm1Hertargeted mutations on a normal chow diet show cholesterol levels corresponding to those seen in the Apoetm1Unc targeted mutant strain. The lipoprotein pattern in homozygous mice also resembles that seen in the Apoetm1Unc targeted mutant strain (VLDL & chylomicron remnants). The double targeted mice have a marked increase in both APOB48 and APOB100. In addition, APOAIV is increased. | ||
| 004162 | B6;129-Scaptm1Mbjg/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for this targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. They posses a loxP-flanked neomycin resistance cassette located 3 kb upstream of exon 1. A third loxP site is located in intron 1. When used in conjunction with a Cre recombinase-expressing strain, this strain is appropriate for generating tissue-specific knockout mutants of Scap. This mutant mouse strain represents a model that may be useful in studies related to cholesterol and fatty acid homeostasis. | ||
| 004362 | B6;129-Scarb1tm1Kri Apoetm1Unc/J | Cryopreserved - Ready for recovery |
| At birth, mice homozygous for both targeted alleles are viable, normal in size and do not display any gross physical or behavioral abnormalities. All double mutants die between 5 to 8 weeks following birth, exhibiting hypercholesterolemia and significantly lower body weights compared to control mice. Mice display an altered appearance several days before death, displaying ruffled fur, an abnormal gate and sometimes labored breathing. Hearts from double mutants are enlarged, exhibit evidence of myocardial infarction and are functionally impaired. Histological examination reveals extensive coronary artery disease characterized by atherosclerotic plaques with evidence of cholesterol clefts and fibrin deposition. As with other Scarb1 homozygous null mutants, females are infertile while the fertility of homozygous males remains intact. This double mutant mouse strain offers a model that may be a useful tool in studies related to coronary heart disease. | ||
| 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 | ||
| 003000 | B6;129S-Ldlrtm1Her Apobtm2Sgy/J | Cryopreserved - Ready for recovery |
| This strain expresses only APO-B100 (normally expressed in the liver and yolk sac) and is deficient in low density lipoprotein receptor (Ldlrtm1Her/Ldlrtm1Her). | ||
| 002465 | B6;129S-Lrpap1tm1Her Ldlrtm1Her/J | Cryopreserved - Ready for recovery |
| Mice homozygous for both the Ldlrtm1Her and Lrpap1tm1Her targeted mutations are viable and fertile. They have a functional deficiency of the low density lipoprotein receptor-related protein (LRP) and low density lipoprotein receptor (LDLR). LRP is reduced in both the liver and the brain of homozygotes. They also show impaired hepatic clearance of alpha2-macroglobulin and plasma accumulation of remnant lipoproteins. | ||
| 003902 | B6;129S-Mttptm2Sgy/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites located 2.5 kb 5' of exon 1 and flanking a neomycin resistance gene inserted into intron 1 of the Mttp gene. Mice that are homozygous for this floxed Mttp allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to a strain expressing interferon inducible Cre recombinase in liver tissue (see Stock No. 003556 for example), this mutant mouse strain may be useful in lipoprotein research. | ||
| 006258 | B6;129S4-Apoa2tm1Bres/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile. Homozygous mice have no detectable transcripts in liver tissues and the high density lipoprotein (HDL) particle size is reduced. Homozygotes have decreased plasma levels of HDL cholesterol and free fatty acids in both fed and fasted states. In addition, the plasma concentration of fasting glucose and insulin is decreased. These mice may be useful in studies of lipid metabolism, atherosclerosis, heart disease, insulin resistance and diabetes. | ||
| 006404 | B6;129S4-Apoa4tm1Bres/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile with no protein detectable in plasma, liver, or intestinal tissues. Homozygotes have decreased plasma levels of cholesterol, free fatty acids, and high density (HDL) and very low density lipoprotein (VLDL). These mice may be useful in studies of lipid metabolism, atherosclerosis, heart disease, appetite regulation, intestinal lipid absorption, or inflammatory bowel disease. | ||
| 004670 | B6;129S6-Abcg5/Abcg8tm1Hobb/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for this targeted allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected in liver or jejunum. A 2 to 3 fold increase in fractional absorption of dietary plant sterols results in plasma sitosterol levels that are elevated 30 fold compared to wildtype levels. Biliary cholesterol levels are low, as are plasma and liver cholesterol levels. Plasma and liver cholesterol levels increase rapidly (2.4 and 18 fold, respectively) following cholesterol feeding. This mutant mouse strain represents a model that may be useful in studies related to sitosterolemia and cholesterol homeostasis. | ||
| 005939 | B6;129S6-Insig1tm1Mbjg Insig2tm1Mbjg/J | Cryopreserved - Ready for recovery |
| Mice homozygous for both targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This double mutant has normal expression of Insig1 and no Insig2 gene expression or protein in liver. As the Insig1 mutant locus contains a loxP, frt-flanked exon 1, Cre-mediated deletion of exon 1 (encoding amino acids 1-113) terminates gene function. The resulting double homozygous "knockout" mice die in utero some time after embryonic day 18.5. These mice may be useful in studies of cholesterol synthesis and feedback suppression, sterol regulatory element-binding protein (SREBP) processing pathways, liver metabolism and storage functions, and may have use in insulin-related topics such as diabetes and endocrine/exocrine function. | ||
| 006208 | B6;129S6-Pdzk1tm1Dls/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile. Liver tissue from homozygous mutant mice lacks endogenous protein expression. Homozygotes, but not heterozygotes, have significantly decreased (~85-95%) hepatic high density lipoprotein (HDL) receptor scavenger receptor B-I (SR-BI) levels. This decrease is further exacerbated following diet supplementation with the PPAR-alpha activator fenofibrate. These mice may be useful in studies of cardiovascular health and atherosclerosis, lipid metabolism, SR-B1 regulation, kidney function, as well as kidney transporter (e.g. urate transporter) regulation and liver organic anion transport. | ||
| 004365 | B6;129S6-Srebf1tm1Mbr/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. The targeted mutation results in a total ablation of the SREBP-1c transcript and only a slight redution in levels of the alternate SREBP-1a transcript. There is a 50% increase in level of SREBP-2 transcript and increases in transcripts of enzymes utilized in cholesterol biosynthesis. Liver cholesterol content is increased while plasma cholesterol and plasma triglycerides levels are reduced. There is a reduction of expression of all genes required for fatty acid and triglyceride synthesis. Administration of liver X receptor (LXR) agonist did not result in increased levels of SREBP-1a transcript or in liver triglycerides. This mutant mouse strain represents a model that may be useful in studies of transcriptional control of fatty acid and triglyceride biosynthesis. | ||
| 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. | ||
| 008408 | B6;D2-Tg(APOE-NPC1L1)20Lqyu/J | Cryopreserved - Ready for recovery |
| These transgenic mice express the human NPC1 (Niemann-Pick disease, type C1, gene)-like 1 (NPC1L1) gene under the control of the human apolipoprotein E (APOE) promoter and hepatic control region. Transgene expression is detected in liver by Western blot analysis and is localized to the canalicular membrane. Transgenic mice exhibit decreased biliary cholesterol levels, which is associated with increased plasma cholesterol levels (mostly apoE-rich HDL particles). Biliary phospholipid and bile acid levels are not affected. Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make this strain homozygous. This mutant mouse strain may be useful in studies of lipid metabolism and cholesterol transport. | ||
| 003393 | B6;SJL-Tg(aP2-SREBF1c)9884Reh/J | Cryopreserved - Ready for recovery |
| This transgenic mouse strain overexpresses human nuclear sterol regulatory element binding protein-1c in adipose tissue under the control of the adipocyte-specific aP2 promoter. The phenotype of transgenic mice resembles congenital generalized lipodystrophy (CGL), a rare autosomal recessive disorder in humans. CGL is characterized by an insufficiency of adipose tissue which is evident at birth and is accompanied by a severe insulin resistance leading to symptoms of type II diabetes mellitis, (hyperinsulinemia and hyperglycemia), and an enlarged fatty liver. Transgenic mice exhibit these symptoms showing defects in differentiation of white fat accompanied by an hypertrophy of brown fat that resembles immature white fat. | ||
| 012383 | B6CBA-Tg(Myh6-Ppard)HEDpk/J | Cryopreserved - Ready for recovery |
| The mouse Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha) promoter drives expression of Ppard (peroxisome proliferator activator receptor delta) in these transgenic mice. Hemizygotes have increased myocardial glucose utilization, do not accumulate myocardial lipid, and have normal cardiac function. Expression levels in this "high expression" (HE) line are increased approximately 100-fold over endogenous levels. This strain may be useful in studies of cardiac function and metabolic modulation during diabetes and ischemia. | ||
| 013042 | B6N;129S-Acacbtm1.1Lowl/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Acc2flox allele are viable, fertile, normal in size, and have no reported physical abnormalities. The Acc2flox allele has loxP sites flanking the biotin-binding motif exon (and the preceding exon) of the targeted locus. When bred to mice that express Cre recombinase, the resulting offspring will have the floxed sequences deleted in the cre-expressing cells/tissues. The exon immediately upstream of the biotin-binding catalytic domain was included so that splicing of the remaining exons following Cre-mediated deletion would introduce a frameshift and nonsense mutation after Asp865 in any translated protein. These mutant mice may be useful to generate conditional mutations for studying malonyl-CoA (the substrate for fatty acid synthesis and the regulator of fatty acid oxidation) synthesis and other metabolic cellular signaling molecules, as well as diet-induced obesity, glucose intolerance and insulin resistance.
NOTE: W ..... | ||
| 002840 | B6SJL-Tg(SREBP1a)7343Reh/J | Cryopreserved - Ready for recovery |
| 005516 | C.129S4-Cyb5r4tm1Hfb/HfbJ | Cryopreserved - Ready for recovery |
| Mice heterozygous for the targeted mutation are viable and fertile, glucose tolerant, have normal blood sugar levels, serum lipid profiles and white adipose tissue mass. No protein from the targeted gene was detected by Western Blot analysis of mice homozygous for the allele. Homozygous mice consume more food, have decreased adipose tissue mass and are hyperlipidemic compared to wildtype controls post-weaning. At 4 weeks of age glucose levels are normal but insulin levels are 40% of wildtype controls. At 7 weeks of age clinical diabetes is present in both male and female of homozygous mice. Histological evaluation of pancreas from 21 week old homozygote animals revealed a significant reduction in the number of islets and decreased cytoplasmic to nuclear ratio in the islet cells and there was no insulitis nor phagocytosis of necrotic beta cell fragments. While there is a progressive loss of beta cells in aging homozygous mice, there is no loss of alpha, delta or PP cells. Electron m ..... | ||
| 003401 | C3H/HeJ-Lpin1fld-2J/J | Cryopreserved - Ready for recovery |
| Homozygous fatty liver dystrophy (fld) mice have an enlarged, fatty liver and hypertriglyceridemia which resolve to normal during the weaning transition. However, decreased overall size, decreased lipid in the fat pads, and a peripheral neuropathy persist throughout the lifespan. This peripheral neuropathy manifests as a tremor and an unsteady gait shortly after 10 days of age and worsens with age. The fld neuropathy is specific to the peripheral nervous system. Electron microscopy of sciatic nerves revealed thin, poorly compacted myelin sheaths, hypertrophic Schwann cells, myelin debris, degenerating axons, bands of Bugner, and regenerative clusters, but no evidence of inflammation (Langner et al, 1991). Western blot analysis of sciatic nerve from two-to-three month old fld/fld mice showed a 7-13-fold reduction in myelin P0, a vast increase in apoE, an increase in GAP-43, and no detectable myelin P2. It was also noted that a ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 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. | ||
| 003285 | C57BL/6-Tg(LIPC)6784His/J | Cryopreserved - Ready for recovery |
| These transgenic mice overproduce a range of human hepatic lipase activities (4-23 fold increase) and help to understand the role of hepatic lipase in lipoprotein metabolism. A 5-fold increase in heparin releasable hepatic lipase activity is accompanied by moderate decreases in plasma total and high density lipoprotein (HDL) cholesterol and phospholipid (PL) but no significant change in triglyceride (TG), whereas a 23-fold increase in hepatic lipase activity causes a more significant decrease in plasma total and HDL cholesterol, PL and TG, and a substantial decrease in lipoprotein lipids amongst IDL, LDL and HDL fractions. High levels of hepatic lipase activity diminish the plasma concentration of apoA-I, A-II and apoE. Increased hepatic lipase activity is associated with a progressive decrease in the levels and an increase in the density of LpAI and LpB48 particles. There is an increased rate of disappearance of 125I-labeled human HDL from the plasma of the transgenic mice and substan ..... For more information please see the full phenotype on the strain data sheet | ||
| 005863 | C57BL/6J-Tg(ACTB-DDAH1)1Jpck/J | Cryopreserved - Ready for recovery |
| Hemizygous mice are viable and fertile with no anatomic abnormalities. Transgene expression is observed in aorta, heart, and brain. Transgenic dimethylarginine dimethylaminohydrolase (DDAH) activity is reflected in a reduction of plasma asymmetric dimethylarginine (ADMA). Nitric oxide synthase (NOS) activity is significantly increased in transgenic skeletal and cardiac muscle. Transgenic mice have lower blood pressure and higher heart rate. Transgenic mice may be useful in studies of atherosclerosis, hypertension, hyperlipidemia, hypercholesterolemia, hyperhomocystinemia, diabetes mellitus, stroke, renal failure, preeclampsia, and other conditions associated with vascular pathophysiology and/or cardiovascular disease. | ||
| 007073 | CByJ.129P2(B6)-Nos3tm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Nos3tm1Unc targeted mutation are viable and fertile. They have elevated blood pressure that is about 20 mmHg higher than that seen in normal wildtype siblings. They also show a decreased heart rate. Female homozygotes are smaller in body weight than normal wildtype siblings. Hyperglycemic-euglycemic clamp studies demonstrate that homozygotes exhibit insulin resistance at the level of the liver and peripheral tissues. This mutant mouse strain may be useful in studies of wound healing, hypertension and other cardiovascular defects, insulin resistance, hyperlipidemia and lung development.
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. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain de ..... | ||
| 007683 | CByJ.129X1(Cg)-Apobtm1.1Zc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this apoB38.9 allele (apoB38.9/38.9) are viable with impaired fertility, bearing a premature stop codon at residue 1767 of the targeted gene. As a result, homozygous plasma shows a truncated apoB38.9 as the sole apoB protein. Plasma from heterozygous (apoB+/38.9) mice have reduced apoB100 and apoB48 compared to wild-type, with apoB38.9 representing 20% of total circulating apoB. This apoB38.9 truncation affects both apoB100 and apoB48 metabolism in mice, and mimics human Familial Hypobetalipoproteinemia (FHBL). Homozygous and, to a lesser extent, heterozygous mice exhibit symptoms of FHBL due to impaired lipoprotein export system/VLDL secretion, including elevated hepatic triglyceride (TG), cholesterol and free fatty acids (FFA), with decreased plasma TG and cholesterol. These BALB/cByJ-apoB38.9 mice are also heterozygous for the BALB/cByJ-derived SCAD deletion (Acadsdel-J). While BALB/cByJ inbred mice have elevated liver TG f ..... For more information please see the full phenotype on the strain data sheet | ||
| 003897 | DBA/1-Abca1tm1Jdm/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the Abca1-null allele are at greater risk of perinatal lethality. Autopsied pups exhibit perivisceral hemorrhaging. Pups that survive beyond birth have no detectable Abca1 gene transcript in the tissues of the liver. Homozygous females suffer from impaired placental development and are unable to produce litters. Both plasma lipids and lipoproteins are markedly reduced. Plasma cholesterol is decreased by approximately 70%. HDL-C and apoAI are decreased by greater than 99%. LDL-C and apoB are also reduced (70 % and 20%, respectively). Other characteristics observed are an increase in intestinal absorption of dietary cholesterol, an impaired ability for macrophages to engulf apoptotic cells and an accumulation of lipid rich macrophages and type II pneumocytes the lungs. These mice display pathophysiologic hallmarks similar to those associated with Tangier disease and provide a tool suitable for use in studies examining membrane lipid homeostasis. ..... For more information please see the full phenotype on the strain data sheet | ||
| 002304 | DBA/1LacJ-Scd1ab-2J/J | Cryopreserved - Ready for recovery |
| The overall appearance of mice homozygous for either the Scd1ab-J allele or the Scd1ab-2J allele (Stock No. 002304
or 005956) includes slightly hunched posture, dry, scaly skin, thin fur sometimes detectable by 7 days of age, and small eyes with encrusted eyelids stuck shut. They have hypoplasia of the sebaceous glands and other hair follicle abnormalities that result in scarring alopecia. These mice have a paucity of adipose tissue, thin subcutis, and a distinctive odor. Hepatic cholesterol ester and triglyceride synthesis has been shown to be deficient in Scd1ab-J homozygotes and could not be restored through diet. Early studies of skin lipids in the original asebia mutant (Scd1ab) revealed a deficiency in wax esters, wax diesters, and sterols esterified with very long-chain fatty acids along with an i ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 006402 | FVB/N-Adrb3tm1Lowl/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. | ||
| 005994 | STOCK Mbtps1tm1Jdh/J | Cryopreserved - Ready for recovery |
| These mice carry a targeted mutation in which exon 2 of the targeted gene is flanked by loxP sites. A loxP-flanked ("floxed") neomycin resistance cassette also is inserted downstream in intron 2. Homozygotes are viable and fertile, and the floxed gene appears to function normally. When homozygotes are crossed with transgenic strains expressing Cre-recombinase, cre-mediated recombination of the loxP-flanked sequences can result in one of three genotypes: a) deletion of the neo cassette only, leaving a loxP-flanked second exon and unimpaired endogenous gene function. b) Deletion of exon 2 only, leaving a loxP-flanked neo cassette and no endogenous gene function. c) Deletion of both the neo cassette and exon 2, leaving a single loxP site and no endogenous gene function. When these floxed mutant mice are bred to mice carrying the Mx1-cre transgene (for example, Stock No. 003556), liver- ..... For more information please see the full phenotype on the strain data sheet | ||
| 004192 | STOCK Mttptm2Sgy Ldlrtm1Her Apobtm2Sgy Tg(Mx1-cre)1Cgn/J | Cryopreserved - Ready for recovery |
| These mice are homozygous for four different induced mutations. The cumulative result of these mutations is a mouse model in which hypercholesterolemia can be reversed. By themselves, the combined presence of the Ldlrtm1Sgy and Apobtm1Sgy targeted alleles results in mice with a high susceptibility to atherosclerosis and total plasma cholesterol levels of approximately 300 mg/dl. A functional microsomal triglyceride transfer protein gene (Mttp) is essential for establishing a hypercholesterolemic condition. By flanking the Mttp gene with loxP sites and including a Mx1-Cre transgene, it is possible to reduce total plasma cholesterol levels from 300 mg/dl to 30 mg/dl upon induction of the Cre recombinase by administering interferon alpha, interferon beta, or synthetic double-stranded RNA. This unique model is useful in research related to the mechanisms and events of atherosclerotic reversal. Mice homozygous for the targeted ..... For more information please see the full phenotype on the strain data sheet | ||
| 004144 | STOCK Nr1h4tm1Gonz/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted Nr1h4 allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Nr1h4 protein product is detected in liver tissue although an aberrant transcript appears to be generated. Homozygous mice display a proatherogenic serum lipoprotein profile characterized by elevated levels of serum and hepatic cholesterol and triglycerides. Serum bile acids are also elevated. When fed a diet supplemented with 1% cholic acid, severe wasting, hypothermia and increased mortality is observed. Wildtype mice fed a similar diet display no ill effects. Levels of fecal bile excretion are reduced in homozygotes. This mutant mouse strain represents a model that may be useful in studies related to bile acid and lipid homeostasis. | ||
| 007679 | SWR.129X1(B6)-Apobtm1.1Zc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this apoB38.9 allele (apoB38.9/38.9) are viable with impaired fertility, bearing a premature stop codon at residue 1767 of the targeted gene. As a result, homozygous plasma shows a truncated apoB38.9 as the sole apoB protein. Plasma from heterozygous (apoB+/38.9) mice have reduced apoB100 and apoB48 compared to wildtype, with apoB38.9 representing 20% of total circulating apoB. This apoB38.9 truncation affects both apoB100 and apoB48 metabolism in mice, and mimics human Familial Hypobetalipoproteinemia (FHBL). Homozygous and, to a lesser extent, heterozygous mice exhibit symptoms of FHBL due to impaired lipoprotein export system/VLDL secretion, including elevated hepatic triglyceride (TG), cholesterol and free fatty acids (FFA), with decreased plasma TG and cholesterol. Because plasma and liver lipid profiles range from mild to severe in populations of heterozygous apoB38.9 mice on a mixed (C57BL/6J;129X1/SvJ) genetic background, apoB+/38. ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 014556 | 129S6/SvEv-Apoetm4Mae/J | Under Development - Now Accepting Orders |
| 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 | ||
| 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 | ||
| 016223 | B6(Cg)-Tg(Phox2b-cre)3Jke/J | Under Development - Now Accepting Orders |
| Phox2b-Cre BAC transgenic mice are viable and fertile, with Cre recombinase expression under control of the Phox2b promoter/enhancer regions within the BAC transgene. cre-expressing neurons co-express PHOX2B (as shown by in situ hybridization). Phox2b-Cre BAC transgenic mice from founder line 3 exhibit cre expression directed primarily to the hindbrain; specifically the dorsal motor nucleus of the vagus (DMV) in parasympathetic visceral and branchial motor neurons, nodose sensory ganglia, and nucleus of the solitary tract (NTS) cells. No transgene expression is reported in hypothalamus or spinal cord. Although endogenous Phox2b expression is reported in peripheral ganglia along with the enteric nervous system, no peripheral transgene expression is reported for these Phox2b-Cre BAC transgenic mice. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequences in the offspr ..... For more information please see the full phenotype on the strain data sheet | ||
| 017443 | B6.129P2-Pdha1tm1Ptl/J | Under Development - Now Accepting Orders |
| These Pdha1flox8 mutant mice possess loxP sites flanking exon 8 of the pyruvate dehydrogenase E1 alpha 1 (Pdha1) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. PDHA1 is catalytic component of the pyruvate dehydrogenase complex (PDC) which is a mitochondrial multienzyme complex involved in lipid synthesis, glucose homeostasis, and metabolism of carbohydrates. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 8 deleted in cre-expressing tissues. For example, when crossed to a strain expressing Cre recombinase in the liver, this mutant mouse strain may be useful for studying lipid metabolism, glucose metabolism, and insulin sensitivity in the liver.
When bred to a strain expressing Cre recombinase in the central and periphal nervous system (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 016108 | B6;129S-Cyp7b1tm1Rus/J | Under Development - Now Accepting Orders |
| In this strain, a neomycin resistance (neo) cassette replaces part of exon 6 of the endogenous cytochrome P450, family 7, subfamily b, polypeptide 1 (Cyp7b1) gene, abolishing gene function. Homozygotes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cyp7b1 encodes oxysterol 7α-hydroxylase, an enzyme of the alternate bile acid synthesis pathway involved in cholesterol homeostasis. Plasma and tissue levels of 25- and 27-hydroxycholesterol, two oxysterol bioactive lipid substrates of oxysterol 7α-hydroxylase, were elevated in homozygotes. Sterol biosynthetic rates showed a 40% decrease in male kidneys. These mice are useful for studying cholesterol and bile acid metabolism, oxysterol synthesis and breakdown, macrophage function, and B cell trafficking and activation in the immune system. | ||
| 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 | ||
| 016131 | C57BL/6J-Sec61a1m1Gek/J | Under Development - Now Accepting Orders |
| Mice homozygous for the ENU-induced missense mutation, called Sec61a1Y344H, 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 Sec61a1Y344H 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 | ||
| 017334 | FVB.129S6(Cg)-Sirt6tm1.1Cxd/J | Under Development - Now Accepting Orders |
| These Sirt6Co floxed mutant mice possess loxP sites flanking exons 2-3 of the sirtuin 6 (Sirt6) 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. Sirt6 is a histone deacetylase highly expressed in the central nervous system, which is involved in the regulation of glucose homeostasis, cell fate, and genomic stability. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 2-3 deleted in cre-expressing tissues.
For example, when crossed to a strain expressing Nestin-Cre in the central and peripheral nervous system (see Stock No. 003771), this mutant mouse strain exhibits reduced post-natal growth and obesity. When crossed to a strain expressing Cre Recombinase in the liver (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
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Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Awaiting Transfer
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New Strains Awaiting TransferThe Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion.
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