Search Criteria: Research Area is "Metabolism Research"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000664 | C57BL/6J | Level 1 |
| C57BL/6 is the most widely used inbred strain. It is commonly used as a general purpose strain and background strain for the generation of congenics carrying both spontaneous and induced mutations. Although this strain is refractory to many tumors, it is a permissive background for maximal expression of most mutations. C57BL/6J mice are used in a wide variety of research areas including cardiovascular biology, developmental biology, diabetes and obesity, genetics, immunology, neurobiology, and sensorineural research. C57BL/6J mice are also commonly used in the production of transgenic mice. Overall, C57BL/6 mice breed well, are long-lived, and have a low susceptibility to tumors. Primitive hematopoietic stem cells from C57BL/6J mice show greatly delayed senescence relative to BALB/c and DBA/2J. This is a dominant trait. Other characteristics include: 1) a high susceptibility to diet-induced obesity, type 2 diabetes, and atherosclerosis; 2) a high incidence of microphthalmia and other a ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 000697 | B6.BKS(D)-Leprdb/J | Level 2 |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) become identifiably obese around 3 to 4 weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at four to eight weeks. Affected mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. On the C57BL/6 background there is compensatory hyperplasia of the islet B cells, and continued hyperinsulinemia throughout an 18- to 20-month life span. Wound healing is delayed and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Leprdb/+) also have increased metabolic efficiency and can survive a prolonged fast longer than controls. Experiments involving destruction of the ventromedial nucleus of the hypothalamus suggest that Leprdb may cause a defect in the hypothalamus. Steroid sulfotransferase enzymes, aberrantly expressed in ..... For more information please see the full phenotype on the strain data sheet | ||
| 000632 | B6.V-Lepob/J | Level 2 |
| Mice homozygous for the obese spontaneous mutation, (Lepob; commonly referred to as ob or ob/ob), are first recognizable at about four weeks of age. Homozygous mutant mice gain weight rapidly and may reach three times the normal weight of wild-type controls. In addition to obesity, mutant mice exhibit hyperphagia, a diabetes-like syndrome of hyperglycemia, glucose intolerance, elevated plasma insulin, subfertility, impaired wound healing, and an increase in hormone production from both pituitary and adrenal glands. They are also hypometabolic and hypothermic. The obesity is characterized by an increase in both adipocyte number and size. Adipose tissue transplants in Lepob homozygotes protect them from obesity, normalize insulin sensitivity, and restore fertility. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight mainte ..... For more information please see the full phenotype on the strain data sheet | ||
| 000642 | BKS.Cg-Dock7m +/+ Leprdb/J | Level 2 |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) become identifiably obese around three to four weeks of age. Elevations of plasma insulin begin at 10 to 14 days of age and of blood sugar at four to eight weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. A number of features are observed on the C57BLKS background, including an uncontrolled rise in blood sugar, severe depletion of the insulin-producing beta-cells of the pancreatic islets, and death by 10 months of age. Exogenous insulin fails to control blood glucose levels and gluconeogenic enzyme activity increases. Peripheral neuropathy and myocardial disease are seen in C57BLKS-Leprdb homozygotes. Wound healing is delayed, and metabolic efficiency is increased. Female homozygotes exhibit decreased uterine and ovarian weights, decreased ovarian hormone production and hypercytolipidemia in fol ..... For more information please see the full phenotype on the strain data sheet | ||
| 000656 | CBA/J | Level 2 |
| CBA/J inbred mice are widely used as a general purpose strain. CBA/J strain is the only CBA substrain that carries the Pde6brd1 mutation, which causes blindness by wean age. CBA/J mice are not histocompatible with the CBA/CaJ (Stock No. 000654) substrain (Green and Kaufer, 1965). The CBA/J inbred mouse strain is used to study granulomatous experimental autoimmune thyroiditis (G-EAT), are relatively resistant to diet-induced atherosclerosis (Paigen et al. 1990), and develop a mild hearing loss late in life, with most of the hearing loss occurring in the higher frequencies (Sweet et al. 1988). Renal tubulointerstitial lesions have been observed in this strain at a high frequency (Rudofsky 1978). Some CBA/J mice spontaneously develop exocrine pancreatic insufficiency syndrome (Eppig and Leiter 1977, Leiter et al. 1977). | ||
| 000671 | DBA/2J | Level 2 |
| DBA/2J is a widely used inbred strain that is valuable in a large number of research areas, including cardiovascular biology, neurobiology, and sensorineural research. Its characteristics are often contrasted with those of the C57BL/6J inbred strain (Stock No. 000664). DBA/2J mice show a low susceptibility to developing atherosclerotic aortic lesions (20 to 350 um2 atherosclerotic aortic lesions /aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). They also exhibit high-frequency hearing loss beginning roughly at the time of weaning/adolescence (between three to four weeks of age) and becoming severe by two to three months of age. The age related hearing loss 8 mutation arose spontaneously in DBA/2J between 1951 and 1975. This strain possesses three recessive alleles that cause progressive cochlear pathology initially affecting the organ of Corti. Decreasing anteroven ..... For more information please see the full phenotype on the strain data sheet | ||
| 000686 | SJL/J | Level 2 |
| SJL mice display a very high incidence of reticulum cell sarcomas resembling Hodgkin's disease by approximately one year of age. Sarcomas first appear in the Peyer's patches and mesenteric lymph nodes and later in the spleen, liver, thymus and other lymph nodes. Most of the tumors are mixed-cell types classified as type B reticulum cell neoplasms, but a few are type A histiocytomas. This strain is also characterized by extreme aggression in males and its susceptibility to experimental autoimmune encephalomyelitis (EAE) for multiple sclerosis research. SJL/J mice develop a spontaneous myopathy resulting from a splice-site mutation in the Dysferlin gene. This Dysfim allele has been shown to result in decreased levels of dysferlin protein in SJL/J mice and makes this strain a good model for limb girdle muscular dystrophy 2B. This spontaneous myopathy is characterized by a progressive loss of muscle mass and strength corresponding with an increase in muscle pathology incl ..... For more information please see the full phenotype on the strain data sheet | ||
| 000648 | AKR/J | Level 3 |
| Originally inbred at the Rockefeller Institute, AKR mice are widely used in cancer research for their high leukemia incidence (60-90%) and in immunology as a source of the Thy1.1 (theta AKR) antigen. AKR/J mice are viremic from birth, and express the ecotropic retrovirus AKV in all tissues. The hair interior defect (hid) mutation, a strain characteristic of AKR mice, causes alterations in hair development that is only evident microscopically. Adrenocortical lipid depletion (ald) in AKR mice is caused by a mutation in sterol O-acyltransferase 1 (Soat1), and leads to a truncated SOAT1 protein. AKR/J mice are relatively resistant to aortic lesion formation on a semi-synthetic high fat diet and are hyporesponsive to diets containing high levels of fat and cholesterol. | ||
| 002726 | B6SJL-Tg(SOD1*G93A)1Gur/J | Level 3 |
| Mice hemizygous for this SOD1-G93A (also called G93A-SOD1) transgene are viable and fertile, with transgenic expression of a G93A mutant form of human SOD1. This founder line (often referred to as G1H) is reported to have high transgene copy number. Hemizygotes exhibit a phenotype similar to amyotrophic lateral sclerosis (ALS) in humans; becoming paralyzed in one or more limbs with paralysis due to loss of motor neurons from the spinal cord. Transgenic mice have an abbreviated life span: 50% survive at 128.9+/-9.1 days (in contrast to C57BL/6J background where 50% survival is observed at 157.1+/-9.3 days). These SOD1-G93A (also called G93A-SOD1) transgenic mice may be useful in studying neuromuscular disorders, including Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig's Disease). | ||
| 000690 | 129P3/J | Level 4 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently, 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson et al. 1997. | ||
| 002087 | B6.129P2-B2mtm1Unc/J | Level 4 |
| Mice homozygous for the B2mtm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8+ cytotoxic T-cells and under some circumstances a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+ T-cells are severely deficient providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). 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 ..... For more information please see the full phenotype on the strain data sheet | ||
| 002365 | B6.129S-Cybbtm1Din/J | Level 4 |
| Chronic granulomatous disease (CGD) is a recessive disorder characterized by a defective phagocyte respiratory burst oxidase, life-threatening pyogenic infections and inflammatory granulomas. Gene targeting was used to generate mice with a null allele of the gene involved in X-linked CGD, which encodes the 91 kD subunit of the oxidase cytochrome b. Affected hemizygous male mice lack phagocyte superoxide production, manifest an increased susceptibility to infection with Staphylococcus aureus and Aspergillus fumigatus and have an altered inflammatory response in thioglycollate peritonitis. This animal model should aid in developing new treatments for CGD and in evaluating the role of phagocyte-derived oxidants in inflammation. | ||
| 000662 | C57BLKS/J | Level 4 |
| Although C57BLKS/J is estimated to have more than 70% of its genome derived from C57BL/6J, these strains are phenotypically distinct. Diet-induced atherosclerotic lesions are much more severe in C57BLKS/J than in C57BL/6J or many other inbred strains. Compared with a panel of inbred strains, C57BLKS/J was found to have low total cholesterol and low HDL cholesterol when fed a normal diet and high total cholesterol and HDL cholesterol in an atherogenic diet. Paigen et al. found high levels of plasma bile salts in C57BLKS/J females after eight weeks on an atherogenic diet. The mutations diabetes (Leprdb) and obese (Lepob) each express a much more severe phenotype on the C57BLKS/J background than on the C57BL/6J background. The Cpefat mutation causes severe obesity, hyperinsulinemia, and hyperglycemia on the C57BLKS/J background rather than the hyperinsulinemia, and mild obesity without hyperglycemia found on the HRS/J background ..... For more information please see the full phenotype on the strain data sheet | ||
| 000668 | C57L/J | Level 4 |
| C57L/J mice are used widely in research as a general purpose strain. Mice have a high incidence of Hodgkin's-like reticulum cell neoplasm at 18 months of age and pituitary tumors in old multiparous females. C57L/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE) and highly responsive to phytohemagglutinin. In addition, C57L/J mice are highly susceptible to developing atherosclerotic aortic lesions (4500 to 8000 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat) (Paigen et al. 1990). On a lithogenic diet, C57L/J mice develop gallstones as a result of abnormal regulation of cholesterol synthesis (Xua et al. 2004). C57L/J mice carry no detectable endogenous ecotropic MuLV DNA sequences. | ||
| 000928 | CAST/EiJ | Level 4 |
| 000676 | LP/J | Level 4 |
| LP/J mice display a high susceptibility to audiogenic seizures. This strain is also reported to have a fairly high incidence of tumors that develop later in life, including mammary tumors, lymphoma, lung and soft-tissue sarcomas. LP/J mice are also homozygous for the spontaneous mutation piebald in the endothelin receptor type B gene (Ednrbs). The piebald spontaneous mutation is the result of a mutation in the endothelin receptor type B gene, Ednrb. Mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. They also have dark eyes. The white areas of the coat are completely lacking in neural crest-derived melanocytes, and there is a reduction in the number of melanocytes in the choroid layer of the eye is reduced. | ||
| 000684 | NZB/BlNJ | Level 4 |
| NZB/BlNJ mice display a number of autoimmune abnormalities including hemolytic anemia, elevated levels of immunoglobulin, anti-DNA antibodies, anti-thymocyte antibodies, and circulating immune complexes causing glomerulonephritis. F1 hybrids of NZB/BlNJ and NZW/LacJ (NZBWF1/J, Stock No. 100008) are widely used as a model for autoimmune disease resembling human systemic lupus erythematosus. NZB/BlNJ mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, Stock No. 000667, and SM/J, Stock No. 000687). | ||
| 000689 | SWR/J | Level 4 |
| SWR/J mice are used widely in research as a general purpose strain. Aging mice exhibit a high incidence of lung and mammary gland tumors. They also develop extreme polydipsia and polyuria (nephrogenic diabetes insipidus) with increasing age. SWR/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE). Germline deletion of about 50% of T-cell receptor V beta-chain gene segments and a T-cell receptor V alpha polymorphism are responsible for the resistance of SWR/J mice to collagen type II-induced arthritis. SWR/J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions (1670 to 1690 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). SWR/J mice have been recommended for generation and propogation of transgenic mice because they are high responders to exogenous hormones, have large and prominant pronuclei with good resistance to l ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 013039 | 129S-Spictm1Kmm/J | Repository- Live |
| In these mutant mice a loxP-flanked neomycin resistance (neo) cassette replaces exons 2-5 of the Spi-C transcription factor (Spi-1/PU.1 related) gene (Spic), abolishing gene function. Heterozygous mice are viable and fertile, while homozygotes are born at a frequency lower than the expected Mendelian ratio and they have small litters. Spi-C is highly expressed in red pulp macrophages which are a distinct splenic subset required for red blood cell recycling and iron homeostasis. These Spi-C-/- mice exhibit a defect in the development of red pulp macrophages, which fail to efficiently phagocytose red blood cells trapped in the spleen. They also develop an iron overload localized selectively to splenic red pulp. These mice may be useful for studying the development and function of red pulp macrophages. | ||
| 007853 | 129S/SvEv-Tg(Alb1-Ren)2Unc/CofJ | Repository- Live |
| Mice heterozygous for the RenTgMK transgene are viable and fertile. The RenTgMK transgene contains a liver-specific albumin promoter/enhancer controlling the expression of a synthetic renin gene (engineered to allow efficient cleavage and secretion of the prorenin transgene product by the liver). This, and because the transgene was targeted to the apolipoprotein locus on Chromosome 9, results in active renin secretion from the liver independently of renal or other homeostatic cardiovascular control mechanisms (i.e. genetically clamped). RenTgMK heterozygotes have high ectopic levels of active mouse renin in the liver and elevated plasma levels of prorenin and active renin. Heterozygous mice display significantly elevated blood pressure, enhanced thirst, high urine output, proteinuria, and kidney damage. Because active renin overexpression results in increased circulating levels of angiotensin II (Ang II), heterozygotes also exhibit cardiac hypertrophy and 50% male mortality between 6-8 ..... For more information please see the full phenotype on the strain data sheet | ||
| 003580 | 129S4/SvJae-Pparatm1Gonz/J | Repository- Live |
| Mice homozygous for the Pparatm1Gonz targeted mutation are viable, fertile and appear normal in appearance and behavior. An altered response to a group of compounds (peroxisome proliferators) that induce peroxisome proliferation and hapatocarcinogenesis is observed. No peroxisome proliferation response is detected when these mice are challenged with classical peroxisome proliferators. Typically, such a response includes hepatomegaly, peroxisome proliferation and transcriptional activation of a set of target enzyme genes. Accumulation of lipid droplets observed in liver tissue suggests that Ppara is involved in maintaining the homeostasis of hepatic lipid metabolism. | ||
| 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 ..... | ||
| 002211 | 129S7/SvEvBrd-Mt1tm1Bri Mt2tm1Bri/J | Repository- Live |
| Mice homozygous for the Mt1tm1Bri Mt2tm1Bri mutation are viable and fertile. They show an increased sensitivity to hepatic poisoning by cadmium. Most homozygous mice given daily injections of cadmium die within 4 days, with most of the males dying within 2 days. | ||
| 003070 | ALR/LtJ | Repository- Live |
| ALS/LtJ (Stock No. 003072) and ALR/LtJ inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. ALR/LtJ mice are of particular interest to investigators studying the immunogenetics of NOD/ShiLtJ mice in that the ALR/LtJ MHC haplotype (H2gx) is a variant of the diabetogenic NOD H2g7 haplotype. The (H2gx) haplotype is identical to the H2g7 haplotype from the H2-K end of the complex through the class II and class III region distal to Hsp70. However, at the distal H2-D end of the complex, ALR/LtJ mice have a rare H2-Dgx allele. Despite the ..... For more information please see the full phenotype on the strain data sheet | ||
| 003072 | ALS/LtJ | Repository- Live |
| ALS/LtJ and ALR/LtJ (Stock No. 003070) inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. By 34 weeks of age, both untreated ALS/Lt and ALR/Lt males fed a 6% fat-containing chow diet attain a mean body weight of around 50 grams. Genome wide scan comparison shows that ALS/LtJ mice are more closely related to NON/ShiLtJ mice (they share the H2nb1 haplotype) than to NOD/ShiLtJ. Like two other ICR-derived inbred strains selected in Japan (NON and NSY), alloxan-untreated ALS/Lt males exhibit impaired glucose tolerance when tested by intraperitoneal administration of glucose. However, unlike NON/ShiLt males ..... For more information please see the full phenotype on the strain data sheet | ||
| 016235 | B6(Cg)-Narfltm1.1Fsl/J | Repository- Live |
| These Iop1flox mutant mice possess loxP sites flanking exon 1 of the nuclear prelamin A recognition factor-like (Narfl or Iop1) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. IOP1 is required for cytosolic iron-sulfur protein assembly pathways. Iron-sulfur proteins are involved in the Krebs Cycle, oxidative phosphorylation, translation, iron regulatory pathways, and purine metabolism. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exon 1 deleted in the cre-expressing tissues. This strain may be useful for conditional deletion of IOP1 to study the cytoplasmic iron-sulfur complex assembly pathway. | ||
| 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 | ||
| 008195 | B6.129-Adipoqtm1Chan/J | Repository- Live |
| Homozygous mice are viable and fertile, with absence of targeted allele expression confirmed in adipose tissue (mRNA) and plasma (adiponectin protein). While homozygous mice have normal glucose tolerance and insulin resistance, beta-oxidation activity is significantly increased in muscle and liver. Homozygotes also have endothelial dysfunction (increased leukocyte rolling and leukocyte adhesion), are protected from DSS-induced colitis, and are more susceptible to myocardial ischemia/reperfusion. When fed a high fat diet, obese homozygotes are significantly heavier with increased insulin levels and altered insulin resistance. These adiponectin-deficient (Adipoq-/- or Adipo-/-) mice may be useful in studying obesity, diabetes, insulin resistance, metabolism, inflammation, leukocyte-endothelium interactions, and colitis. | ||
| 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. | ||
| 007741 | B6.129-Arg1tm1Rki/J | Repository- Live |
| Homozygous AI-mutant mice completely lack hepatic arginase (AI) activity, exhibit hyperagrininemia, severe symptoms of hyperammonemia (ncluding decerebrate posture, lethargy, and high-frequency tremor of the extremities, particularly the tail) and die between 10-14 days after birth. Neural stem cells (NCSs) isolated from homozygous mice exhibit abnormal proliferation and differentiation. In addition, haploid germ cells carrying the disrupted AI allele may be less fit/less effective in forming zygotes compared to wild-type spermatozoa. Heterozygotes are viable and fertile. These AI-mutant mice may be useful in studying metabolic defects of arginase I deficiency, urea cycle (excretion of excess nitrogen), and neuronal development and function. | ||
| 009100 | B6.129-Arntltm1Bra/J | Repository- Live |
| These targeted mutation mice exhibit a loss of both behavioral and molecular circadian rhythms. When placed in constant darkness, the mice undergo an immediate loss of circadian rhythmicity. Locomotor activity is impaired in both light and constant dark cycles. Reduced total activity is seen as the mice age. They display a progressive noninflammatory arthropathy. Little pathology is seen prior to 11 weeks of age, but virtually all homozygotes develop joint ankylosis due to flowing ossification of ligaments and tendons by 35 weeks of age. Bone density and articular cartilage are unaffected.
Inactivation of the gene suppresses diurnal variation in glucose and triglycerides. Gluconeogenesis is abolished in homozygotes, but the counterregulatory response of corticosterone and glucagon to insulin-induced hypoglycemia is retained.
Homozygotes are viable but not fertile and have an increased mortality rate after 26 weeks of age. A truncated, non-functional protein is ..... | ||
| 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 | ||
| 012772 | B6.129-Sirt2tm1.1Fwa/J | Repository- Live |
| 005775 | B6.129P2-Adipor2tm1Dgen/J | Repository- Live |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 004155 | B6.129S2-Alox5tm1Fun/J | Repository- Live |
| Mice homozygous for the Alox5tm1Fun targeted mutation are viable and fertile. In general, homozygous mutant mice are selectively resistant to inflammatory insults. They are resistant to the lethal effects of platelet activating factor but reaction to endotoxin shock is normal. Phorbol ester induced inflammation is normal but arachidonic acid induced inflammation is reduced. | ||
| 009641 | B6.129S4-Adcyap1tm1Clw/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, but experience high postnatal mortality between postnatal week 1 and 2 due to thermoregulatory defect. The Donating Investigator reports that postnatal survival is improved if temperature is kept at 82.5 F. Homozygous males are fertile, homozygous females are subfertile. No gene product (protein) is detected by RIA (radioimmunoassay) analysis of hypothalamus, cerebral cortex, kidney, and stomach tissues in homozygotes. Homozygotes exhibit sustained hyperactivity, shortened circadian period and abnormal circadian phase shifting with 50% reduction in the magnitude of light cued phase shift. Homozygous mice lack the light stimulation increase of sympathetic nerve activity and plasma corticosterone that is observed in wildtype mice. Testicular aging is delayed in 15-month old male homozygotes; reactive oxygen species generation and apoptosis in the testis is reduced. Young male homozygotes (4 month old) exhibit decreased steroi ..... For more information please see the full phenotype on the strain data sheet | ||
| 015857 | B6.129S4-Arg1tm1Lky/J | Repository- Live |
| A targeting vector was designed to insert an internal ribosome entry site (IRES)-enhanced yellow fluorescent protein (eYFP) fusion protein, downstream of the endogenous stop codon of the arginase (Arg1) gene. These homozygous YARG mice are viable, fertile, and normal in size. Located in the cytoplasm of the liver and specifically in macrophages, arginase I converts L-arginine into L-ornithine and urea as the final step in the urea cycle. L-arginine can also be catabolized into nitric oxide (NO), a secreted free radical which causes tissues damage and is toxic to bacteria. Arginase I suppresses NO production by decreasing the amount of L-arginine available to the nitric oxide synthase (NOS) enzyme for conversion into NO and other reactive oxygen species (ROS). Nine days after infection with the helminth, Nippostrongylus brasiliensis, YARG mice exhibit accumulation of arginase I-expressing macrophages in the lung and peritoneum. As soon as two days afte ..... For more information please see the full phenotype on the strain data sheet | ||
| 012932 | B6.129S4-Ftmttm1Mdf/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis of testes from homozygotes. Homozygotes do not exhibit any overt phenotype. | ||
| 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. | ||
| 002973 | B6.129S7-Sod2tm1Leb/J | Repository- Live |
| Mice homozygous for the Sod2tm1Leb targeted mutation die within 21 days after birth. They exhibit severe wasting and are clearly much smaller, weaker,and less coordinated than their wildtype and heterozygous littermates. Homoyzotes exhibit several novel pathogenic phenotypes including severe anemia, degeneration of neurons in the basal ganglia and brainstem, progressive motor disturbances, and myocardial injury. | ||
| 004855 | B6.129X-Mmp12tm1Sds/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. Homozygous females have reduced litter sizes (~60% of wildtype). No gene product (mRNA or protein) is detected by Northern or Western blot analysis of peritoneal macrophages and fluid. Casein substrate gel zymographic analysis of thioglycollate-stimulated cultured macrophages and peritoneal fluid reveals there is no lytic activity. In whole lung extracts, no elastase activity was detected by zymography. Immunohistochemistry of lung tissue does not detect macrophage elastase. Macrophages from homozygous mice are unable to penetrate artificial basement membrane matrix. Addition of plasminogen to cultured macrophages does not increase elastase activity. When challenged with chronic exposure to cigarette smoke, mutant mice do not develop emphysema. IL-13 induced tissue inflammation is reduced in homozygotes. This mutant mouse strain may b ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 ..... | ||
| 004265 | B6.129X1-Mpotm1Lus/J | Repository- Live |
| Mice that are homozygous null for the targeted gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Mpo gene product (mRNA or protein) is detected. Mutant mice exhibit total white blood cell counts and differentials similar to wildtype mice. Neutrophils and monocytes in periperhal blood and bone marrow have no endogenous peroxidase activity. Superoxide production levels in peritoneal exudate cells of mutant mice are similar to levels found in wildtypes mice. Hypochlorous acid production is undetectable in both isolated leukocytes and peritoneal exudate cells. Mutant mice display impaired fungicidal activity due to myeloperoxidase deficiency. When maintained under hyperlipidemic conditions, mutant mice develop atherosclerotic lesions 50% larger than those seen in control mice. | ||
| 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 | ||
| 008599 | B6.Cg-Cyp1a2/Cyp1a1tm2Dwn Ahrd Tg(CYP1A1,CYP1A2)1Dwn/DwnJ | Repository- Live |
| These "humanized" hCYP1A1_1A2_Cyp1a1/1a2(-/-)_Ahrd mice carry the human CYP1A1 and CYP1A2 genes in the absence of functional mouse Cyp1a1 and Cyp1a2 orthologs, and also mimic the human poor-affinity aryl hydrocarbon receptor (AHR) by carrying the poor-affinity Ahrd allele derived from DBA/2J mice (rather than the high-affinity Ahrb1 allele normally present on a C57BL/6J genetic background); all on a C57BL/6J (reported >99.8%) genetic background. Mice homozygous for the Cyp1a2/Cyp1a1 targeted allele [Cyp1a1/1a2(-/-)], homozygous for the Ahrd allele, and carrying the hCYP1A1_1A2 transgene are viable and fertile with normal lifespan. As the Cyp1a2/Cyp1a1(-) targeted allele lacks the coding regions of both Cyp1a1 and Cyp1a2 genes, no mouse CYP1A1 or CYP1A2 mRNA expression is observed in liver, lung or kidney. Transgene expression of the orth ..... | ||
| 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 | ||
| 004435 | B6.Cg-Tg(SOD1*G93A)1Gur/J | Repository- Live |
| Mice hemizygous for this SOD1-G93A (also called G93A-SOD1) transgene are viable and fertile, with transgenic expression of a G93A mutant form of human SOD1. This founder line (often referred to as G1H) is reported to have high transgene copy number. Hemizygotes exhibit a phenotype similar to amyotrophic lateral sclerosis (ALS) in humans; becoming paralyzed in one or more limbs with paralysis due to loss of motor neurons from the spinal cord.
Transgenic mice have an abbreviated life span: 50% survive at 157.1+/-9.3 days (in contrast to the mixed B6SJL background where 50% survival is observed at 128.9+/-9.1 days).
Female hemizygotes are poor breeders, and rarely produce more than one litter before the onset of disease. These SOD1-G93A (also called G93A-SOD1) transgenic mice may be useful in studying neuromuscular disorders, including Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig's Disease).
In an attempt to offer alleles on well-characterized or multiple genetic bac ..... | ||
| 002921 | B6.D2N-Ahrd/J | Repository- Live |
| 003923 | B6.HRS(BKS)-Cpefat/J | Repository- Live |
| Mice homozygous for the fat spontaneous mutation (Cpefat) on a C57BL/6J genetic background (N10) become noticeably obese by 14-15 weeks of age. There is also some sexual dimorphism; female homozygous mutant mice develop obesity at a later age than males. Cpefat mice actually weigh less than wildtype controls prior to weaning age. Homozygous mutant mice develop a diabetic phenotype characterized by hyperglycemia and insulin resistance. Cpefat mice appear healthier on the C57BL/6J genetic background, avoiding the hereditary hydronephrosis present in C57BLKS/J and a lower incidence of malocclusion. | ||
| 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. | ||
| 002972 | B6;129S7-Sod1tm1Leb/J | Repository- Live |
| Mice homozygous for the Sod1tm1Leb targeted mutation produce no SOD1 protein. Female homozygous mice are infertile, while male homozygous mice reproduce normally. | ||
| 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 | ||
| 002297 | B6SJL-Tg(SOD1)2Gur/J | Repository- Live |
| This transgenic strain carries the normal allele of the human SOD1 gene. Originally published as N1029, it has been reported that the SOD1 protein level is the same as in the transgenic strain carrying the SOD1*G93A transgene (002726), even though the copy number in the SOD1*G93A transgenic is higher. This strain serves as a control for the B6SJL-Tg(SOD1*G93A)1Gur/J (002726) and the B6SJL-Tg(SOD1*G93A)dl1Gur/J (002300) strains. | ||
| 001592 | BALB/cByJ-Lpin1fld/J | Repository- Live |
| The original fld (fatty liver dystrophy) mutation arose spontaneously at The Jackson Laboratory in the Animal Resources BALB/cByJ colony in 1981, and was maintained by sibling mating for 47 generations, then backcrossed once in 2001 to a male BALB/cByJ via homozygous ovarian transplant, then sibling mating resumed. Homozygotes can be identified soon after birth by an enlarged, pale liver and smaller overall body size. Although the hepatic steatosis resolves to normal at wean age, a neurological phenotype manifests by day 14 as a tremor and an unsteady gait which is most pronounced in the rear legs (Sweet et al. 1988). Both phenotypes stem from improper cellular processing of lipid. fld/fld mice are smaller than their normal littermates by three days of age and remain smaller throughout life. Hair growth is retarded and abnormal resulting in a ruffled, unkempt appearance in the adult. Homozygotes experience increased mortality between 19 and 35 days of age. A ..... | ||
| 003092 | BALB/cNctr-Npc1m1N/J | Repository- Live |
| Mice homozygous for the recessive NIH allele of the Niemann Pick type C1 gene (Npc1m1N) show a dual deficiency of sphingomyelinase and glucocerebrosidase activity. The overall phenotype resembles the sphingomyelinosis condition seen in mice homozygous for the sphingomyelinosis allele (Npc1spm, Stock No. 002760). Sphingomyelinosis mutant mice begin to lose weight and to show tremor and ataxic gait at about 7 weeks of age. Weight loss continues and tremor and ataxia become more severe until death at about 12 to 14 weeks of age. The liver and spleen are also enlarged and Purkinje cells in the cerebellum are severely depleted. Sphingomyelin and free cholesterol are markedly elevated in liver and spleen but not in brain. Sphingomyelinosis closely resembles that of human Niemann-Pick Type C disease patients. | ||
| 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 | ||
| 004824 | BTBR.V(B6)-Lepob/WiscJ | Repository- Live |
| Mice homozygous for the obese spontaneous mutation, (Lepob commonly referred to as ob or ob/ob) exhibit obesity hyperphagia, a diabetes-like syndrome of hyperglycemia, glucose intolerance, elevated plasma insulin, subfertility, impaired wound healing, and an increase in hormone production from both pituitary and adrenal glands. They are also hypometabolic and hypothermic. The obesity is characterized by an increase in both number and size of adipocytes. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase body weight and is probably the result of it. Homozygotes do have an abnormally low threshold for stimulation of pancreatic islet insulin secretion even in very young preobese animals. As is the case with mice carrying the diabetes mutation (Leprdb ..... For more information please see the full phenotype on the strain data sheet | ||
| 004626 | C3H/HeDiSnJ-Vamp1lew/GrsrJ | Repository- Live |
| Mice homozygous for this recessive mutation are recognized by their wasting pre-weaning lethal phenotype, they curl up, waste away and die by 21 days. Mutants do not live to breed but no lesions have been found pathologically. | ||
| 009062 | C57BL/6-Magel2tm1Stw/J | Repository- Live |
| The mouse locus 7qB4/B5 (syntenic with the Prader-Willi region at chromosome position 15q11-q13 in humans) encompasses the cluster of paternally-expressed imprinted genes Magel2, Ndn, Mkrn3, and Peg12. As maternal imprinting silences the Magel2 allele, only the paternally inherited Magel2 allele is expressed. The Magel2-lacZ knock-in allele abolishes endogenous gene function and expresses a β-galactosidase fusion protein. Under control of the upstream promoter/enhancer elements, lacZ expression is directed to the same tissues as the wildtype gene. For example, β-galactosidase expression during embryogenesis is detected in central nervous system (neural tube, forebrain, midbrain and embryonic hypothalamus), peripheral nervous system (dorsal root ganglia and peripheral neurons innervating limb and trunk muscles), and some non-neuronal tissues (genital tubercle, midgut region and placenta). Adult β-galactosidase ..... For more information please see the full phenotype on the strain data sheet | ||
| 001139 | C57BL/6ByJ | Repository- Live |
| 5 SNP differences have been identified that distinguish C57BL/6J from C57BL/6ByJ and C57BL/6NJ. Both C57BL/6ByJ and C57BL/6NJ type as follows: 08-015199792-M is C; 11-004367508-M is A; 13-041017317-M is C; 15-057561875-M is G; 19-049914266-M is T. C57BL/6J types as follows: 08-015199792-M is T; 11-004367508-M is G; 13-041017317-M is T; 15-057561875-M is A; 19-049914266-M is G (Petkov and Wiles, 2005.) | ||
| 000629 | C57BL/6J-Lystbg-J/J | Repository- Live |
| Mice homozygous for the beige-J spontaneous mutation (Lystbg-J) are identical to the original beige mutation (Lystbg). The phenotype closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syn ..... For more information please see the full phenotype on the strain data sheet | ||
| 009345 | C57BL/6J-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 | ||
| 000667 | C57BR/cdJ | Repository- Live |
| C57BR/cdJ mice develop early-onset hearing loss that is moderate at seven weeks of age, is severe by 20 weeks and progresses with increasing age (Henry 1982; Zheng et al. 1999). The loss is greatest in the higher frequency range; at seven weeks, Henry reported 50% of the mice showed no 64 kHz auditory brainstem response (ABR), and by 100 days both the 2 kHz and 32 kHz responses were absent. Both labs found this strain to be least vulnerable to loss of the16 kHz response, which persisted through 200 days but was lost before 300 days of age (Henry 1982). C57BR/cdJ did not exhibit aberrant ABR wave patterns, suggesting that the hearing loss results from defects of the peripheral, rather than central auditory system (Zheng et al. 1999). F1 hybrid progeny from matings with the good-hearing strain CAST/Ei exhibited good hearing even at advanced ages, indicating that the allele(s) responsible for hearing loss in C57BR/cdJ are recessive. An allelism test between C57BR/cdJ and NOD ..... For more information please see the full phenotype on the strain data sheet | ||
| 000669 | C58/J | Repository- Live |
| This strain was developed by MacDowell in 1921 from litter mates 58 and 52 of Miss Lathrop's stock. A mating of the same male but a different female gave rise to the commonly used C57BL group of strains. C58/J mice exhibit a high incidence of leukemia (>90% by one year of age). C58/J mice also exhibit an intermediate susceptibility to developing atherosclerotic aortic lesions (1670 to 1690 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). | ||
| 000926 | CAROLI/EiJ | Repository- Live |
| 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 | ||
| 000657 | CE/J | Repository- Live |
| CE/J mice are very responsive to phytohemagglutinin and resistant to amyloid induction and development of amyloidosis. Amyloidosis is the extracellular deposition of the acute phase protein 'serum amyloid A' (SAA), which is induced in response to inflammation. CE/J mice express a single isoform of SAA designated SAA2.2, which is structurally unable to form amyloid fibrils. Viral expression of amyloidogenic proteins in CE/J mice does result in amyloid depostion, making this a useful model to examine the amyloid deposition potential of altered SAA proteins. Early studies by Dr. Margaret Dickie reported that approximately 1/3 of CE females and of reciprocal DBA x CE F1 hybrids were found to have ovarian tumors at 20 months of age. Virgin reciprocal DBA x CE F1 hybrids were found to develop hyperplasia of the uterus and an increased uterine sensitivity to estrogen that increases with age. This pathology results from a hormonal imbalance characteristic of this F1 cross and breed ..... | ||
| 000351 | CXB1/ByJ | Repository- Live |
| Like BALB/cByJ, this recombinant inbred carries the mutation hippocampal lamination defect or Hld, an allele responsible for abnormal neuronal migration to the pyramidal cell layer (Nowakowski RS, et al, Jnl Neurogen, 1984). | ||
| 000356 | CXB6/ByJ | Repository- Live |
| 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. | ||
| 008311 | FVB.129S2(B6)-Hmox1tm1Poss/J | Repository- Live |
| Mice that are homozygous for this targeted mutation are slightly smaller in size than wildtype littermates and exhibit poor grooming and hypoactivity. As early as 20 weeks of age, homozygotes develop anemia with diminished serum iron and increased serum ferritin. Histological analysis reveals iron accumulation in kidney and liver. Elevated oxidized proteins and lipid peroxidation develop in the liver and kidney. Homozygotes develop progressive chronic inflammatory
disease, including enlarged spleen and lymph nodes, inflammatory infiltrates, glomerulonephritis, fibrosis. Homozygous male mice have smaller testis than wildtype controls. Homozygotes occur at a lower than expected frequency, or are not produced, from heterozygous crosses and have decreased postnatal survival. An almost undetectable abnormal gene product (mRNA) is detected by Northern blot analysis of total splenic RNA. This mutant mouse strain may be useful in studies of hemochromatosis, inflammation and iron meta ..... For more information please see the full phenotype on the strain data sheet | ||
| 006654 | FVB.BKS(D)-Leprdb/ChuaJ | Repository- Live |
| The congenic "FVB-db" strain differs from that previously published on other genetic backgrounds in that it presents a marked obesity/diabetes phenotype intermediate between the severe uncompensated hyperglycemia observed in C57BLKS/J and DBA2/J backgrounds and the mild, compensated syndrome reported on the C57BL/6J and 129/J backgrounds. The literature reports that obese FVB-db mice of both sexes show long-term hyperglycemia primarily due to severe insulin resistance. The hyperglycemia in the fed state persists despite continued extreme hyperinsulinemia correlated with a marked pancreatic cell hypertrophy and hyperplasia. These phenotypes have been replicated in the stock at The Jackson Laboratory. However, the diabetic nephropathy (glomerulosclerosis) reported in the literature was not evident in the stock imported to JAX at the age evaluated (24 weeks).
As the phenotype varies by genetic background, these mutant mice, along with db mutants on other ge ..... | ||
| 000674 | I/LnJ | Repository- Live |
| I/LnJ mice were originally derived by Dr. LC Strong in 1926 from an unpedigreed stock of mice. A high proportion of mice from this strain lack a corpus callosum. This absence is associated with slow growth of the medial septum subadjacent to the cavum septi. I/LnJ mice are resistant to mmtv induced mammary tumor development and generate neutralizing antibodies to mmtv and MuLv virions that effectively block viral transmission. Due to a frameshift mutation in alpha 1 phosphorylase kinase these mice have increased glycogen content in resting skeletal muscle. The reproductive performance of I/LnJ mice is very poor. Further analysis indicates that oocytes from I/LnJ mice display retarded kinetics of meiotic maturation and a high frequency of metaphase I arrest. Some oocytes fail to resume meiosis. Oocytes have many very small centrosomes with an absence of microtubules. I/LnJ mice, in addition to carrying several other coat color alleles, are homozygous for the piebald mutation (Ednrb<> ..... For more information please see the full phenotype on the strain data sheet | ||
| 010498 | ISS.ILS-Lore5ILS/TejJ | Repository- Live |
| This allele of the loss of righting induced by ethanol 5 (Lore5) gene from ILS/TejJ (Inbred Long Sleep) exhibits a 50% increase in the loss of righting response time (LORR)and a decrease in blood ethanol concentration following sedative intraperitoneal ethanol injection on the ISS/TeJ (Inbred Short Sleep) background as compared to the strain ISS/TejJ. This congenic also exhibits an increased ability to maintain body weight under dietary restriction. The congenic interval is believed to include a quantitative trait locus (QTL) for fuel efficiency in response to dietary restriction. This strain may be used to study the genetics of neurogenetic, neuropharmacological, and behavioral phenotypes involved in alcohol-related traits and the genetics of metabolic efficiency. | ||
| 000675 | LG/J | Repository- Live |
| LG/J mice develop antinuclear antibodies and rheumatoid factor as well as renal disease characterized by glomerulonephritis, interstitial nephritis, and perivasculitis (Peng et al., 1996). LG/J was the predominant strain used to develop the MRL/LpJ (Stock No. 000486) inbred strain, a model for autoimmunity. LG/J mice are often compared to SM/J (Stock No. 000687) for quantitative trait locus analysis in the areas of atherosclerosis, obesity, and mandible size . These mice are susceptible to diet-induced obesity and diet-induced atherosclerosis. This strain is among the least responsive to phytohemagglutinin (Heiniger et al., 1975). | ||
| 000677 | MA/MyJ | Repository- Live |
| A characteristic of MA/MyJ is the spontaneous mutation hf (hepatic fusion), which results in varying degrees of fusion in the hepatic lobes. | ||
| 000550 | MOLF/EiJ | Repository- Live |
| A 7 base pair deletion was reported in the Cd4 5' untranslated region of MOLF/EiJ (Wade et al. 1993, Capparelli et al. 2004). Subsequent testing at The Jackson Laboratory indicated that MOLC/EiJ, MOLD/EiJ and MOLG/EiJ also carry the variant sequence. The deletion is not believed to affect gene expression. | ||
| 003925 | MRL.129P2(B6)-B2mtm1Unc/Dcr-Dab1scm-2J/J | Repository- Live |
| See Stock No. 000486 for important information on the MRL/MpJ background. | ||
| 010636 | NOD.Cg-B2mtm1Unc Prkdcscid Il2rgtm1Wjl/SzJ | Repository- Live |
| The NOD.Cg-Prkdcscid B2mtm1Unc Il2rgtm1Wjl/SzJ mice, commonly known as NOD-scid Il2rynull B2m null (NSG-B2m), do not express the Prkdc gene, the X-linked Il2rg gene nor the B2m gene. Triple mutant mice are viable, normal in size and do not display any gross physical or behavioral abnormalities, but can be poor breeders. Mutant mice combine the features of the NOD/ShiLtJ background, the severe combined immune deficiency mutation (scid), IL2 receptor gamma chain deficiency and the MHC class I molecule, beta-2 microglobulin, deficiency and are relatively resistant to graft versus host disease (GVHD). The mean survival time (MST) of NOD-scid Il2rynull B2mnull irradiated with 2 Gy and injected with 5 x 106 human peripheral blood mononuclear cells (PBMC) is 44 days compared to the MST of 21 days in the NOD-scid Il2rynull treated similarly. The bl ..... For more information please see the full phenotype on the strain data sheet | ||
| 012480 | NOD.Cg-Prkdcscid Il2rgtm1Wjl Hprtb-m3/EshJ | Repository- Live |
| Mice that are homozygous/hemizygous for these alleles are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mutant mice combine the following characteristics: NK cell deficiency (NOD/ShiLtJ background), T and B cell deficiency (Prkdcscid), reduced numbers of lymphocytes and myeloid dendritic cells (Il2rgtm1Wjl) and biochemically defective stromal cells (Hprtbm-3). These mice can be used for transplantation of human primary cancers. During tumor growth, Hprt-defective murine fibroblast and stromal cells replace human stromal cells. In culture, the addition of HAT selection media eliminates murine fibroblasts and other stromal cells and facilitates the isolation of human cancer cells. These mice may be used to generate patient-specific low passage cell lines from primary cancers for use in chemosensitivity profiling and other applications. | ||
| 000726 | RBF/DnJ | Repository- Live |
| The RBF inbred strain arose from crosses with wild mice, originally known as "tobacco mouse", captured in Valle di Poschiavo in S.E. Switzerland. The wild mice originally known as 'tobacco mouse' because of the coat colour. The strain was transferred to Dr. M. Davisson (Dn) in 1981 and subsequently to the production colony of The Jackson Laborotory (J). Mice are homozygous for Robertsonian translocation Rb(1.3)1Bnr, Rb(8.12)5Bnr and Rb(9.14)6Bnr. This strain is useful for production of antibody producing hybridomas. | ||
| 000644 | SEA/GnJ | Repository- Live |
| 001146 | SPRET/EiJ | Repository- Live |
| The wild-derived inbred strain SPRET/Ei is often used in crosses with common inbred strains to create highly polymorphic panels for genetic mapping. SPRET/Ei mice are resistant to high doses of tumor necrosis factor alpha (TNFa) (Staelens et al 2002). Mice from a C57BL/6 x SPRET/Ei F1 cross were protected from TNFa-induced arthritis and partially protected against induced allergic asthma (Staelens et al 2004). SPRET/Ei may be useful in understanding certain inflammatory diseases. | ||
| 003810 | STOCK Adrb1tm1Bkk Adrb2tm1Bkk/J | Repository- Live |
| Mice that are homozygous null for the Adrb1 and Adrb2 genes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Stimulation of beta adrenergic receptor function in these mice by agonists or exercise reveals significant impairments in chronotropic range, vascular reactivity and metabolic rate. A severely attenuated chronotropic and hypotensive response is observed after administration of the non-selective beta adrenergic receptor agonist isoproterenol. An abnormal response to epinephrine is also seen, with bradycardia and a monophasic hypertensive blood pressure change being observed rather than the tachycardia and biphasic hypertensive/ hypotensive response seen in wildtype mice. When exercised, heart rates in null mice are lower than that of wild type mice. No difference is noted in the resting heart rate. | ||
| 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 | ||
| 002364 | STOCK Cftrtm1Unc Tg(FABPCFTR)1Jaw/J | Repository- Live |
| These FABP-hCFTR-CFTR bitransgenic mice harbor the FABP-hCFTR transgene (human fatty acid binding protein 1 liver (FABP1) promoter directing expression of a human cystic fibrosis transmembrane conductance regulator (ATP-binding cassette sub-family C, member 7) (CFTR) gene) and a targeted mutation of the cystic fibrosis transmembrane conductance regulator homolog gene (Cftrtm1Unc). Mice homozygous for both the Cftr targeted mutation and the FABP-hCFTR transgene have normal longevity up to nine months (longest time examined). There is correction of ileal goblet cell and crypt cell hyperplasia and cAMP-stimulated chloride secretion. There is little or no expression of the transgene in the lung. This more robust model may be used to assess the effects of the null mutation on the nose and lungs, and may be useful as a mouse model of Cystic Fibrosis.
Of note, colonies maintained at The Jackson Laboratory report poor breeding performance when using ..... | ||
| 009340 | STOCK Eif2ak3tm1Dron/HotaJ | Repository- Live |
| These mice harbor a targeted mutation of the Eif2ak3 (eukaryotic translation initiation factor 2 alpha kinase 3 [also called Perk]) locus that abolishes endogenous gene expression. To date (Feb 2010), the donating investigator has not been able to generate homozygous mice on a C57BL/6J congenic background. The following phenotype describes mice on a mixed albino Swiss Webster;129/SvEv genetic background. Heterozygous mice are viable and fertile. Homozygous (Perk-/-) mice appear runty within a few days of birth and develop a rapid and progressive decline in endocrine and exocrine pancreatic function. This results in a complex pleiotropic phenotype including hyperglycemia, exocrine pancreatic insufficiency, diabetes, growth retardation, inability to breed, and early mortality. The phenotype of the Perk-/- mice is very similar to that observed in humans with Wolcott-Rallison syndrome; the consistent feature of which is severe diabetes mellitus developing in infancy. Heterozygous mi ..... For more information please see the full phenotype on the strain data sheet | ||
| 008755 | STOCK Tg(Ins2-rtTA)2Efr Tg(teto-DTA)1Gfi/J | Repository- Live |
| This strain was generated by breeding Stock No. 008168 and Stock No. 008250 together at The Jackson Laboratory. The resulting double transgenic colony was established as Stock No. 008755. The Ins2-rtTA (or RIP7-rtTA) transgene expresses the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the rat insulin 2 (Ins2) promoter. The tet-DTA (or tetO-DTA) (transgene expresses diphtheria toxin A (DTA) under the control of a tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator) and a cytomegalovirus minimal promoter. Mice harboring both of these transgenes has doxycycline-inducible expression of DTA in pancreatic beta cells; i.e. addition of the tetracycline analogue doxycycline (dox) results in ablation of pancreatic beta cells. | ||
| 000693 | WC/ReJ KitlSl/J | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing ..... For more information please see the full phenotype on the strain data sheet | ||
| 003423 | BXSB.129P2(B6)-B2mtm1Unc/Dcr | Research Strain |
| BXSB mice develop spontaneous autoimmune disease characterized by moderate lymph node and spleen enlargement, hemolytic anemia, hypergammaglobulinemia, and immune complex glomerulonephritis. The disease process in BXSB is strikingly accelerated in males, which live little more than a third as long as females. The acceleration is due to the presence of the Yaa gene on the Y chromosome. Characteristics of mice homozygous for the B2mtm1Unc targeted mutation include a lack of MHC class I protein expression on the cell surface. There are few CD8+ cytotoxic T-cells and under some circumstances a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+ T-cells are severely deficient providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93: ..... For more information please see the full phenotype on the strain data sheet | ||
| 002485 | 129-Alox5tm1Fun/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Alox5tm1Fun targeted mutation are viable and fertile. In general, homozygous mutant mice are selectively resistant to inflammatory insults. They are resistant to the lethal effects of platelet activating factor but reaction to endotoxin shock is normal. Phorbol ester induced inflammation is normal but arachidonic acid induced inflammation is reduced. Commonly referred to as 5-LO. | ||
| 002484 | 129-Alpltm1Sor/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the Alpltm1Sor targeted mutation appear normal and viable. Homozygous mutant mice are perinatal lethals but can be rescued by pyridoxal treatment. Surviving homozygotes develop epilepsy due to reduced GABA levels in the brain. Bone formation does not appear to be grossly affected in untreated animals, but treated animals exhibit cranial dysmorphology. The targeting vector contained both a b-galalactosidase and a neomycin genes (beta-geo), both of which are under the control of the Alpl promoter and are thus expressed in a tissue specific manner. Specifically, expression occurs in developing bones and in primordial germ cells (PGC), and the beta-galactosidase thus serves as a marker for these tissues. The marker for PGC's is particularly significant because the current marker (alkaline phosphatase staining) is only useful to study early germ cell migration. | ||
| 002387 | 129-Asgr2tm1Her/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Asgr2tm1Her targeted mutation are viable and have no obvious phenotype. There is no detectable ASGR2 expression and a pronounced reduction in ASGR1 expression. Expression of Asgr1 mRNA is not affected. Homozygous mutant mice are unable to clear 125I labeled asialoorosmomucoid. Plasma desialylated glycoprotein levels are not increased. The plasma lipoprotein protein profile level of mice deficient in both LDLR and ASGR2 does not differ from the LDLR deficient strain arguing against a major role of ASGR in lipoprotein metabolism. | ||
| 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 | ||
| 005063 | 129-Hfetm1.1Nca/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable and fertile. These mice carry the "C282Y" mutant Hfe allele, which encodes a tyrosine to cysteine amino acid substitution at codon 282. Expression of the missense mutation is detected by RT-PCR analysis. Homozygotes exhibit hemochromatosis, accumulating hepatic iron postnatally. These mice have a phenotype that is intermediate between wildtype mice and mice that are homozygous for the null allele, Hfetm2Nca. This mutant mouse strain may be useful in studies of hereditary hemochromatosis. | ||
| 004446 | 129-Lta4htm1Bhk/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected in isolated bone marrow cells. No final product of the reaction catalyzed by the targeted gene product enzyme is detected in peritoneal lavage fluids from mice with experimental peritonitis. Acute inflammatory reaction induced by topical arachidonic acid application to the inner surface of the ear produces a reduced vascular and cellular response in homozygous mice. Edema formation, as assessed by weight of ear biopsies, and protein extravasation into the inflamed tissue is diminished. Neutrophil infiltrate and myeloperoxidase activity is significantly decreased. Inflammatory response to zymosan-A induced peritonitis is characterized by reduced polymorphonuclear neutrophil infiltration into the peritoneal cavity. Homozygous mice are resistant to platelet-activating factor induced systemic shock. This ..... For more information please see the full phenotype on the strain data sheet | ||
| 005966 | 129-Prdx6tm1Pgn/Pgn | Cryopreserved - Ready for recovery |
| 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 | ||
| 002910 | 129/Sv-Cyp2e1tm1Gonz/J | Cryopreserved - Ready for recovery |
| 000709 | 129P3/J-Leprdb-3J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the diabetes 3J spontaneous mutation (Leprdb-3J) become identifiably obese around three to four weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at four to eight weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. Homozygous mutant mice on the 129P3/J background exhibit severe obesity but the diabetes phenotype is much reduced. | ||
| 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. | ||
| 008077 | 129S1/Sv-Bchetm1Loc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this BChE mutant allele are viable and fertile with no reported spontaneous abnormalities. All tissues and plasma from homozygous mice are devoid of BChE activity. As BChE (butyrylcholinesterase) is a bioscavenger molecule protecting acetylcholinesterase (AChE) activity against nerve agents and organophosphates, homozygous BChE-deficiency leads to impaired protection from toxic compounds. These BChE mutant mice are a model for human butyrylcholinesterase deficiency and may be useful for studying metabolic effects of organophosphorus toxicants or nerve agents, neurotransmitter function, and anti-Alzheimer's drug therapies.
Of note, the donating investigator has multiple strains available that may be useful for testing toxic compounds, including the AChE-deficient (Stock No. 005987), G117H BChE transgenic (Stock No. 007577), and BChE-deficient (see Stock ..... | ||
| 004302 | 129S1/Sv-Hprttm1(cre)Mnn/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable and fertile. This is a Cre-deleter induced mutation strain on a 129S1 background. A Cre expression cassette was inserted into the X-linked Hprt gene. When male mice carrying a neomycin selection cassette flanked by loxP sites are mated to female mice heterozygous for this targeted mutation, the cassette is excised without detectable mosaicism, irrespective of cre inheritance. Heterozygous female mice have sufficient Cre recombinase in their oocytes to excise floxed sequence at the zygote or early cleavage stage. | ||
| 005358 | 129S6/SvEvTac-Car3tm1Gkim/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted allele are viable, fertile, normal in size and life span and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected. Histological examination of tissues discerns no anomalies. Similarly, gas chromatography-mass spectrometry analysis of the fatty-acid distribution in serum, muscle, liver, and fat reveal no differences between mutant and wildtype mice. When exposed to an atmosphere of 100% oxygen homozygous mice display similar mean survival times as wildtype (~ 70 hours). The contractile properties of soleus muscle derived from mutant mice exhibit some differences from wildtype mice. Mutant mice display shorter relaxation and half-relaxation times for single and tetanic twitches and a minor reduction tetanic force. Microarray analysis detects an increase (~30%) in carbonic anhydrase 13 expression. | ||
| 001425 | A/J-Esdc-mJ/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 000649 | AU/SsJ | Cryopreserved - Ready for recovery |
| 002454 | B10.129P2(B6)-B2mtm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the B2mtm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8+ cytotoxic T-cells and under some circumstances a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+T-cells are severely deficient providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). 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 exact expression pattern of the allele could vary from that originally described. We will modify the strain description if ne ..... For more information please see the full phenotype on the strain data sheet | ||
| 000507 | B6 x B6EiC3 a/A-Otcspf/J | Cryopreserved - Ready for recovery |
| 002533 | B6 x BALB/cByJ-Lpin1fld/J | Cryopreserved - Ready for recovery |
| 002048 | B6 x C57BLKS-Dock7m Leprdb Myo15sh2-J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the shaker 2 Jackson spontaneous mutation (Myo15sh2-J) are viable and fertile, showing only a slight reduction in both compared to wild-type mice. The shaker 2 Jackson remutation is not visibly different from the original shaker 2 (Myo15sh2, Stock No. 000109). Homozygous mutant mice of both alleles display a phenotype very similar to the behavior and pathology to shaker-1 (Myo7ash1) with the exception that the abnormalities are observed a little earlier in shaker 2 mice. This strain is also carrying the misty (Dock7m) and diabetes (Leprdb) spontaneous mutations. | ||
| 002543 | B6 x IDH2/EiJ | Cryopreserved - Ready for recovery |
| 006963 | B6(101)-Mdh1am1H/LvtJ | Cryopreserved - Ready for recovery |
| Homozygotes die at approximately embryonic day 17.5 (E17.5), but heterozygotes are viable and fertile. Homozygous embryos are nearly colorless, are approximately half the size of heterozygous and wildtype littermates, and show altered or delayed brain/body development. There may be a vascular defect. Decreased expression of this gene has previously been implicated with cases of schizophrenia. | ||
| 006564 | B6(C)-KitW-41J Gusbmps/BrkJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. In appearance, homozygous KitW-41J mice are mostly white with black eyes and brown or grey spots. They are fertile, distinct from mice with other alleles of Kit, and have the impaired hemopoiesis causing mild, normochromic, macrocytic anemia. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They ..... For more information please see the full phenotype on the strain data sheet | ||
| 008149 | B6(Cg)-Snord116tm1.1Uta/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Snord116del (1-loxP or knockout) allele are viable and fertile. As the Snord116 gene cluster is imprinted and expressed only from the paternal allele, mice with paternal inheritance of the deletion lack expression of the targeted Snord116 small nucleolar RNAs (snoRNAs) gene cluster in brain tissues. Similarly, paternal transmission of the mutant allele is required to obtain the mutant phenotype in offspring. Affected heterozygotes (paternal deleted/maternal wildtype) recapitulate a subset of Prader-Willi syndrome (PWS) characteristics, including early-onset postnatal growth retardation, delayed sexual maturation, increased anxiety, motor learning deficit and hyperphagia (but not obesity). Other reported abnormalities include altered metabolic fuel usage, prolonged meal time, and increased levels of circulating ghrelin. These Snord116del mice may be useful in studying growth and feeding regulation, mechanisms of obesity, and pa ..... For more information please see the full phenotype on the strain data sheet | ||
| 002920 | B6(D2N).Spretus-Ahrb-3/J | Cryopreserved - Ready for recovery |
| 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 | ||
| 002831 | B6.129-Ahrtm1Bra/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation are viable. Homozygotes do not respond to aryl-hydrocarbon receptor agonists. They show reduced liver weight (25% decrease) delayed extramedullary hematopoiesis, and transient hepatic microvesicular steatosis. | ||
| 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. | ||
| 003178 | B6.129-Arnttm1Mcs/J | Cryopreserved - Ready for recovery |
| Arnt-/- embryonic stem cells fail to activate genes that normally respond to low oxygen tension. They also fail to respond to a decrease in glucose concentration, indicating that ARNT is crucial in the response to hypoxia and to hypoglycaemia. Arnt-/- embryos were not viable past embryonic day 10.5 and showed defective angiogenesis of the yolk sac and branchial arches, stunted development and embryo wasting. The defect in blood vessel formation in Arnt-/- yolk sacs is similar to the angiogenic abnormalities reported for mice deficient in vascular endothelial growth factor or tissue factor. | ||
| 003079 | B6.129-Calb1tm1Mpin/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Calb1tm1Mpin targeted mutation are viable and fertile. Homozygous mutant mice show severe impairment in tests of motor coordination and exhibit ataxia when challenged on a runway. These results suggest functional deficits in cerebellar pathways. Confocal calcium imaging of cerebellar Purkinje cells reveals marked changes of synaptically-evoked postsynaptic calcium transients. | ||
| 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 | ||
| 004068 | B6.129-Iduatm1Clk/J | Cryopreserved - Ready for recovery |
| At birth, mice that are homozygous null for the Idua gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No alpha-L-iduronidase enzyme activity or mRNA is detected. By three weeks of age, homozygous null mice develop a flattened facial profile and a thickening of digits. Defective bone formation is noticeable by fifteen weeks, characterized by a broadening and thickening of long bones. Evidence of lysosomal storage disorder is apparent in cells of the reticuloendothelial system at four weeks. By eight weeks progressive evidence of lysosomal storage is seen in Kupffer cells, splenic sinusoidal lining cells, chondrocytes, glial and Purkinje cells. This animal model is suitable for use in studies investigating the lysosomal storage disorder mucopolysaccharidosis type I (MPS I). | ||
| 005819 | B6.129-Insl5tm1Dgen/J | Cryopreserved - Ready for recovery |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 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. | ||
| 005974 | B6.129-Prdx6tm1Pgn/Pgn | Cryopreserved - Ready for recovery |
| 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. | ||
| 010725 | B6.129-Ugt1tm1Rhtu/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation exhibit very high serum levels of unconjugated bilirubin (UCB) and die within the first two weeks of birth. Newborn mice appear jaundiced within 8 hours of birth. Although UCB levels are 50-60% higher than controls, homozygous mice do not exhibit liver or kidney damage. This mutant mouse strain may be useful as a model of Crigler-Najjar Type 1 Disease. | ||
| 003533 | B6.129P-B2mtm1Unc-rs2J/J | Cryopreserved - Ready for recovery |
| 003461 | B6.129P2(C)-Thratm1Ven/J | Cryopreserved - Ready for recovery |
| The Thra gene encodes the T3 receptor TRa1 (alpha 1) and a non-T3 bindng product TRa2 (alpha 2), generated by alternative splicing in the C-terminal region. This Thra mutant is deleted for the T3 receptor TRa1 (ALPHA ONE) but retains TRa2. These mutants have an average heart rate 20% lower than that of control animals, prolonged QTend and QRS durations, body temperatures 0.5 degrees C lower than that of control animals. A mild hypothyrodism is present but is restricted to males. | ||
| 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 | ||
| 002362 | B6.129P2-Camk2atm1Sva/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Camk2atm1Sva targeted mutation are viable but are reported not to breed. Homozygous mutant mice show no obvious anatomical defects in the nervous system. Postsynaptic mechanisms are intact, but long-term hippocampal potentiation (LTP), an electrophysiological manifestation of increased synapse strength, is deficient. These mutant mice show specific impairment in spatial learning, indicating that LTP is important to spatial though not necessarily to non-spatial memory. In a more recent study heterozygotes displayed normal offensive aggression. Heterozygotes exhibit a decreased fear response and an increase in defensive aggression. Homozygotes (in which both copies of the gene are absent) exhibit more pronounced behavior suggesting a gene dosage effect. | ||
| 002853 | B6.129P2-Cbstm1Unc/J | Cryopreserved - Ready for recovery |
| The phenotype of cystathionine-beta synthase deficient mice on the C57BL/6J background has not been characterized. Homozygous mice on the mixed B6,129 background suffer from severe growth retardation and a majority of them are dead by 5 weeks of age. Histological examination showed that the hepatocytes of homozygotes were enlarged, multinucleated, and filled with microvesicular lipid droplets. Plasma homocysteine levels of the homozygotes were approximately 40 times normal. Homozygotes may be used as a model for severe homocysteinemia. Heterozygous mutants have an approximately 50% reduction in cystathionine beta-synthase mRNA and enzyme activity in the liver and have twice normal plasma homocysteine levels. Thus, the heterozygous mutants are promising for studying the in vivo role of elevated levels of homocysteine in the etiology of cardiovascular diseases. | ||
| 002196 | B6.129P2-Cftrtm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Cftrtm1Unc mutation survive approximately 28 days. Death of the homozygotes is usually due to intestinal obstruction (ileum or large intestine). Pancreatic involvement has been found in some animals. A recent report (Kent, et.al.) has found that this mutation on a C57BL/6J genetic background does cause lung disease. | ||
| 005801 | B6.129P2-Esrratm1Dgen/J | Cryopreserved - Ready for recovery |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 003812 | B6.129P2-Hfetm1Gfn/J | Cryopreserved - Ready for recovery |
| At birth, mice homozygous null for the Hfe gene are viable, normal in size and do not display any gross physical or behavioral abnormalities. Adult mice are fertile. Full-length Hfe transcripts are not detected in either liver or kidney tissue. A poorly expressed, alternate transcript resulting from a direct splicing event between exons 1 and 4 is detected. At twelve weeks of age, a significant elevation in plasma and hepatic iron concentration is evident as is an increase in levels of saturated transferrin. Excess iron stores may be the result of enhanced duodenal iron absorbtion. This strain represents a viable animal model of human hemochromatosis. | ||
| 002171 | B6.129P2-Hprtb-m3/J | Cryopreserved - Ready for recovery |
| HPRT-embryonic stem cells were obtained by selecting for spontaneous mutation by incubation in medium containing 6-thioguanine. HPRT-males have no overt phenotype of abnormal behavior. The mutation is due to a large deletion in the Hprt gene. Mutant mice have no HPRT detectable by Western blot analysis and no detectable HPRT enzyme activity in brain homogenates. They appear to have normal brain purine content, but de novo purine synthesis is accelerated four- to fivefold. The Hprtb-m3 mutation has been used in preimplantation studies to determine when the maternal and paternal alleles of Hprt are activated during early embryonic development. Either administration of amphetamine or inhibition of adenine phosphoribosyltransferase (APRT) activity stimulates locomotor and stereotypic behaviors in HPRT-deficient mice. However, the null mutant for both Hprt and Aprt does not show the characteristics of Lesch-Nyhan disease. | ||
| 005769 | B6.129P2-Htr7tm1Dgen/J | Cryopreserved - Ready for recovery |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005823 | B6.129P2-Lrp5tm1Dgen/J | Cryopreserved - Ready for recovery |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 007620 | B6.129P2-Mrc1tm1Mnz/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. Mice are defective in clearing proteins that bear accessible mannose and N-acetylglucosamine residues and have elevated levels of eight different lysosomal hydrolases. Clearance of a subset of mannose-bearing serum glycoproteins that are normally elevated during inflammation is impaired. Expression is abolished as shown by immunoblot of lymph node lysates. EGFP expression has not been assessed. This strain may be useful in studies of serum glycoprotein homeostasis. | ||
| 005826 | B6.129P2-Ntsr1tm1Dgen/J | Cryopreserved - Ready for recovery |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 002829 | B6.129P2-Plaurtm1Jld/J | Cryopreserved - Ready for recovery |
| Homozygous mice are born and survive to adulthood with no overt phenotypic abnormalities. No Plaur gene product (protein) is detected. In addition, activated peritoneal macrophages collected from homozygous mice fail to promote plasminogen activation in vitro. The loss of the receptor also results in a redistribution of uPA in some tissues but has no impact on pro-PLAU activation in the urogenital tract. Thus, in the absence of other challenging factors such as infection, injury, or other functional deficits, PLAUR deficiency does not compromise fertility, development, or hemostasis. These mice provide a means to test the proposed function of PLAU/PLAUR in wound repair, atherogenesis, and tumor cell invasion in vivo. | ||
| 005828 | B6.129P2-Ppardtm1Dgen/J | Cryopreserved - Ready for recovery |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 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 | ||
| 008087 | B6.129S1-Bchetm1Loc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this BChE mutant allele are viable and fertile with no reported spontaneous abnormalities. All tissues and plasma from homozygous mice are devoid of BChE activity. As BChE (butyrylcholinesterase) is a bioscavenger molecule protecting acetylcholinesterase (AChE) activity against nerve agents and organophosphates, homozygous BChE-deficiency leads to impaired protection from toxic compounds. These BChE mutant mice are a model for human butyrylcholinesterase deficiency and may be useful for studying metabolic effects of organophosphorus toxicants or nerve agents, neurotransmitter function, and anti-Alzheimer's drug therapies.
Of note, the donating investigator has multiple strains available that may be useful for testing toxic compounds, including the AChE-deficient (Stock No. 005987), G117H BChE transgenic (Stock No. 007577), and BChE-deficient (see Stock ..... | ||
| 012768 | B6.129S1-Gnai2tm1.1Rneu/J | Cryopreserved - Ready for recovery |
| A G184S point mutation was created in the Gnai2 (guanine nucleotide binding protein (G protein), alpha inhibiting 2; also called Gαi2) gene which disrupts interactions with regulator of G protein signaling (RGS) proteins that normally deactivate Gα G protein signals. A complex phenotype affecting multiple organ systems (heart, myeloid, skeletal, and central nervous system) can be observed. Homozygous mice and their cardiocytes exhibit enhanced muscarinic (M2) but not adenosine (A1) receptor-mediated responses. Isoproterenol-stimulated beating rates of heterozygous and homozygous hearts are significantly more sensitive to inhibition to carbachol than are those of wildtype mice.
Homozygous mice show slightly reduced adiposity. Unlike females, males placed on a high-fat diet are resistant to weight gain and have decreased body fat as compared to wildtype mice. Both males and females exhibit enhanced insulin sensitivity (protected f ..... | ||
| 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. | ||
| 002509 | B6.129S2-Plautm1Mlg/J | Cryopreserved - Ready for recovery |
| Homozygotes develop normally, have a normal life span, and are poor breeders. Pups often need fostering. Rectal prolapse of a non-infectious origin develops in 9% of homozygotes and/or extensive non-healing ulcerations occur at the eyelids and around the face. Small, focal fibrin deposits are occasionally seen in the intestines and in the sinusoids of the liver, and excessive fibrin deposits are seen in ulcerated skin or prolapsed rectum. Pulmonary clot lysis is comparable to that seen in normal wildtype siblings. Endotoxin induced venous thrombosis is increased over normal wildtype siblings. Fibrin dissolution by PLAU-deficient macrophages is greatly reduced but macrophage invasion into the peritoneal cavity after thioglycollate injection is unaffected. Homozygous knockout mice have increased levels of Abeta42 and Abeta40 in plasma. Brain Abeta levels are not significantly different than controls. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 003322 | B6.129S4-Soat1tm1Far/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Soat1tm1 targeted mutation display tissue specific decreases in cholesterol esterification. Fibroblasts and adrenal membranes of homozygous mutant mice show diminished cholesterol esterification and markedly reduced cholesterol ester levels in adrenal glands and peritoneal macrophages. However, the livers of SOAT1-deficient mice contained substantial amounts of cholesterol esters and exhibited no reduction in cholesterol esterification activity. These findings support the presence of more than one form of esterification enzyme in mammals. A second sterol O-acyltransferase gene (Soat2), expressed in the liver and intestine, has subsequently been identified in mice and humans. | ||
| 007147 | B6.129S4-Soat1tm1Far/Pgn | Cryopreserved - Ready for recovery |
| Phenotypically similar to B6.129S4-Soat1tm1Far/J (003322), B6.129S4-Soat1tm1Far/Pgn has a reduced congenic interval making the closely linked Apoa2 gene of C57BL/6 rather than 129S4 origin. The donating investigator indicates that HDL levels exhibit a 24% increase on high fat diet in this strain in contrast to the 73% increase observed in the original strain. Triglyceride levels are unchanged. This strain may be useful in atherosclerosis research. | ||
| 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 | ||
| 002515 | B6.129S6-Cftrtm1Kth/J | Cryopreserved - Ready for recovery |
| The Cftrtm1Kth targeted mutation corresponds to the delta 508 mutation in humans. Homozygous mutant mice show an increased mortality within the first month after birth, with ~60% mortality by post-weaning. Those that survive are fertile, but females are poor breeders. Mutant mice are also reduced in size compared to normal wildtype mice. Those that do not survive to adulthood show bowel obstructions, bowel strictures and peritonitis. Lungs, pancreas, gall bladder, male reproductive tract, lacrimal gland, and submandibular glands from homozygous mice appear normal regardless of the survival of the animal. Homozygous mice also show a tissue-specific loss of CFTR transcripts in the intestine. | ||
| 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 ..... | ||
| 002741 | B6.129S7-Alpltm1Sor/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the Alpltm1Sor targeted mutation appear normal and viable. Homozygous mutant mice are perinatal lethals but can be rescued by pyridoxal treatment. Surviving homozygotes develop epilepsy due to reduced GABA levels in the brain. Bone formation does not appear to be grossly affected in untreated animals, but treated animals exhibit cranial dysmorphology. The targeting vector contained both a b-galalactosidase and a neomycin genes (beta-geo), both of which are under the control of the Alpl promoter and are thus expressed in a tissue specific manner. Specifically, expression occurs in developing bones and in primordial germ cells (PGC), and the beta-galactosidase thus serves as a marker for these tissues. The marker for PGC's is particularly significant because the current marker (alkaline phosphatase staining) is only useful to study early germ cell migration. | ||
| 003881 | B6.129S7-Sod1tm1Leb/DnJ | Cryopreserved - Ready for recovery |
| 005643 | B6.129X-Gusbtm1Sly/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable but have reduced neonatal survival. Homozygotes are infertile, but fertility can be restored with enzyme replacement therapy. No residual enzyme activity is observed. Homozygous mice are indistinguishable from heterozygous and wild type mice at birth, but show distinct growth retardation, shortened extremities, and facial dysmorphism observable at wean and increasing in severity with age. Long bones of the lower extremities are shortened, broad, and sclerotic. Compared to wild-type, this model has increased urinary glycosaminoglycan and secondary elevation of other lysosomal storage enzymes. Further, homozygous mice show abundant lysosomal storage in liver, kidney, leptomeningeal cells, cornea, spleen, neurons, and retinal pigment epithelium. The phenotype exhibited by this mutant mouse strain is more severe than that observed in a similarly constructed mutant (Stock No. 005644) which bears a L175F point ..... For more information please see the full phenotype on the strain data sheet | ||
| 005644 | B6.129X-Gusbtm3Sly/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable but infertile. Fertility can be restored with enzyme replacement therapy. Less than 1% residual enzyme activity is observed. Homozygous mice are indistinguishable from wild type mice at birth, but show distinct growth retardation, shortened extremities, and facial dysmorphism observable at three months with a moderate increase in severity with age. Long bones of the lower extremities are shortened, broad, and sclerotic. Compared to wild-type, this model has increased urinary glycosaminoglycan and secondary elevation of other lysosomal storage enzymes. Further, homozygous mice show abundant lysosomal storage in liver, kidney, leptomeningeal cells, cornea, and retinal pigment epithelium. The phenotype exhibited by this mutant mouse strain is less severe than that observed in a similarly constructed mutant (Stock No. 005643) which bears a E536A point mutation. This strain represents a model of human GUS def ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 009365 | B6.129X1-Mark2tm1Hpw/J | Cryopreserved - Ready for recovery |
| Homozygous targeted mice show and increased metabolic rate, decreased adiposity, resistance to high fat diet-induced weight gain, and insulin hypersensitivity. Western blot analysis demonstrates that expression is eliminated in brain, spleen, kidney and liver, lymph nodes, thymus, white and brown adipose tissues, large and small intestines, stomach. Homozygous pups are born slightly below predicted Mendelian ratios and show both embryonic and postnatal growth retardation as well as increased mortality as compared to wildtype animals. The age of death can range from 3 weeks to several months. Approximately 85% of homozygotes exhibit some combination of immunological disorders between the ages of 5 and 12 months. B and T cell development is normal, but CD4+ T cells lacking this protein exhibit a marked upregulation of the memory marker CD44 and produce more gamma interferon and interleukin 4 on stimulation through the T cell receptor in vitro. B cell responses to T ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 006559 | B6.C-H2-Kbm1/ByBir-Gusbmps/BrkJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Gusbmps allele exhibit skeletal dysplasia as well as cognitive, hearing and visual deficits. Lifespan of the homozygotes is approximately six months. Homozygotes lack the lysomal enzyme, beta-glucoronidase, and, as a result, glycosaminoglycans accumulate in tissues throughout the body. Female homozygotes rarely conceive and do not lactate. This strain is a model for the human lysomal storage disease, mucopolysaccharidosis type VII. | ||
| 000256 | B6.C-H2-Kbm1/ByBir-Gusbmps/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Gusbmps allele exhibit skeletal dysplasia as well as cognitive, hearing and visual deficits. Lifespan of the homozygotes is approximately six months. Homozygotes lack the lysomal enzyme, beta-glucoronidase, and, as a result, glycosaminoglycans accumulate in tissues throughout the body. Female homozygotes rarely conceive and do not lactate. This strain is a model for the human lysomal storage disease, mucopolysaccharidosis type VII. | ||
| 000136 | B6.C-H34c/(HW22)ByJ | Cryopreserved - Ready for recovery |
| 006557 | B6.C3-Gusbmps-2J/BrkJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Gusmps-2J allele exhibit a phenotype similar to Gusmps homozygotes including skeletal deformities, lysosomal storage disease and elevated levels of the lysosomal enzymes alpha-galactosidase and beta-hexosaminidase (Gwynn et al., 1998). Like the Gusmps heterozygote, Gusmps-2J heterozygotes have a 26-85% reduction in beta-glucuronidase activity. depending on tissue type (Gwynn et al., 1998, Birkenmeier et al., 1989). Homozygotes of both alleles have beta-glucuronidase activity levels at 1% of the control level. Unlike the Gusmps homozygote, Gusmps-2J homozygotes on the C3H background live longer, are fertile and can raise litters to weaning age (Gwynn et al., 1998). In addition to a difference in the nature of the mutations between these two alleles, it is also likely that the phenotypic differences are the result of strain background. C3H/HeOuJ mice carry a ..... For more information please see the full phenotype on the strain data sheet | ||
| 000204 | B6.C3Rl-Lystbg/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the beige spontaneous mutation (Lystbg) are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syngeneic tumor cells grow better in beige mice than in l ..... For more information please see the full phenotype on the strain data sheet | ||
| 006562 | B6.CBy(Cg)-Gusbmps Gpi1a-m1J/BrkJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage diseases. | ||
| 000535 | B6.Cg-Atp7aMo-blo/J | Cryopreserved - Ready for recovery |
| Female mice heterozygous for the blotchy alleles (Atp7aMo-blo) are viable and fertile. They have irregular patches of light-colored fur. Hemizygous males and homozygous females have reduced viability and many are infertile. Hemizygotes and homozygotes are light all over with no blotching, are usually small, and occasionally have deformed hindlegs. Most hemizygotes and homozygotes have defective elastin in the aorta and usually die with aortic aneurysm. Hemizygous males have enlarged air spaces in the lung (emphysema), probably because of defective elastin and collagen. Skin collagen and aortic elastin have defective crosslinking at the step at which lysine residues are converted to aldehydes. Hemizygous males have a deficiency of noradrenalin in the brain, probably because a deficiency of copper shown to exist in the brain causes defective activity of the enzyme dopamine-beta-hydroxylase. Copper absorption from the gut and hepatic copper concentration are reduced to 6 ..... For more information please see the full phenotype on the strain data sheet | ||
| 001381 | B6.Cg-Atp7aMo-pew2J/J | Cryopreserved - Ready for recovery |
| 000053 | B6.Cg-Atp7aMo-to/J | Cryopreserved - Ready for recovery |
| 000699 | B6.Cg-Dock7m Leprdb/+ +/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) become identifiably obese around 3 to 4 weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at 4 to 8 weeks. Affected mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. On the C57BL/6 background there is compensatory hyperplasia of the islet B-cells, and continued hyperinsulinemia throughout an 18- to 20-month life span. Wound healing is delayed, and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Leprdb/+) also have increased metabolic efficiency, and can survive a prolonged fast longer than controls. Experiments involving destruction of the ventromedial nucleus of the hypothalamus suggest that Leprdb may cause a defect in the hypothalamus. Steroid sulfotransferase enzymes, aberrantly expressed in diabe ..... For more information please see the full phenotype on the strain data sheet | ||
| 006407 | B6.Cg-Gusbmps/BrkJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. These mice have the H2b haplotype typical of inbred C57BL/6 mice. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage diseases. | ||
| 002086 | B6.Cg-Gusbmps Tg(Gussx)1Wat/J | Cryopreserved - Ready for recovery |
| Androgen induction of Gus is faster but lower in M. saxicola than in Mus musculus. However, growth hormone induces Gus upregulation in Mus musculus but has no affect on Gus induction in Mus saxicola. When transferred to a Mus musculus background in the absence of endogenous Gus the Mus saxicola derived Gus (Gussx) also showed no growth hormone enhancement of induction supporting the idea that an evolutionary change in regulatory sequence underlies this variation in response. These mice do not exhibit the phenotypic characteristics of Gusmps homozygotes indicating rescue by Gussx. (Niermann and Watson, 1999; Paigen 1989.) | ||
| 006558 | B6.Cg-H2-Kbm1 Tg(GUSB)4Sly/SndsJ | Cryopreserved - Ready for recovery |
| Mice that are homozygous for this transgene and the Gusbmps allele have approximately 20-fold higher beta-glucuronidase enzyme activity than wildtype controls. Distribution of human enzyme activity throughout various tissues mimics the endogenous mouse enzyme activity pattern. Of note, mice homozygous for both the transgene and the Gusbmps allele do not exhibit an accumulation of undegraded glycosaminoglycans. These transgenic mice do not carry the Gusbmps allele. Mice that are hemizygous for this transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of lysomal storage diseases and mucopolysaccharidosis VII (Sly syndrome). | ||
| 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. | ||
| 000827 | B6.Cg-Pgk1a/J | Cryopreserved - Ready for recovery |
| 000571 | B6.Cg-Whrnwi Tyrp1b/+ +/J | Cryopreserved - Ready for recovery |
| At 9 to 10 days of age Whrnwi homozygotes display increased activity, decreased ability to right their selves, and are generally smaller than unaffected siblings. By 14 to 16 days of age homozygotes display head bobbing, circling, and an unsteady gate. Adults display head tossing and circling behavior and deafness is indicated by 20 days of age. Sackler and Weltman reported the average number of circles by a prodded 12-week old female homozygote to be 407 in 10 minutes. They found female homozygotes to have an increased metabolic rate and adrenocorticosteroid activity and decreased body weights. Homozygous males were reported to have decreased blood glucose and liver glycogen levels, decreased white blood cell and eosinophil counts, increased plasma albumin levels, and decreased globulin levels, in addition to decreased weight and increased food intake. (Lane 1963; Sackler and Weltman 1967, 1970, 1971.)
While the organ of Corti in whirler homozygotes shows normal ..... | ||
| 010901 | B6.Cg-Tg(ACTA1-Il15)10941Lsq/J | Cryopreserved - Ready for recovery |
| In both mouse and human, the interleukin-15 (Il15) gene encodes two IL-15 mRNA variants that utilize different signal sequences but produce identical mature IL-15 proteins following signal peptide cleavage. The long signal peptide IL-15 (LSP-IL-15) isoform is inefficiently secreted from cells, whereas the short signal peptide (SSP)-IL-15 isoform is not secreted and localization is intracellular. Mice hemizygous for the HSA-natLSP-IL15 transgene are viable and fertile, with overexpression of the inefficiently secreted native LSP-IL-15 mRNA and protein directed to skeletal muscle tissue by the human α-skeletal actin (HSA or ACTA1) promoter. Compared to wildtype littermates, IL-15 mRNA/protein expression in skeletal muscle is approximately 300-fold/400-fold greater in hemizygous males (and approximately 100-fold/400-fold greater in hemizygous females), respectively. No overexpression of IL-15 protein is detectable in the serum of hemizygous males or females. These HS ..... For more information please see the full phenotype on the strain data sheet | ||
| 011002 | B6.Cg-Tg(ACTA1-Il15*)11650Lsq/J | Cryopreserved - Ready for recovery |
| In both mouse and human, the interleukin-15 (Il15) gene encodes two IL-15 mRNA variants that utilize different signal sequences but produce identical mature IL-15 proteins following signal peptide cleavage. The long signal peptide IL-15 (LSP-IL-15) isoform is inefficiently secreted from cells, whereas the short signal peptide (SSP)-IL-15 isoform is not secreted and localization is intracellular. Mice hemizygous for the HSA-IL2SP-IL15 transgene are viable and fertile, with overexpression of the IL2SP-IL15 mRNA and protein directed to skeletal muscle tissue by the human α-skeletal actin (HSA or ACTA1) promoter. Compared to wildtype littermates, IL-15 mRNA/protein expression in skeletal muscle is approximately 1000-fold greater in hemizygous males (and approximately 800-fold/1000-fold greater in hemizygous females, respectively). Because the native IL-15 LSP is replaced with the IL-2 signal peptide, efficient secretion of mature IL-15 leads to overexpression in the ..... For more information please see the full phenotype on the strain data sheet | ||
| 012379 | B6.Cg-Tg(Ckm-Ppara)HEDpk/J | Cryopreserved - Ready for recovery |
| This transgenic strain expresses mouse Ppara (peroxisome proliferator activated receptor alpha) cDNA carrying a C-terminal FLAG tag under the control of the mouse Ckm (creatine kinase, muscle) promoter. Expression levels in this "high expression" (HE) line are increased approximately 100-fold over endogenous levels. Highest expression is found in fast-twitch muscle and less expression occurs in heart and soleus. Hemizygotes develop glucose intolerance (as early as 6 weeks of age) and insulin resistance despite being protected from diet-induced obesity. This strain may be useful in studies of diabetes, obesity, and muscle lipotoxicity. | ||
| 008221 | B6.Cg-Tg(IGFBP1)2Miel/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the hIGFBP-1 transgene are viable and fertile with no reported gross morphological or developmental changes. The hIGFBP-1 transgene encompasses the entire human IGFBP-1 structural gene and its regulatory sequences, allowing transgene expression of IGFBP-1 to remain responsive to normal hormonal regulation. Transgenic mice overexpress hIGFBP-1, with hIGFBP-1 mRNA expression in a tissue-specific fashion more similar to the human pattern than the murine pattern. Fasting transgenic mice have elevated total serum IGFBP-1 levels that fluctuate according to nutritional status (as they do in humans), and exhibit postprandial hyperinsulinemia with preservation of normal glucocompetence and insulin sensitivity. Transgenic mice also have significantly greater hyperinsulinemic response to glucose challenge and cardiovascular abnormalities in response to carbohydrate load and vasoconstrictors. Transgenic mice exhibit fasting hyperglycemia and hyperinsulinemia and glucose intoler ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 002298 | B6.Cg-Tg(SOD1)2Gur/J | Cryopreserved - Ready for recovery |
| This transgenic strain carries the normal allele of the human SOD1 gene. Originally published as N1029, it expresses the same SOD1 protein level as the transgenic strain carrying the SOD1*G93A transgene (002726), even though the copy number in the SOD1*G93A transgenic is higher. This strain serves as a control for the B6.Cg-Tg(SOD1*G93A)dl1Gur/J mutant strain (Stock No. 002299). | ||
| 002299 | B6.Cg-Tg(SOD1*G93A)dl1Gur/J | Cryopreserved - Ready for recovery |
| Mice carrying the transgene exhibit paralysis resulting in a reduced life expectancy. They serve as a model for human amyotrophic lateral sclerosis (ALS). The transgene carries a variant of the human Superoxide dismutase-1 gene (glycine to alanine at position 93). Paralysis is due to loss of motor neurons from the spinal cord. The onset of the ALS phenotype is delayed compared to the original high copy number strain (SOD1*G93A)1Gur, Stock No. 002726) because of a reduction in transgenic copy number. This reduction most likely occurred during the importation and establishment of the original high copy number mutant transgenic strain. Mice on the B6SJL background (Stock No. 002300) become paralyzed in one or more limbs beginning around six to seven months of age. Life expectancy is normally four to six weeks beyond onset of symptoms. The transgene was backcrossed to C57BL/6J 5 ..... For more information please see the full phenotype on the strain data sheet | ||
| 001623 | B6.D2-Car2n/J | Cryopreserved - Ready for recovery |
| In human, CAR2 deficiencies can result in osteopetrosis, renal tubular acidosis, impaired growth, cerebral calcification, and mental retardation. Mice homozygous for Car2<n> do not display cerebral calcification or osteopetrosis, although medial calcification of small arteries has been found in several organs, most notably the male genital tract. The phenotype of these mice includes renal tubular acidosis, doubled urine output, increased urine pH and Cl-, decreased blood pH and HCO-3, phosphatemia, lower plasma bicarbonate, and a smaller body size. Despite smaller body weight, the kidneys are of normal size and plasma potassium and creatinine levels are normal. Type A and B intercalated cells of the kidney are severely depleted. Car2n homozygotes have reduced susceptibility to audiogenic and chemogenic seizures and hippocampal slices from homozygotes are more resistant to hypoxia than are those of wild type controls. Increase ..... For more information please see the full phenotype on the strain data sheet | ||
| 008222 | B6.FVB-Tg(IGFBP2)1Miel/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the IGFBP-2 transgene are viable and fertile with no reported gross morphological or developmental changes. Transgenic mice overexpress human IGFBP-2 (hIGFBP-2), with hIGFBP-2 mRNA detected in a variety of organs and tissues, including adipose tissue. Overexpression of hIGFBP-2 is associated with reduced susceptibility to obesity and improved insulin sensitivity; transgenic mice are protected from glucose intolerance and increased blood pressure with age, and are also resistant to obesity and insulin resistance on a high fat diet. The phenotype of hIGFBP-2 overexpressing mice may vary between male and female mice. These IGFBP-2 transgenic mice may be useful in studying metabolic homeostasis, adipocyte biology, and the role of insulin-like growth factor binding protein in protecting against obesity- and age-associated complications (such as hypertension and diabetes).
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alle ..... | ||
| 003063 | B6.NOD-(D6Mit54-D6Mit14)/J | Cryopreserved - Ready for recovery |
| This strain is congenic for a 24 cM segment of Chr 6 extending from D6Mit54through D6Mit14that includes the insulin dependent diabetes susceptibility locus Idd6.The name given this segment in the primary reference is c6. Upon histologic examination of the pancreas, the incidence and severity of periinsulitis (perivascular, periductal and/or periislet infiltration by mononuclear cells) of B6.NOD-(D6Mit54-D6Mit14) mice were found to be similar to those of C57BL/6 controls. | ||
| 001372 | B6.PERU-Sordb/J | Cryopreserved - Ready for recovery |
| 001371 | B6.SW-Ldr1b Gsrb/J | Cryopreserved - Ready for recovery |
| 002727 | B6;129-Ahrtm1Bra/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Ahrtm1Bra targeted mutation are viable and fertile. Homozygotes do not respond to aryl-hydrocarbon receptor agonists. They show reduced liver weight (25% decrease) delayed extramedullary hematopoiesis, and transient hepatic microvesicular steatosis. | ||
| 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. | ||
| 004154 | B6;129-Gaatm1Rabn/J | Cryopreserved - Ready for recovery |
| At birth, mice that are homozygous for the targeted allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. Low levels of transcript are detectable, but functional protein is absent. By 3 weeks of age, light microscopy (PAS staining) reveals a progressive accumulation of lysosomal glycogen in heart and skeletal muscle, and diaphragm. Concomitant with accumulating glycogen is a significant reduction in the number of myofibrils and signs of damaged muscle structure. Reduced mobility and progressive muscle weakness is observed by 3-4 weeks of age. By 8-9 months of age, muscle wasting and weakness are obvious. Adults are fertile. These mice recapitulate key features of glycogen storage disease type II (GSDII) and provide a model for studying the underlying mechanism of GSDII. | ||
| 012625 | B6;129-Glatm1Kul wblo/GrsrJ | Cryopreserved - Ready for recovery |
| Mice both homozygous for the wblo mutation and homozygous or hemizyogus for the Glatm1Kul mutation develop a wobbly gait by approximately 5 weeks of age that decreases in severity with age. | ||
| 003535 | B6;129-Glatm1Kul/J | Cryopreserved - Ready for recovery |
| This knockout is a model for Fabry disease, an X-linked inherited metabolic disorder that is caused by a deficiency of alpha-galactosidase A. In Fabry disease, deposition of glycosphingolipids with alpha-galactosyl terminal moieties causes renal failure, myocardial infarctions, and strokes. | ||
| 003138 | B6;129-Hprttm1Detl/J | Cryopreserved - Ready for recovery |
| Mutant mice develop a phenotype similar to the human translated CAG repeat disorders showing a late onset neurological phenotype. Mice have handling-induced seizures, weight gain, reduced vertical activity, clasping response, impaired performance on the rotarod task, and premature death. Mice subjected to frequent handling have a median age of death of 45 weeks. There is the presence of neuronal intranuclear inclusions containing at least part of the polyglutamine-containing HPRT protein and ubiquitin. These results indicate that expanded CAG repeats need not be located within one of the classic repeat disorder genes to have a neurotoxic effect. Note that the size of the CAG repeat may not be stable and any reduction in repeat size may lead to a later onset phenotype. | ||
| 002963 | B6;129-Pcsk2tm1Dfs/J | Cryopreserved - Ready for recovery |
| 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 | ||
| 005323 | B6;129P2 Pemttm1J-tnyw/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the tiny wasting mutation are runted and some have abnormal locomotion or are unable to right themselves. Mutants can be identified by 2 weeks of age and most die by 3 weeks of age. All have vacuoles in the brain. | ||
| 002070 | B6;129P2-B2mtm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the B2mtm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8+ cytotoxic T-cells and under some circumstances a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+T-cells are severely deficient providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). 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 ..... For more information please see the full phenotype on the strain data sheet | ||
| 002461 | B6;129P2-Cbstm1Unc/J | Cryopreserved - Ready for recovery |
| Mice deficient in cystathionine-beta synthase suffer from severe growth retardation and a majority of them are dead by 5 weeks of age. Histological examination showed that the hepatocytes of homozygotes were enlarged, multinucleated, and filled with microvesicular lipid droplets. Plasma homocysteine levels of the homozygotes were approximately 40 times normal. Homozygotes may be used as a model for severe homocysteinemia. Heterozygous mutants have an approximately 50% reduction in cystathionine beta-synthase mRNA and enzyme activity in the liver and have twice normal plasma homocysteine levels. Thus, the heterozygous mutants are promising for studying the in vivo role of elevated levels of homocysteine in the etiology of cardiovascular diseases. | ||
| 008333 | B6;129P2-Dldtm1Ptl/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the Dld (dihydrolipoamide dehydrogenase or E3 component) targeted mutation are viable and fertile. Heterozygous mice exhibit approximately half of wild-type enzymatic activity levels for E3 and all affected mitochondrial multienzyme complexes. Heterozygotes (on a C57BL/6;129P2 genetic background) exhibit increased vulnerability to treatments with MPTP (dopaminergic neurotoxin used to induce Parkinson's disease-like lesions), malonate (inhibitor of cellular respiration used to mimic Huntington's disease features), and 3-NP (mitochondrial toxin used to mimic Huntington's disease features). Homozygous mice exhibit normal development and metabolism during the preimplantation period, explained by the persistence of E3 enzyme from the oocyte. Homozygotes exhibit developmental delays shortly after implantation (7.5 to 8.5 days postcoitum (dpc)) and cease development within the subsequent two days. These Dld mutant mice may be useful to study early murine em ..... For more information please see the full phenotype on the strain data sheet | ||
| 003187 | B6;129P2-Pemttm1J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Pemttm1J are viable and fertile. Pemt encodes an enzyme that converts phosphatidylethanolamine to phosphatidylcholine. Homozygotes completely lack PEMT activity and are no longer able to catalyze this reaction. Homozygotes are indistinguishable from controls in terms of development, behavior, and fecundity. Hepatocyte morphology, plasma lipid levels, and bile composition are normal. However, feeding homozygotes a choline deficient (CD) diet causes rapid onset of a severe liver pathology. Mice lose weight, develop grossly enlarged and pale colored livers, develop bright yellow plasma, and their gall bladders become engorged. In addition, a 50% decrease in liver phosphatidylcholine concentration and greater than 90% decrease in plasma triacylglyceride and cholesterol levels is observed in homozygotes on the CD-deficient diet. | ||
| 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. | ||
| 004858 | B6;129S1-Tshrtm1Rmar/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation exhibit delayed eye opening, are runted by day 21, and will die within 1 week if weaned at day 21. Homozygotes will survive by extending weaning to 28 days but will not reproduce. Homozygotes are viable and fertile when weaned at day 21 and subsequently placed on a hormone replacement therapy diet consisting of a 100ppm desiccated thyroid powder supplement. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis of thyroid membranes. Enhanced Green Fluorescent Protein (EGFP) gene product is detected by RT-PCR and Western blot analysis of thyroid tissue. Hypothyroidism is exhibited by mutant mice that have a longer weaning period and a non-supplemented diet, as indicated by low T4 and T3 serum levels, and high thyrotropin (TSH) serum levels. Treatment with exogenous TSH does not result in a thyroid hormone release response. Mutant mice produce uniodinated thyroglobulin and do not accumulate radioactive iodide in ..... For more information please see the full phenotype on the strain data sheet | ||
| 002263 | B6;129S2-Alox5tm1Fun/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Alox5tm1Fun targeted mutation are viable and fertile. In general, homozygous mutant mice are selectively resistant to inflammatory insults. They are resistant to the lethal effects of platelet activating factor but reaction to endotoxin shock is normal. Phorbol ester induced inflammation is normal but arachidonic acid induced inflammation is reduced. Commonly referred to as 5-LO. | ||
| 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. | ||
| 002367 | B6;129S4-Hexatm1Rlp/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Hexatm1Rlp targeted mutation are viable and fertile. GM2 ganglioside accumulates in the central nervous system of homozygous mice and the neuropathology is similar to that of Tay-Sachs patients with the exception that not all neurons are affected in the mouse as in human beings. No neuronal storage was found in the cerebellum, the anterior horn of the spinal cord or the spinal ganglia. Only minor storage was present in the posterior horn of the spinal cord. There are no abnormal neurologic signs in homozygous mice by 5 months of age. | ||
| 002914 | B6;129S4-Hexbtm1Rlp/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Hexbtm1Rlp targeted mutation develop motor defects beginning at about 3 months of age. The defects progressively worsen and homozygous mice die by 4.5 months of age. Mice display gangliosidosis; mice abnormally accumulate GM2 and GA2 ganglioside and serve as a model of Sandhoff disease. | ||
| 002896 | B6;129S4-Soat1tm1Far/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Soat1tm1 targeted mutation display tissue specific decreases in cholesterol esterification. Fibroblasts and adrenal membranes of homozygous mutant mice show diminished cholesterol esterification and markedly reduced cholesterol ester levels in adrenal glands and peritoneal macrophages. However, the livers of SOAT1-deficient mice contained substantial amounts of cholesterol esters and exhibited no reduction in cholesterol esterification activity. These findings support the presence of more than one form of esterification enzyme in mammals. A second sterol O-acyltransferase gene (Soat2), expressed in the liver and intestine, has subsequently been identified in mice and humans. | ||
| 005937 | B6;129S4-Ucp3tm1Lowl/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable and fertile and do not express full length mRNA in skeletal muscle and brown adipose tissue. In skeletal muscle mitochondria, endogenous protein was undetectable. Skeletal muscle mitochondria from homozygous mice show decreased state 4 respiration. Further, skeletal muscle, but not liver, mitochondria produce more superoxide anions and reactive oxygen species both in vitro (lucigenin-derived chemiluminescence) and in vivo (aconitase activity). Skeletal muscle ATP synthesis under fasting conditions is approximately 4-fold greater in mutant mice. This mouse may be useful in studies of energy metabolism, thermogenesis, aerobic respiration (including mitochondrial respiration coupling), and age-related progressive deterioration of fatty acid homeostasis. | ||
| 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. | ||
| 002317 | B6;129S7-Alpltm1Sor/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the Alpltm1Sor targeted mutation appear normal and viable. Homozygous mutant mice are perinatal lethals but can be rescued by pyridoxal treatment. Surviving homozygotes develop epilepsy due to reduced GABA levels in the brain. Bone formation does not appear to be grossly affected in untreated animals, but treated animals exhibit cranial dysmorphology. The targeting vector contained both a b-galalactosidase and a neomycin genes (beta-geo), both of which are under the control of the Alpl promoter and are thus expressed in a tissue specific manner. Specifically, expression occurs in developing bones and in primordial germ cells (PGC), and the beta-galactosidase thus serves as a marker for these tissues. The marker for PGC's is particularly significant because the current marker (alkaline phosphatase staining) is only useful to study early germ cell migration. | ||
| 002361 | B6;129S7-Asgr2tm1Her/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Asgr2tm1Her targeted mutation are viable and have no obvious phenotype. There is no detectable ASGR2 expression and a pronounced reduction in ASGR1 expression. Expression of Asgr1 mRNA is not affected. Homozygous mutant mice are unable to clear 125I labeled asialoorosmomucoid. Plasma desialylated glycoprotein levels are not increased. The plasma lipoprotein protein profile level of mice deficient in both LDLR and ASGR2 does not differ from the LDLR deficient strain arguing against a major role of ASGR in lipoprotein metabolism. | ||
| 002189 | B6;129S7-Ass1tm1Bay/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Ass1tm1Bay mutation stop gaining weight at about 10 hours after birth and usually die prior to 24 hours after birth. They have a plasma ammonia concentration of 2670 microM, 16 times greater than normal siblings. There is a significantly higher plasma concentration of citrulline and decreased level of arginine. This corresponds to the human disease. There is an overall 2 to 4 fold increase in the plasma levels of almost all amino acids, an effect not found in the human disease. Heterozygous mice are healthy and develop normally. They do, however, have a 2-fold increase in the plasma citrulline level over that seen in normal siblings. | ||
| 002751 | B6;129S7-Cyp7a1tm1Rus/J | Cryopreserved - Ready for recovery |
| Heterozygous carriers of the disrupted Cyp7a1 gene are phenotypically normal, viable, and fertile. Homozygous animals appear normal at birth but most die within the first 18 days of life. The 10-15% of homozygotes that survive are fertile. Newborn animals with a homozygous mutation in the Cyp7a1 gene lack bile acids, causing fat malabsorption as manifest by severe steatorrhea (fatty stools), deficiency of fat-soluble vitamins, and wasting due to malnutrition. Approximately 40% of the homozygotes die between postnatal days 1-4; 45% between days 11-18. Vitamin supplements given to nursing mothers can prevent deaths during the early period; cholic acid supplements in the mother's diet can prevent deaths in the later period. Mutant pups born to homozygous mothers not maintained on dietary supplements are noticeably smaller than age-matched heterozygous and wild type siblings. The skin of nursing homozygotes can be dry and scaly in appearance. Nursing heterozygous and homozygo ..... For more information please see the full phenotype on the strain data sheet | ||
| 002793 | B6;129S7-Srd5a1tm1Mahe/J | Cryopreserved - Ready for recovery |
| 002223 | B6;129S7-Uoxtm1Bay/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this mutation are viable and fertile although about 65% of homozygous mice die by 4 weeks of age unless maintained on allopurinol. Homozygous mice show severe hyperuricemia and urate nephropathy. | ||
| 004728 | B6;129X1-Prdx6tm1Pgn/Pgn | Cryopreserved - Ready for recovery |
| 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. | ||
| 000785 | B6;D2-a Ces1ce/EiJ | Cryopreserved - Ready for recovery |
| Mice homozygous for Ces1ce are viable and fertile and exhibit no apparent defect. Ces1ce was discovered in a screen of progeny of triethylenemelamine (TEM) treated male mice for mutations at specific loci, but appears to have pre-existed in the male. The screen employed analysis of blood and kidney homogenates by "standard starch gel electrophoresis techniques" and focused on enzymes known to differ in electrophoretic mobility between the parental strains (DBA/2J and C57BL/6J). Ces1ce was initially thought to be a null allele, but characterization of homozygous F2 mice demonstrated presence of a faint band migrating between those of the parental strains, which was not perceived in the presence of either parental band. Thus, Ces1ce was shown to be a hypomorphic electrophoretic variant (Soares 1979). | ||
| 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. | ||
| 000829 | B6BALB Pgm1c/Pgm1a/J or Pgm1c/Pgm1b/J | Cryopreserved - Ready for recovery |
| 000604 | B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J | Cryopreserved - Ready for recovery |
| 000624 | B6C3Fe a/a-anx/J | Cryopreserved - Ready for recovery |
| Compared with their wildtype siblings, anx/anx homozygotes are characterized by a thinning in the neck and tail at 5 days of age, lower body weight detectable by 9 days of age, and death by 22 days of age on the B6C3H-a/a background. Outbreeding to CAST/Ei modifies the phenotype such that homozygotes live to approximately 5 weeks of age. Evaluation of stomach content shows that anx/anx mice ingest less than their siblings. They show headweaving, body tremors, uncoordinated gait, and hyperactivity along with diminished adipose tissue and reduced serum leptin levels. (Maltais et al., 1984; Johansen et al., 2000)
Intraperitoneal injection of 20 day old pups with 5,7-dihydroxytryptamine, a seratonin antagonist, reduces the severity of the neurological phenotypes. Homozygotes have extensive serotonergic hyperinnervation in normal target fields including the hippocampus, frontal cortex, olfactory bulb, and cerebellum, yet they have normal catecholamine ..... | ||
| 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. | ||
| 000909 | B6CBy-Gpi1a/Gpi1b/J or Gpi1a-m1/Gpi1b/J | Cryopreserved - Ready for recovery |
| 002044 | B6Ei.Cg-Atp7aMo-blo/J | Cryopreserved - Ready for recovery |
| Female mice heterozygous for the blotchy alleles (Atp7aMo-blo) are viable and fertile. They have irregular patches of light-colored fur. Hemizygous males and homozygous females have reduced viability and many are infertile. Hemizygotes and homozygotes are light all over with no blotching, are usually small, and occasionally have deformed hindlegs.. Most hemizygotes and homozygotes have defective elastin in the aorta and usually die with aortic aneurysm. Hemizygous males have enlarged air spaces in the lung (emphysema), probably because of defective elastin and collagen. Skin collagen and aortic elastin have defective crosslinking at the step at which lysine residues are converted to aldehydes. Hemizygous males have a deficiency of noradrenalin in the brain, probably because a deficiency of copper shown to exist in the brain causes defective activity of the enzyme dopamine-beta-hydroxylase. Copper absorption from the gut and hepatic copper concentration are reduced to ..... For more information please see the full phenotype on the strain data sheet | ||
| 001811 | B6EiC3Sn a/A-Otcspf-ash/J | Cryopreserved - Ready for recovery |
| 002343 | B6EiC3Sn a/A-Otcspf/J | Cryopreserved - Ready for recovery |
| 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 ..... | ||
| 002300 | B6SJL-Tg(SOD1*G93A)dl1Gur/J | Cryopreserved - Ready for recovery |
| Mice carrying the transgene exhibit paralysis resulting in a reduced life expectancy. They serve as a model for human amyotrophic lateral sclerosis (ALS). The transgene carries a variant of the human Superoxide dismutase-1 gene (glycine to alanine at position 93). Paralysis is due to loss of motor neurons from the spinal cord. The onset of the ALS phenotype is delayed compared to the original high copy number strain (SOD1*G93A)1Gur, Stock No. 002726) because of a reduction in transgenic copy number. This reduction most likely occurred during the importation and establishment of the original high copy number mutant transgenic strain. Mice become paralyzed in one or more limbs beginning around six to seven months of age. Life expectancy is normally four to six weeks beyond onset of symptoms. | ||
| 002840 | B6SJL-Tg(SREBP1a)7343Reh/J | Cryopreserved - Ready for recovery |
| 000652 | BDP/J | Cryopreserved - Ready for recovery |
| 000700 | BKS.Cg-Dock7m Leprdb/+ +/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the diabetes spontaneous mutation (Leprdb) become identifiably obese around three to four weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at four to eight weeks. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. A number of features are observed on the C57BLKS background, including an uncontrolled rise in blood sugar, severe depletion of the insulin-producing beta-cells of the pancreatic islets, and death by 10 months of age. Exogenous insulin fails to control blood glucose levels and gluconeogenic enzyme activity increases. Peripheral neuropathy and myocardial disease are seen in C57BLKS Leprdb homozygotes. Wound healing is delayed and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Leprdb/+) also have increased metabolic ..... For more information please see the full phenotype on the strain data sheet | ||
| 001192 | BKS.Cg-meaJ Leprdb +/+ + Dock7m/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the meander tail-J spontaneous mutation (meaJ) have variably shortened and kinked tails. At about two weeks an unsteadiness of gait, often amounting to a tremor, appears. Homozygous mutant mice are smaller and less vigorous than wild-type controls but are fertile. The anterior lobe of the cerebellum is disorganized. Purkinje cells are scattered, some cellular layers never form, and Bergmann glial processes are absent. The cytoarchitecture of the posterior lobe is normal, and the transition from normal to disorganized areas is sharply demarcated. This mutation occurred in the BKS.Cg-Leprdb +/+ Dock7m strain so it is also segregating for the diabetes (Leprdb) and misty (Dock7m) mutations. See strain description for Stock No. 000642 for more information. | ||
| 000696 | BKS.V-Lepob/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the obese spontaneous mutation (Lepob, commonly referred to as ob or ob/ob) are first recognizable at about 4 weeks old. Homozygous mutant mice increase in weight rapidly and may reach three times the normal weight of wildtype controls. In addition to obesity, mutant mice exhibit hyperphagia; a diabetes-like syndrome of hyperglycemia, glucose intolerance, and elevated plasma insulin; subfertility; and increased hormone production from both pituitary and adrenal. They are also hypometabolic and hypothermic. The obesity is characterized by both an increased number and size of adipocytes. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase body weight and is probably the result of it. Homozygotes do have an abnormally low threshold for stimulati ..... For more information please see the full phenotype on the strain data sheet | ||
| 002391 | BKSChpLt.HRS-Cpefat/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the fat spontaneous mutation (Cpefat) on a C57BLKS/J genetic background (N10) have a diabetes phenotype that is primarily restricted to males and is more severe than what is seen on the original HRS/J or C57BLKS/J (N5) genetic backgrounds. At weaning both males and female homozygous mutant mice were significantly lighter than wildtype or heterozygous littermates. Obesity develops between 6 and 8 weeks of age and mutant mice can be distinguished from wildtype littermates between 8 and 12 weeks of age. By 18 weeks fat mutant mice will reach 45-55 g and may reach 60-70 g by 6 months of age. Thus, the obesity is thus slower to develop than in the obese (Lepob) and diabetes (Leprdb) mutant mice. The excess adiposity is distributed throughout the body's fat stores, in contrast to the largely axial and inguinal fat deposition of the obese and diabetes mutant mice. Hyperinsulinemia is severe by 4 weeks of age and contin ..... For more information please see the full phenotype on the strain data sheet | ||
| 002232 | BTBR-Pahenu2/J | Cryopreserved - Ready for recovery |
| Homozygous mutant mice show severe hyperphenylalanemia. They are hypopigmented unless maintained on a low phenylalanine diet. Females are fertile but do not rear their young when maintained on a standard mouse diet. The coat color of the background strain, BTBR +T tf/tf, is black and tan (at/at). This strain is also homozygous for the gene tufted (tf/tf) resulting in various molting patterns in the mouse coat. These effects, limited to the mouse coat, may make the mice appear malformed. | ||
| 002231 | BTBR.Cg-Pahenu1/J | Cryopreserved - Ready for recovery |
| Homozygous mutant mice show a delay in the clearing of a load of phenylalanine. | ||
| 002449 | BXSB.129P2(B6)-B2mtm1Unc/J | Cryopreserved - Ready for recovery |
| BXSB mice develop spontaneous autoimmune disease characterized by moderate lymph node and spleen enlargement, hemolytic anemia, hypergammaglobulinemia, and immune complex glomerulonephritis. The disease process in BXSB is strikingly accelerated in males, which live little more than a third as long as females. The acceleration is due to the presence of the Yaa gene on the Y chromosome. Characteristics of mice homozygous for the B2mtm1Unc targeted mutation include a lack of MHC class I protein expression on the cell surface. There are few CD8+ cytotoxic T-cells and under some circumstances a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+ T-cells are severely deficient providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93: ..... For more information please see the full phenotype on the strain data sheet | ||
| 002420 | C.129P2(B6)-B2mtm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the B2mtm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8+ cytotoxic T-cells and under some circumstances a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+ T-cells are severely deficient providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Other traits of B2M deficient mice include: NK cells deficiency, NK1+ T cells deficiency and decreased levels of serum Ig. Some forms of lupis autoimmunity are severely reduced. (Christianson, J Immunol 156:4932-9, 1996). Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from ..... For more information please see the full phenotype on the strain data sheet | ||
| 002328 | C.129S2-Plautm1Mlg/J | Cryopreserved - Ready for recovery |
| Homozygotes develop normally, are fertile and have a normal life span. Rectal prolapse of a non-infectious origin develops in 9% of homozygotes and/or extensive non-healing ulcerations occur at the eyelids and around the face. Small, focal fibrin deposits are occasionally seen in the intestines and in the sinusoids of the liver, and excessive fibrin deposits are seen in ulcerated skin or prolapsed rectum. Pulmonary clot lysis is comparable to that seen in normal wildtype siblings. Endotoxin induced venous thrombosis is increased over normal wildtype siblings. Fibrin dissolution by PLAU-deficient macrophages is greatly reduced but macrophage invasion into the peritoneal cavity after thioglycollate injection is unaffected. Homozygous knockout mice have increased levels of Abeta42 and Abeta40 in plasma. Brain Abeta levels are not significantly different than controls. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 ..... | ||
| 004040 | C3.129P2(B6)-B2mtm1Unc/Dcr | Cryopreserved - Ready for recovery |
| Mice homozygous for the B2mtm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD4- CD8+ cytotoxic T-cells and under some circumstances there is a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+T-cells are severely deficient, providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds. | ||
| 002439 | C3.129P2(B6)-B2mtm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the B2mtm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8+ cytotoxic T-cells and under some circumstances a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+T-cells are severely deficient providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). 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 ..... For more information please see the full phenotype on the strain data sheet | ||
| 000509 | C3.Cg-Lystbg-2J/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the beige 2J spontaneous mutation (Lystbg-2J) display characteristics very similar to the original beige mutation (Lystbg). The mouse phenotype closely resembles Chediak-Higashi syndrome in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to a ..... For more information please see the full phenotype on the strain data sheet | ||
| 001906 | C3Ga.Cg-Catb/J | Cryopreserved - Ready for recovery |
| 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 | ||
| 003525 | C3H/HeOuJ-Gusbmps-2J/BrkJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Gusmps-2J allele exhibit a phenotype similar to Gusmps homozygotes including skeletal deformities, lysosomal storage disease and elevated levels of the lysosomal enzymes alpha-galactosidase and beta-hexosaminidase (Gwynn et al., 1998). Like the Gusmps heterozygote, Gusmps-2J heterozygotes have a 26-85% reduction in beta-glucuronidase activity. depending on tissue type (Gwynn et al., 1998, Birkenmeier et al., 1989). Homozygotes of both alleles have beta-glucuronidase activity levels at 1% of the control level. Unlike the Gusmps homozygote, Gusmps-2J homozygotes live longer, are fertile and can raise litters to weaning age (Gwynn et al., 1998). In addition to a difference in the nature of the mutations between these two alleles, it is also likely that the phenotypic differences are the result of strain background. C3H/HeOuJ mice carry ..... For more information please see the full phenotype on the strain data sheet | ||
| 001576 | C3HeB/FeJ-Atp7btx-J/J | Cryopreserved - Ready for recovery |
| 002566 | C57BL/6-Atp7aMo-br/J | Cryopreserved - Ready for recovery |
| Heterozygous females carrying the brindled allele (Atp7aMo-br) are very similar to mottled heterozygous females (Atp7aMo/+) in appearance but have normal viability. They have curly vibrissae, but the coat is not noticeably waved. Hemizygous males are almost devoid of pigment except in the eyes and ears. The vibrissae are strongly curled, and the coat is wavy. Males usually die by two weeks of age, but a few have lived and been fertile. They have a behavioral abnormality consisting of a slight tremor, uncoordinated gait, and clasping of the hindfeet when held up by the tail. Histological examination of the brain of brindled males shows widespread neuronal degeneration in the cerebral cortex and thalamic nuclei and scattered degeneration in the cerebellum. Heterozygous females have been shown to have neurochemical abnormalities as well. In contrast to mice bearing other Atp7a alleles, brindled mice have no aortic lesions and no defect in crossli ..... 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. | ||
| 008231 | C57BL/6-Tg(Ckm-Ppargc1a)31Brsp/J | Cryopreserved - Ready for recovery |
| These transgenic mice express mouse peroxisome proliferative activated receptor, gamma, coactivator 1 alpha under the direction of the mouse muscle creatine kinase promoter. Transgene expression is specific to skeletal muscle. The increased levels of the transgene product induces expression of energy and mitochondrial oxidative metabolism genes such as cytochrome c oxidase II and IV. Muscle fibers from transgenic mice exhibit a more type II oxidative phenotype than wildtype mice. Isolated extensor digitorum longus muscle from transgenic mice exhibit increased fatigue resistance when compared to wildtype. Muscle fiber diameter loss in response to denervation and fasting is less severe in transgenic animals when compared to controls. Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of muscle physiology and disease, exercise and oxidative capacity, ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 002628 | C57BL/6-Tg(SOD1)10Cje/J | Cryopreserved - Ready for recovery |
| Transgenic mice are viable and express human SOD1. Transgenic mice express three times the normal level of SOD1 in the blood, brain, and fibroblasts. Homozygote males for the Tg(SOD1)10Cje transgene are sterile; homozygote females for the Tg(SOD1)10Cje transgene are fertile. Described in the literature as 218/10 denoting that the transgene insertion site maps to Chr 10. | ||
| 002629 | C57BL/6-Tg(SOD1)3Cje/J | Cryopreserved - Ready for recovery |
| Transgenic mice are viable and express human SOD1. Transgenic mice express three times the normal level of SOD1 in the blood, brain, and fibroblasts. Homozygotes for the Tg(SOD1)3Cje transgene are fertile. Described in the literature as 218/3 denoting that the transgene insertion site is maps to Chr 3 (Shi, et al., 1994). Of the two lines (the other being C57BL/6-Tg(SOD1)10Cje/J, Stock No. 002628), this is the most widely used. | ||
| 003333 | C57BL/6-Tg(TF-CAT)48Gsa/J | Cryopreserved - Ready for recovery |
| Transferrin is regulated by iron at the level of translation. This transgenic strain carries a chimeric gene composed of the human TF 5'-flanking sequences fused to the CAT reporter gene. Iron administration to transgenic mice results in a significant decrease of transferrin-directed CAT enzyme activity and CAT protein in the liver. This strain is useful for understanding the expression of the human TF gene and its age-related regulation. During aging, expression of the transgene decreases in the liver, but not in the brain, and liver expression is suppressed by iron and lipopolysaccharide. | ||
| 000663 | C57BL/6By | Cryopreserved - Ready for recovery |
| 005598 | C57BL/6J-Arsbm1J/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Arsbm1J mutation have a combination of delayed muscle and nerve degeneration along with a skeletal phenotype consisting of a shortened snout, wide-set eyes and shortened limbs that becomes more noticeable with age. Mutants can be poor breeders yielding small litters. Of 10 litters the average number of pups was 3.9. | ||
| 001672 | C57BL/6J-Otcspf-J/J | Cryopreserved - Ready for recovery |
| 006699 | C57BL/6J-Pcsk1N222D/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this ENU-induced "Pc1N222D" mutation are viable and fertile, although the donating investigator reports that homozygous breeders have diminished reproductive performance. Unlike mice homozygous for the traditional knockout allele, Pc1N222D homozygotes are not runted. Homozygous mice exhibit obesity, abnormal proinsulin processing and multiple endocrinological defects. Increased energy intake and a more efficient metabolism contribute to the obesity. Defective proinsulin processing leads to glucose intolerance, but neither insulin resistance nor diabetes develop despite obesity. Obesity is associated with impaired autocatalytic and neuropeptide processing. These mutant mice are a model of human PC1 deficiency, and may be useful in studying obesity, fat metabolism, propeptide processing, and neuroendocrinology. | ||
| 000219 | C57BL/6J-Slc30a4lm/J | Cryopreserved - Ready for recovery |
| Female mice homozygous for the lethal milk mutation (Slc30a4lm, formerly Znt4lm) produce milk that is lethal to mice nursed during the first week of life and detrimental to mice nursed thereafter. The lethal and detrimental effects are due to a deficiency of zinc in the milk. If foster nursed on normal dams, lethal milk homozygotes survive and become reproductively mature. Zinc supplementation of the drinking water of dams enables them to nurse their young successfully. All homozygous mutant mice lack utricular otoliths and this defect is not prevented by zinc supplementation. They have varying loss of saccular otoliths and show mild behavioral abnormalities related to the otolith defect. Homozygotes over eight months of age show progressive hair loss, dermatitis, and skin lesions, symptoms of zinc deficiency. | ||
| 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. | ||
| 002760 | C57BLKS/J-Npc1spm/J | Cryopreserved - Ready for recovery |
| The sphingomyelinosis mutation (Npc1spm) arose in the C57BLKS inbred strain. Homozygous mutant mice begin to lose weight and to show tremor and ataxic gait at about 7 weeks of age. Weight loss continues and tremor and ataxia become more severe until death at about 12 to 14 weeks of age. The liver and spleen are also enlarged and Purkinje cells in the cerebellum are severely depleted. Sphingomyelin and free cholesterol are markedly elevated in liver and spleen but not in brain. Sphingomyelinosis closely resembles that of human Niemann-Pick Type C disease patients. A dual deficiency of sphingomyelinase and glucocerebrosidase activity has been described in BALB/c mice (npc1N) with resemblance to the sphingomyelinosis condition. | ||
| 000707 | CBA.Cg-Dock7m Leprdb/+ +/J | Cryopreserved - Ready for recovery |
| Leprdb/Leprdb mice on the CBA strain background are characterized by exocrine pancreatic necrosis and kidney lesions in aging mice. In contrast to the obesity observed in other strain backgrounds, five month old homozygous males exhibit weight loss in comparison to controls. Homozygous males develop severe hyperglycemia exhibiting blood sugar levels of +/-475 mg/dl by three months of age and increasing to +/- 517 mg/dl by five months. Five month old homozygous males do not exhibit hyperinsulinemia, however homozygous females reach levels of +/-540 uU/ml. Homozygous males do not survive beyond six months (Leiter EH et al, 1981).
Because of the sterility of Leprdb homozygotes, misty has been incorporated into stocks for maintenance of the diabetes mutation. The repulsion double heterozygote (Leprdb +/+ Dock7m) facilitates identification of heterozygotes for breeding, while the coupling ..... | ||
| 000813 | CBA/J-Atp7aMo-pew/J | Cryopreserved - Ready for recovery |
| The Atp7 genes encode Cu2+ ATPases. Atp7a is the mouse ortholog of the human ATP7A gene, which is mutated in children with Menke's syndrome. The range of defects in both Menke's syndrome and in mice having mutations of Atp7a--the mottled series of mutants--are due to deficiencies in a number of copper-requiring enzymes, in turn attributed to an intracellular copper transport defect. Thus, it is likely that the Atp7a gene product functions as a copper transport protein. (For brief review and references, see Levinson et al., 1994.) Atp7aMo-pew, the mottled-pewter mutation, has the mildest effect of the known mutations at this locus. The sole phenotype noted in hemizygous males and homozygous females is their pale, silvery gray coat color. The coats of affected mice of both sexes are initially agouti; males become pewter by about 4 weeks and females at 5-6 weeks of age. Heterozygous females have normal, agouti coats throug ..... | ||
| 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 | ||
| 002208 | CFW-Mpv17/J | Cryopreserved - Ready for recovery |
| 002937 | D2.B6-Ahrb-1/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 008784 | FVB-Tg(Lactb)74.2Lus/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the mouse Lactb (lactamase, beta) transgene are viable, fertile, normal in size and do not display any gross behavioral abnormalities. The transgene encompasses the entire mouse structural gene and its regulatory sequences. Transgenic mice have a higher fat-mass-to-lean-mass (FMLM) ratio compared to wild-type littermates when fed a 6% fat diet. Over time the FMLM ratio difference between transgenic and wild-type animals increases. This mutant mouse strain may be useful in studies of metabolic syndrome and obesity. | ||
| 012662 | FVB-Tg(Ttr-Igf1)1Sykr/J | Cryopreserved - Ready for recovery |
| These "HIT" transgenic mice overexpress rat IGF1 specifically in the liver, with normal tissue IGF-I but have increased serum IGF-I levels. Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator reports that there is no difference between the phenotype exhibited by homozygotes compared to hemizygotes. | ||
| 012563 | FVB.129(Cg)-Slc9a3tm1Ges/J | Cryopreserved - Ready for recovery |
| These mice harbor a targeted mutation of the Na+/H+ exchanger isoform 3 locus (Nhe3 or Slc9a3) that abolishes endogenous gene expression. While no full-length mRNA is detected in kidney or intestine of homozygous mice, a truncated mutant mRNA lacking codons 320-831 (encoding sequences required for Na+/H+ exchange) is observed but expected to impart no dominant negative effects. When maintained as congenic on the FVB/N genetic background, homozygous mice exhibit a high mortality rate beginning just after weaning, with ~30% surviving to adulthood. Homozygous females are fertile, but homozygous males are infertile.
Homozygous (Nhe3-null) mice lack Na+/H+ exchanger isoform 3 function, and exhibit impaired intestinal absorption; resulting in severe diarrhea, altered salt and water homeostasis, and increased luminal fluid throughout the intestinal tract. Nhe3-null mice have increased PCNA-positive cells in the cryp ..... For more information please see the full phenotype on the strain data sheet | ||
| 002539 | FVB.129P2-Abcb4tm1Bor/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Abcb4tm1Bor mutation lack the ability to secrete phospholipid into the bile from the liver. They develop a degenerative liver disease. Portal inflammation ensues at an early age followed by hepatocellular carcinoma development after the age of 1 year. Bile from heterozygous mice has half the level of phospholipid when compared to bile from homozygotes. No liver pathology has been shown in heterozygotes. | ||
| 008660 | FVB.129S2(B6)-Hmox2tm1Poss/J | Cryopreserved - Ready for recovery |
| Homozygotes have reduced total heme oxygenase activity in brain and testes, diminished inflammatory pain response and are more susceptible to hyperoxia with attenuated hypoxic ventilatory response. Cultured neurons from homozygotes exhibit increased neurotoxicity and cell death. Neuronal and endothelial cell damage due to transient focal ischemia and glutamate induced cytotoxicity is increased. Olfactory epithelial neurons have decreased proliferation of neuronal precursors and increased apoptosis. Mutant pulmonary venous myocardium is hypertrophic. After hyperoxic exposure, total lung iron content increased 3.5 fold in homozygotes compared to wild-type. Homozygotes have a slower overall gastrointestinal transit time than wild-type. Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Although homozygous male animals exhibit ejaculatory abnormalities, both male and female homozygotes are fertile ..... For more information please see the full phenotype on the strain data sheet | ||
| 002329 | FVB.129S2-Plautm1Mlg/J | Cryopreserved - Ready for recovery |
| Homozygotes develop normally, are fertile and have a normal life span. Rectal prolapse of a non-infectious origin develops in 9% of homozygotes and/or extensive non-healing ulcerations occur at the eyelids and around the face. Small, focal fibrin deposits are occasionally seen in the intestines and in the sinusoids of the liver, and excessive fibrin deposits are seen in ulcerated skin or prolapsed rectum. Pulmonary clot lysis is comparable to that seen in normal wildtype siblings. Endotoxin induced venous thrombosis is increased over normal wildtype siblings. Fibrin dissolution by PLAU-deficient macrophages is greatly reduced but macrophage invasion into the peritoneal cavity after thioglycollate injection is unaffected. Homozygous knockout mice have increased levels of Abeta42 and Abeta40 in plasma. Brain Abeta levels are not significantly different than controls. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a ..... For more information please see the full phenotype on the strain data sheet | ||
| 005215 | FVB.129X1(B6)-Trfr2tm1Slu/J | Cryopreserved - Ready for recovery |
| These Tfr2Y245X mice have codon 245 of the targeted gene converted to a stop codon; this mutation corresponds to the human truncation mutation Y250X which is the cause of hemochromatosis (HH type 3). Mice that are homozygous for the targeted mutation are viable and fertile. Northern blot analysis of total RNA from liver tissue detects a reduced level of full length gene product (mRNA). PCR analysis of liver tissue detects the C to G point mutation in exon 6. Western blot analysis of hepatic membrane preparations does not detect truncated gene product (protein). By 4 weeks of age, homozygotes display ~5-fold increase in liver iron levels and ~1.5-fold increase in serum transferrin saturations levels over wildtype control. Iron deposition in the liver is hepatocellular and periportal. Mice homozygous for the mutation have decreased iron concentrations in the spleen, indicating reticuloendothelial iron sparing. These Tfr2Y245X mutant mice may be useful ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 002384 | FVB/N-Tg(UcpDta)1Kz/J | Cryopreserved - Ready for recovery |
| Transgenic mice fed a "Western diet" developed marked obesity, insulin resistance, hyperglycemia, and hyperlipidemia. Mice hemizygous for the TgN(UcpDta)1Kz transgene develop early obesity in the absence of hyperphagia indicating an increased metabolic efficiency. Hyperphagia does follow and is present in mice over 7 weeks of age. | ||
| 003265 | FVB;129-Adatm1Mw Tg(PLADA)4118Rkmb/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Adatm1Mw targeted mutation die perinatally. They show defects in purine metabolism and have liver cell degeneration. Death is most likely the result of accumulation of ADA precursors. Mice from the double mutant strain FVB,129-Adatm1Mw Tg(PLADA)4118Rkmb/J (Stock No. 003265) are rescued from embryonic lethality by transgenic ADA expression in the placenta. Rescued mice that are homozygous for the null Ada allele exhibit a severe combined immunodeficiency. In addition, mice develop a severe lung eosinophilia reminescent of that seen in humans with asthma. Abnormalities were also found in the bone and kidney. ADA deficient mice die from severe respiratory distress by three weeks of age. Mice carrying a transgene overexpressiong ADA in both the placenta and forestomach, FVB;129-Adatm1Mw Tg(PLFSADA)2465Rkmb/J (Stock No. 003297), are rescued from postna ..... For more information please see the full phenotype on the strain data sheet | ||
| 003297 | FVB;129-Adatm1Mw Tg(PLFSADA)2465Rkmb/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Adatm1Mw targeted mutation die perinatally. They show defects in purine metabolism and have liver cell degeneration. Death is most likely the result of accumulation of ADA precursors. Mice from the double mutant strain FVB,129- Adatm1Mw Tg(PLADA)4118Rkmb/J (Stock No. 003265) are rescued from embryonic lethality by transgenic ADA expression in the placenta. Rescued mice that are homozygous for the null Ada allele exhibit a severe combined immunodeficiency. In addition, mice develop a severe lung eosinopilia reminescent of that seen in humans with asthma. Abnormalities were also found in the bone and kidney. ADA deficient mice die from severe respiratory distress by three weeks of age. Mice carrying a transgene overexpressiong ADA in both the placenta and forestomach, FVB,129- Adatm1Mw Tg(PLFSADA)2465Rkmb/J (Stock No. 003297), are rescued from postnatal lethality at three weeks of age. Rescued mice that ..... For more information please see the full phenotype on the strain data sheet | ||
| 002452 | J.129P2(B6)-B2mtm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the B2mtm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8+ cytotoxic T-cells and under some circumstances a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+T-cells are severely deficient providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). 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 ..... For more information please see the full phenotype on the strain data sheet | ||
| 000494 | J.Cg-Oca2+ Tyr+ Lystbg/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the beige spontaneous mutation (Lystbg) are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syngeneic tumor cells grow better in beige mice than in l ..... For more information please see the full phenotype on the strain data sheet | ||
| 001266 | LDH2/EiJ | Cryopreserved - Ready for recovery |
| 000790 | LT.MOL-Esdc/J | Cryopreserved - Ready for recovery |
| 002455 | MRL-Faslpr.129P2(B6)-B2mtm1Unc | Cryopreserved - Ready for recovery |
| Mice homozygous for both the lymphoproliferation spontaneous mutation (Faslpr) and the B2mtm1Unc targeted mutation are viable and fertile. Class I molecule-deficient B2mtm1Unc mice were backcrossed to MRL/MpJ-Faslpr to study the role of MHC class I molecules in the development of systemic autoimmune disease. Double homozygous mutant mice demonstrated a substantial reduction in CD4-CD8- T cells and a diminution of autoimmune disease. Specifically, hypergammaglobulinemia; autoantibodies including anti-DNA, anti-Smith antigen, and rheumatoid factor; and glomerulonephritis were significantly reduced compared to MRL/MpJ-Faslpr homozygous mice. Moreover, the pattern of hypergammaglobulinemia suggests that the requirement for MHC class I proteins is restricted temporally to later stages of the disease. | ||
| 002453 | MRL.129P2(B6)-B2mtm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the B2mtm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8+ cytotoxic T-cells and under some circumstances a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+ T-cells are severely deficient providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). 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 ..... For more information please see the full phenotype on the strain data sheet | ||
| 005356 | NOD.129(B6)-B2mtm1Unc Ciitatm1Ccum/BhsJ | Cryopreserved - Ready for recovery |
| NOD.129(B6)-B2mtm1UncC2tatm1Ccum/BhsJ is homozygous for linkage markers delineating Idd1-5, 7-10 and 13-15 loci of NOD origin and do not become diabetic. Histology indicates normal islet tissue structure with no cellular infiltration. Islets are intact and produce insulin. FACs analysis of peripheral blood cells of mice homozygote for B2mtm1Unc and C2tatm1Ccum confirmed the absence of MHC I or MHC II cell surface expression, reduced peripheral T-cell populations, deficiency of CD4+ and CD8+ T-cells and there is no difference in B-cell numbers when compared with wild-type controls. Additionally, B2mtm1Unc,C2tatm1Ccum double homozygous animals exhibit lower IgG titers and higher IgM titers than wild-type controls. Diabetic NOD females receiving purified islets from NOD.129(B6)-B2mtm1UncC2tatm1Ccum/BhsJ transplanted under the kidney capsule remain normal ..... For more information please see the full phenotype on the strain data sheet | ||
| 004083 | NOD.129(B6)-Prkdcscid Iduatm1Clk/J | Cryopreserved - Ready for recovery |
| At birth, mice that are homozygous null for the Idua gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No alpha-L-iduronidase enzyme activity or mRNA is detected. By three weeks of age, homozygous null mice develop a flattened facial profile and a thickening of digits. Defective bone formation is noticeable by fifteen weeks, characterized by a broadening and thickening of long bones. Evidence of lysosomal storage disorder is apparent in cells of the reticuloendothelial system at four weeks. By eight weeks progressive evidence of lysosomal storage is seen in Kupffer cells, splenic sinusoidal lining cells, chondrocytes, glial and Purkinje cells. This animal model is suitable for use in studies investigating the lysosomal storage disorder mucopolysaccharidosis type I (MPS I). | ||
| 006611 | NOD.129P2(B6)-B2mtm1Unc Tg(HLA-A/H2-D/B2M)1Dvs/DvsJ | Cryopreserved - Ready for recovery |
| NOD mice carrying only the HLA-A/H2-D/B2M transgene, commonly referred to as NOD.HHD, (Stock No. 006604) develop significantly accelerated diabetes onset compared to NOD/ShiLtDvs (NOD) inbred mice.
This mutant stock is also homozygous for the B2mtm1Unc mutation which normally prevents the development of of CD8+ T cells. The presence of the transgene in the B2m-deficient background, however, restores CD8+ T cells, but at a significantly lower level than in NOD inbred mice. Due to the covalently linked nature of the B2M component encoded into the transgene, the transgenic construct is unable to rescue murine MHC class 1 molecules in the NOD.B2m deficient (Stock No. 002309) mice. Thus, these double mutant mice only express human HLA-A2.1. Fifty-five percent of these NOD transgenic B2m-deficient mice develop diabetes b ..... For more information please see the full phenotype on the strain data sheet | ||
| 010565 | NOD.129P2(B6)-B2mtm1Unc Tg(HLA-A24/H2-D/B2M)3Dvs/J | Cryopreserved - Ready for recovery |
| NOD mice carrying only the HLA-A24/H2-D/B2M transgene and homozygous for the B2mtm1Unc mutation, commonly referred to as NOD.B2mnull. A24/HHD, are viable, normal in size, do not display any gross physical or behavioral abnormalities and are reported to be poor breeders. The presence of the transgene in the B2m deficient background restores CD8+ T cells, but at a significantly lower level than in NOD inbred mice. Due to the covalently linked nature of the B2m component incorporated into the transgene, the transgenic construct is unable to rescue expression of murine MHC class I molecules in the NOD. B2m deficient (Stock No. 003914) mice. FACS analysis confirms the NOD. B2m null. A24/HHD mice express human HLA-24, but no murine MHC class I molecules. NOD.B2m null, A24/HHD mice develop insulitis, but progression to overt diabetes is reported to be rare.
This model provides humanized HLA-24 restricted T cells that will be useful tools ..... For more information please see the full phenotype on the strain data sheet | ||
| 002309 | NOD.129P2(B6)-B2mtm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the B2mtm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8+ cytotoxic T-cells and under some circumstances a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+ T-cells are severely deficient providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Other traits of B2M deficient mice include: NK cell deficiency, NK1+ T cells deficiency and decreased levels of serum Ig. Some forms of lupus autoimmunity are severely reduced. (Christianson, J Immunol 156:4932-9, 1996). Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). The B2mtm1Un mutation backcrossed to the NOD/Lt strain serves as a MHC class I-negative, CD8+ deficient diabetes resistant stock ..... For more information please see the full phenotype on the strain data sheet | ||
| 003355 | NOD.Cg-B2mtm1Unc Tg(B2M)55Hpl/Dvs | Cryopreserved - Ready for recovery |
| 008542 | NOD.Cg-B2mtm1Unc Tg(GFAP-B2m)9Mdos/J | Cryopreserved - Ready for recovery |
| Mice carrying the GFAP-B2m transgene and homozygous for the B2mtm1Unc allele, commonly referred to as GFAP-B2m, are viable, fertile and diabetes resistant. Western blot analysis and histological analysis of brain and pancreas confirmed transgene expression in the astrocytes and peri-islet Schwann cells. FACs analysis indicates the absence of CD8+ T cells in the spleens of both NOD.GFAP-B2m and NOD.B2m deficient mice. Similar to the NOD.B2m deficient mice, NOD.GFAP-B2m mice do not develop spontaneous diabetes by forty weeks of age. In adoptive transfer experiments NOD.GFAP-B2m mice receiving splenocytes from diabetic NOD females develop diabetes at a significantly faster rate and higher incidence than non-transgenic littermates. No diabetes occurred in NOD.GFAP-B2m mice receiving splenocytes from AI4 TCR transgenic mice. This strain is useful for studying the role of GFAP in autoimmunity and the development of immunotherapies. | ||
| 004548 | NOD.Cg-B2mtm1Unc Tg(B2M)55Hpl Tg(HLA-A2.1)1Enge/DvsJ | Cryopreserved - Ready for recovery |
| 002570 | NOD.Cg-Prkdcscid B2mtm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for both the B2mtm1Unc and Prkdcscid (commonly referred to as scid) mutations on the NOD/ShiLtSz background are class I deficient, B and T cell deficient, C-5 deficient (Hc0), and have low NK cells. This strain is an ideal model for xenograft transplantation studies and is an excellent source for insulitis-free, MHC class I-negative islets for transplantation studies. | ||
| 005053 | NOD.Cg-Prkdcscid Gusbmps/SndsJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the mps allele exhibit skeletal dysplasia as well as cognitive, hearing and visual deficits. Lifespan of the homozygotes is approximately six months. Homozygotes lack the lysomal enzyme, beta-glucoronidase, and, as a result, glycosaminoglycans accumulate in tissues throughout the body. This strain is a model for the human lysomal storage disease, mucopolysaccharidosis type VII. On the NOD-Prkdcscid background, this strain can be used for xenotransplantation experiments and cell trafficking studies (Hofling et al., 2003). | ||
| 008777 | NZG/KgmJ | Cryopreserved - Ready for recovery |
| The New Zealand Ginger (NZG) mouse is characterized by rapid growth and a large body size as a result of excessive lean body mass. This inbred strain is not obese, diabetic or insulin resistant. Both sexes exhibit a rapid growth rate which plateaus at 60 days, however, males are heavier than females. ELISA assay indicates that mice have higher levels of circulating insulin-like growth factor I (IGF1) than C57BL/6 mice, but comparable levels of insulin and growth hormone. Mice have an unusual pattern of fat distribution compared to C57BL/6 mice with higher percentages of retroperitoneal, gonadal and inguinal fat rather than visceral fat. NZG mice have less total body fat (6%) than C57BL/6 mice (13.8%). These mice are susceptible to high fat (45%) diet-induced obesity, but not diet-induced diabetes.
Genetic analysis indicates that the yellow (ginger) coat is not the result of alleles at either agouti or the melanocortin 1 receptor (Mc1r) genes. The fur is described ..... | ||
| 000059 | PRO/ReJ | Cryopreserved - Ready for recovery |
| Mice exhibit hyperprolinemia and hyperprolinuria. Proline levels in the blood are increased by seven-fold in comparison to the two parental strains, C57BL/6J and 129P1/ReJ. Proline is detected in the urine of all PRO/ReJ mice, however, it is undetectable in the parental strains. This strain may be useful in studies of human hyperprolinemia. | ||
| 000682 | RF/J | Cryopreserved - Ready for recovery |
| Derived from an unknown stock at the Rockefeller Institute, RF/J are commonly used in research in genetics, immunology, oncology and virology. This strain displays a high cancer incidence including leukemia (reportedly between 40 and 66%) and reticulum cell sarcomas (approximately 50%). Mice also have a high incidence of spontaneous glomerular hyalinisation and glomerulosclerosis developing between eight and twenty months. | ||
| 000269 | SB/LeJ | Cryopreserved - Ready for recovery |
| The SB/Le inbred strain is homozygous for both the satin (Foxq1sa) and beige (Lystbg) mutations. Most of the immunological phenotype is due to the beige mutation. Homozygous mutant beige mice are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. They have a severe deficiency of natural killer (NK) cells. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibo ..... For more information please see the full phenotype on the strain data sheet | ||
| 010968 | SB;C3Sn-Lrp4mdig-2J/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Lrp4mdig-2J mutation have toes missing from each foot, have a coarse tail, and some, but not all, have one or two extra upper incisors. | ||
| 001224 | SOD1/EiJ | Cryopreserved - Ready for recovery |
| SOD1/EiJ carries a spontaneous mutation in the Sod1 gene (Luche et al., 1997). The mutation differs from the C57BL/6J sequence at position 231 and changes a glutamate to a lysine in a positively charged amino acid domain within the Zn-subloop. This strain is fertile and exhibits no obvious phenotype. | ||
| 000688 | ST/bJ | Cryopreserved - Ready for recovery |
| 002493 | STOCK Adatm1Mw/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Adatm1Mw targeted mutation die perinatally. They show defects in purine metabolism and have liver cell degeneration. Death is most likely the result of accumulation of ADA precursors. Mice from the double mutant strain FVB;129- Adatm1Mw-TgN(PLADA)4118Rkmb/J (Stock No. 003265) are rescued from embryonic lethality by transgenic ADA expression in the placenta. Rescued mice that are homozygous for the null Ada allele exhibit a severe combined immunodeficiency. In addition, mice develop a severe lung eosinopilia reminescent of that seen in humans with asthma. Abnormalities were also found in the bone and kidney. ADA deficient mice die from severe respiratory distress by three weeks of age. Mice carrying a transgene overexpressiong ADA in both the placenta and forestomach, FVB;129- Adatm1Mw-TgN(PLFSADA)2465Rkmb/J (Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 002974 | STOCK Ces1ce H2d/J | Cryopreserved - Ready for recovery |
| Mice homozygous for Ces1ce are viable and fertile and exhibit no apparent defect. Ces1ce was discovered in a screen of progeny of triethylenemelamine (TEM) treated male mice for mutations at specific loci, but appears to have pre-existed in the male. The screen employed analysis of blood and kidney homogenates by "standard starch gel electrophoresis techniques" and focused on enzymes known to differ in electrophoretic mobility between the parental strains (DBA/2J and C57BL/6J). Ces1ce was initially thought to be a null allele, but characterization of homozygous F2 mice demonstrated presence of a faint band migrating between those of the parental strains, which was not perceived in the presence of either parental band. Thus, Ces1ce was shown to be a hypomorphic electrophoretic variant (Soares 1979). | ||
| 003582 | STOCK Cptm1Hrs/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Cp gene demonstrate a progressive accumulation of iron in hepatocytes and reticuloendothelial cells. By one year of age, iron content of the liver and spleen reaches three to six-fold that observed in wild-type litter mates. The Cp gene product appears to be necessary for proper iron efflux from these cell types. This strain represents a viable murine model for aceruloplasminemia. At one year of age there is no evidence of anemia, diabetes, or neurological symptoms despite iron accumulation at the corresponding tissue sites. | ||
| 006999 | STOCK Dbttm1Geh Tg(Cebpb-tTA)5Bjd Tg(tetO-DBT)A1Geh/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Dbt (E2) targeted mutation and carrying both the LAP-tTA and TRE-E2 transgenes are viable and fertile. The E2-targeted mutation leads to absence of branched-chain keto acid dehydrogenase (BCKDH) activity and E2 protein in liver tissue, but this absence is rescued by the two transgenes: liver-directed expression of the modified human BCKDH E2 subunit from the complimentary "Tet-off" transgenes abrogates the severity of Maple Syrup Urine Disease (MSUD) phenotype observed in E2-deficient single mutant mice. Triple mutant mice are a model for intermediate MSUD (iMSUD); BCKDH activity is only 5-6% of that found in wildtype mice. This low level of BCKDH activity is sufficient to allow survival, but insufficient to normalize circulating branched chain amino acids levels. Because these mice have near normal amounts of E2 protein, but only 5-6% of normal BCKDH enzyme activity, it is probable that the c-myc tag at the carboxy-terminus of the human E2 transge ..... For more information please see the full phenotype on the strain data sheet | ||
| 008598 | STOCK Galptm1Stei/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis. Homozygotes are indistinguishable from wildtype when maintained on ad libitum diet. After fasting, male homozygotes consume less food than wildtype controls. When fed a high fat diet homozygotes gain less weight than wildtype controls. This mutant mouse strain may be useful in studies of energy homeostasis, nutrition and obesity. | ||
| 001880 | STOCK Gusbmps Tg(GUSB)4Sly/BirJ | Cryopreserved - Ready for recovery |
| 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. | ||
| 006327 | STOCK Pcsk1tm1Dfs/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the targeted mutation are viable and fertile. No gene product (mRNA or protein) is detected in the homozygotes by Northern blot analysis of hypothalamic tissue or Western blot analysis of pituitary and brain tissue. Homozygote mice experience perinatal lethality, as the number of homozygotes born is less than the expected Mendelian ratio, and high postnatal lethality. By postnatal day 3, homozygotes are smaller in size than littermates. By 6 weeks of age, the surviving homozygotes are approximately 60% of wildtype body weight. Homozygotes have chronic mild diarrhea with bulky moist stools. Pituitary growth hormone transcript levels are only 25-20% of normal levels. Somatotroph cells in the anterior pituitary are reduced in size and inactive. Insulin-like growth factor 1 serum levels are significantly reduced. Transcript (mRNA) levels are greatly increased for growth hormone-releasing hormone in the hypothalamus and proopiomelanocortin in the pituitary. Ma ..... For more information please see the full phenotype on the strain data sheet | ||
| 005701 | STOCK Pdx1tm1Macd/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation fail to develop a pancreas. Heterozygous mice have normal pancreas development but partially impaired glucose tolerance in adulthood. The substitution of the targeted gene with tTAoff inactivates the endogenous allele and places tTAoff expression under the control of the endogenous transcriptional regulatory sequences. tTA expression from the modified locus is identical to that of the normal allele; tTA mRNA is detectable in the pancreas but not in other visceral organs or salivary glands. This mutant may be useful in studies of pancreatic endocrine/exocrine function and diabetes. Heterozygotes also can be bred with transgenic mice that express a target gene under the regulation of a tetracycline-responsive element (TRE; tetO) for pancreas-specific applications.
This mutant was originally designed to be mated with mutant mice with a TRE-controlled transgene coding for the endogenous Pdx1 (Ipf1) gene alon ..... | ||
| 005740 | STOCK Ppiftm1.1Mmos/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. Brain architecture and cerebrovasculature are normal. No gene product (protein) is detected by immunoblot analysis of mitochondria isolated from liver tissue of mutant mice. Mitochondria from mutant mice have an increased capacity to retain calcium and fail to swell/rupture in response to CaCl2, suggesting abnormal permeability transition pore (PTP) function. Mouse embryonic fibroblasts (MEFs) derived from mutant mice are less susceptible to oxidative stress induced in vitro by exposure to hydrogen peroxide than MEFs derived from wildtype mice. In a model of ischemic brain injury employing a middle cerebral artery occlusion protocol, mutant mice exhibited a reduced infarct volume (37% in heterozygotes, and 62% in homozygotes) when compared to wildtype mice. This mutant mouse strain may be useful in studies investigat ..... For more information please see the full phenotype on the strain data sheet | ||
| 005737 | STOCK Ppiftm1Mmos/J | Cryopreserved - Ready for recovery |
| In this strain loxP sites flank exons 3-5 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. Cre-mediated recombination results in the deletion of the loxP-flanked region. This strain represents an effective tool for generating tissue-specific targeted mutants useful in studies examining the consequences of disrupting Ppif-dependent pathways. | ||
| 010503 | STOCK Smtnl1tm1Tajh/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable, fertile and normal in size. No gene product is detected by Western blot analysis. Mutant mice exhibit better performance during endurance training and, males in particular, exhibit increased time to fatigue, distance run and vertical work in stress tests after endurance training. Vasorelaxation and contractile responses are improved in mutant mice and the ratio of type 2a muscle fibers is increased in sedentary mice, however, this ratio does not change following exercise. This mutant mouse strain may be useful in studies of muscle and vascular adaptation to exercise. | ||
| 007577 | STOCK Tg(Gt(ROSA)26Sor-BCHE*G117H)837Loc/J | Cryopreserved - Ready for recovery |
| Transgenic "G117H BChE" mice are viable and fertile. These mice express a mutant form of human butyrylcholinesterase (BCHE or BChE), harboring a single amino acid change at codon 117 (His for Gly), under the control of the ROSA26 promoter. This mutation has the unusual ability to hydrolyze organophosphorus toxicants (OP), as well as acetylcholine and is resistant to inhibition by OP. All tested tissues show G117H BChE enzymatic activity. In the founder mice and immediate offspring, plasma concentrations of the mutant protein are approximately 25% of endogenous wildtype mouse BChe. No reported abnormalities result from BChE overexpression in homozygous mutant mice. Transgenic mice injected with the OP echothiophate are protected from the severe toxicity and lethality observed in wildtype controls. This is the first transgenic mouse strain that expresses human BChE as well as the first mammal with hereditary OP resistance. These G117H BChE transgenic mice may be useful for biodefe ..... For more information please see the full phenotype on the strain data sheet | ||
| 005699 | STOCK Tg(tetO-Ipf1,EGFP)956.6Macd/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the transgene are viable, fertile, normal in size, and do not display any behavioral abnormalities. At the Jackson Laboratory, no homozygous mice were produced from mating hemizygotes together, suggesting that homozygous transgenic animals die in utero. Expression of the bicistronic transgene is under the regulation of a tetracycline promoter element (TRE; tetO). By themselves, these transgenic mice do not express EGFP, but when these mice are mated with a second transgenic strain expressing tetracycline-transactivator (tTA) protein under the control of a tissue-specific promoter, Ipf1 and EGFP are highly expressed in the appropriate tissue of bitransgenic offspring.
This mouse was originally designed to be mated to an apancreatic targeted mutant with tTAoff in place of the endogenous Ipf1 gene (see Stock No. 005701). The combined mutations allow normal pancreatic dev ..... | ||
| 005728 | STOCK Tg(tetO-Ipf1,lacZ)958.1Macd/J | Cryopreserved - Ready for recovery |
| Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Expression of the bicistronic transgene is under the regulation of a tetracycline-responsive promoter element (TRE; tetO). When transgenic mice are bred to a second transgenic strain expressing tetracycline-transactivator (tTA) protein under the control of a tissue-specific promoter, the bitransgenic offspring express Ipf1 and lacZ in the appropriate target tissue. Further, Ipf1 and lacZ expression in bitransgenic mice can be suppressed by administration of the tetracycline analog, doxycycline. All cells expressing Ipf1 coexpress the reporter, and mRNA levels of the transgenic and endogenous Ipf1 fluctuate in concert during development. This mouse was designed originally to be mated to an pancreatic targeted mutant with tTAoff in place of the Ipf1 gene (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 000623 | TR/DiEiJ | Cryopreserved - Ready for recovery |
| 000147 | WLHR/LeJ | Cryopreserved - Ready for recovery |
| WLHR/Le is a balanced stock with wabbler-lethal (wl) and hairless (hr) spontaneous mutations maintained in repulsion on Chromosome 14. Homozygous wabbler-lethal mutant mice are first recognizable at 12 days of age and usually die at about four weeks. They have an abnormal wobbly gait and a pronounced tremor when walking. In an extensive study of behavioral development of this mutant, homozygous wabbler-lethal mice were shown to be deficient in nearly all behaviors tested. Histological examination showed myelin degeneration widely distributed throughout the CNS, particularly in the vestibulocerebellar and spinocerebellar systems. Electron microscopy showed widespread axonal (Wallerian) degeneration in the medulla with secondary myelin dissolution. Similar abnormalities were present to a lesser extent in the basal ganglia, spinal cord, and cerebellum and in the optic nerve. Homozygous hairless mutant mice have a higher incidence and earlier onset of leukemia, reducible by v ..... For more information please see the full phenotype on the strain data sheet | ||
| 000933 | YBR/EiJ | Cryopreserved - Ready for recovery |
| 009126 | B6.Cg-Nos2tm1Lau Tg(Thy1-APPSwDutIowa)BWevn/Mmjax | Transferred |
| 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 | ||
| 014137 | B6.129S4-Pmchtm1Emf/J | Under Development - Now Accepting Orders |
| Mice that are homozygous for this knockout are viable, fertile, and exhibit a smaller stature and increased locomotor activity when compared to wildtype controls. No gene product (mRNA or protein) is detected by RT-PCR and in situ hybridization analysis of hypothalamus tissue, RT-PCR of pancreatic islets from homozygotes and immunocytochemical analysis of brain tissue from homozygotes.
Homozygotes appear smaller, are leaner than wildtype controls and when placed on a chow diet, display increased basal metabolic rates and locomotor activity.
When fed a high-fat diet, the oxygen consumption ( by 15.7%) and activity levels are further increased and homozygotes do not gain as much weight as controls. The lean phenotype persists in homozygous mice more than 12 months of age. Homozygotes, 12-19 months of age, are more sensitive to insulin, have reduced aging-associated weight and visceral adiposity gain, maintain increased locomotor activity, and are resistant to aging-associated glu ..... For more information please see the full phenotype on the strain data sheet | ||
| 016197 | B6.Cg-Tg(CAG-OTC/CAT)4033Prab/J | Under Development - Now Accepting Orders |
| MCAT transgenic mice have a CMV enhancer/chicken beta-actin promoter (CAG; from the pCAGGS vector) driving the expression of a human Catalase (CAT) gene in mitochondria. Hemizygous MCAT mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Catalase is a an enzyme, normally expressed in peroxisomes, that reduces hydrogen peroxide (H2O2) to water and molecular oxygen, mitigating the potential for H2O2 to cause damage to molecules. Mitochondrial catalase expression in MCAT mice results in a 5.5-month increase in median life span for both males and females. Catalase activity is elevated in heart, skeletal muscle, and brain. Cardiac mitochondria have 50 times higher catalase activity than in wild-type littermates leading to a delay in cardiac pathology. They also display improved cardiac performance with age, reducing their susceptibility to cardiac hypertrophy a ..... 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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