Search Criteria: Research Area is "Cardiovascular Research: Other"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 006050 | 129-Sirt6tm1Fwa/J | Repository- Live |
| Homozygous neonates are smaller than their wildtype and heterozygous littermates. They develop normally until approximately 21 days of age, when they develop an acute and rapid, aging-like degenerative pathology resulting in death by postnatal day 24. Homozygous mutant mice exhibit subcutaneous fat loss, lordokyphosis (hunchbacked spine) with osteopenia (30% loss of bone mineral density), colitis, and severe lymphopenia due to increased lymphocyte apoptosis. At day 12, mice have reduced insulin-like growth factor I (IGF-1) levels in serum, and develop severe hypoglycemia. Mouse embryonic fibroblasts (MEFs) prepared from homozygous embryos exhibit reduced proliferation, defective base excision repair function, as indicated by increased sensitivity to alkylating agents and ionizing radiation, and increased chromosomal aberrations. The donating investigators report that no gene product (mRNA or protein) is detected by RT-PCR or immuoblot analysis of tissues, MEFs or embryonic stem cells f
..... For more information please see the full descriiption on the strain data sheet | ||
| 007175 | 129S-Cyp4a14tm1Jhc/J | Repository- Live |
| Mice homozygous for this "Cyp 4a14" mutant allele are viable and fertile. Homozygous deficiency of the targeted gene leads to spontaneous hypertension (more severe in males) that is androgen-sensitive. Homozygotes also exhibit other interrelated metabolic and regulatory effects; increased renal vascular resistance, impaired renal hemodynamics, elevated plasma androgens (5α-dihydrotestosterone (DHT) and testosterone), upregulated Cyp4a12 gene expression, and increased formation of prohypertensive 20-HETE. These "Cyp 4a14" mutant mice may be useful studying kidney function and metabolism, cardiovascular physiology, hypertension, and the relationships between blood pressure, sex hormones, and p450 ω-hydroxylases. | ||
| 006201 | B6.129-Scd1tm1Ntam/J | Repository- Live |
| 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
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| 006879 | B6.129-Scd2tm1Myz/J | Repository- Live |
| 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. | ||
| 006503 | B6.129S4-Lpltm1Ijg/J | Repository- Live |
| 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. | ||
| 007809 | B6.129S4-Mc3rtm1Cone/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and fertile. Female homozygotes at approximately 50 to 60 days of age exhibit significantly heavier body weight when compared to heterozygotes. No gene product (mRNA) is detected by RT-PCR analysis of hypothalamus tissue. Male homozygotes exhibit an approximately 40% increase in body fat at 15-20 weeks of age when compared to wildtype. Heterozygotes display an intermediate increase in body fat percentage of approximately 36%. Although homozygotes have increased adiposity, there is no increased food intake or weight gain and resting basal or total oxygen consumption is lower in mutant mice when compared to wildtype. High fat diet causes an increased respiratory quotient within 24 hours of the diet change. Homozygotes on a low fat diet have a lower respiratory quotient than wildtype. Male homozygotes exhibit an approximately 50% decrease in wheel running behavior. Mutant mice become hypertensive with increased gamma-melanocyt
..... For more information please see the full descriiption on the strain data sheet | ||
| 006133 | B6.129S4-Vdrtm1Mbd/J | Repository- Live |
| Heterozygous mice are phenotypically indistinguishable from wildtype siblings. Homozygous mice are viable and fertile with normal survival until approximately 14 months. RNA isolated from the intestine and kidney show a truncated deletion of the second zinc finger coding region followed by a premature termination codon, resulting in the absence of receptor protein. Homozygous mice exhibit an identical phenotype as the human disease hereditary vitamin D-dependent rickets type II (HVDDR). As early as 21 days of age, mutant mice demonstrate hypocalcemia, hypophosphatemia, hyperparathyroidism, increased serum parathyroid hormone, abnormal blood mineral levels, and growth retardation. In addition, renin and plasma angiotensin II levels are increased. Homozygous mice are hypertensive and exhibit cardiachypertrophy. At 4 weeks of age, homozygous mice exhibit perioral and periorbital alopecia that progresses over the entire body by 4 months of age. Rickets and osteomalacia develop by 35 days.
..... For more information please see the full descriiption on the strain data sheet | ||
| 006878 | B6.129S6-Taglntm2(cre)Yec/J | Repository- Live |
| Mice homozygous for this SM22alpha-CreKI allele are viable and fertile. These mice have a Cre-recombinase gene inserted into the endogenous transgelin (SM22alpha) locus. The donating investigator reports that this mutation results in a loss of function of the targeted gene. Cre recombinase activity is shown in adult smooth muscle cells (such as arteries, veins, and visceral organs) and cardiac myocytes, but activity is not observed in the same embryonic tissues. These SM22alpha-CreKI mice may be useful for Cre-lox technology applications in studying smooth muscle and cardiac gene function, as well as cardiovascular disease. | ||
| 007682 | B6.129X1-Apobtm1.1Zc/J | Repository- Live |
| 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 descriiption on the strain data sheet | ||
| 006580 | B6.Cg-Ins2Akita Ldlrtm1Her/J | Repository- Live |
| 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. | ||
| 006883 | B6.Cg-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. | ||
| 006877 | B6.Cg-Ldlrtm1Her Tg(H2-K-AKR1B1)1Tj/J | Repository- Live |
| 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 | Repository- Live |
| 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. | ||
| 008221 | B6.Cg-Tg(IGFBP1)2Miel/J | Repository- Live |
| 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 descriiption on the strain data sheet | ||
| 007742 | B6.Cg-Tg(Myh11-cre,-EGFP)2Mik/J | Repository- Live |
| Mice hemizygous for the smMHC/Cre/eGFP transgene (smMHCCre/eGFP) are viable and fertile, with the smooth muscle myosin heavy chain (smMHC or Myh11) promoter directing bicistronic Cre and EGFP protein expression to smooth muscle cells during development as well as in the adult mouse. Hemizygotes from founder line SMCG2 (SM2Cre/GFP) display intense EGFP fluorescence restricted to vascular and nonvascular smooth muscle, with strong concordance between cre expression and EGFP fluorescence (verifying the use of fluorescence as a marker for conditional gene recombination). When bred with mice containing a loxP-flanked sequence of interest, the resulting offspring can have Cre-mediated recombination of the flanked sequence in smooth muscle. Homozygotes are viable and fertile, with smaller litter sizes and a higher incidence of perinatal mortality. These smMHC/Cre/eGFP transgenic mice may be useful in studies utilizing "Cre-lox" technology or fluoresc
..... For more information please see the full descriiption on the strain data sheet | ||
| 006470 | B6;129S-Hopxtm1Eno/J | Repository- Live |
| Homozygous mice are viable and fertile on this mixed genetic background. Absence of the targeted protein is confirmed in heart and brain tissues from homozygotes. The lacZ expression pattern is similar to that of the endogenous gene. Homozygous heart tissues show altered serum response factor (SRF)-associated gene expression. Mice homozygous for this null allele segregate into two phenotypic classes characterized by an excess or deficiency of cardiac myocytes. These mutant mice may be useful in studying cardiac growth and development. | ||
| 006028 | B6;129S6-Epha2tm1Jrui/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile with no overt developmental or behavioral abnormalities. The Jackson Laboratory is distributing these mice on their original C57BL/6;129S6 mixed background. The published phenotype of these mutant mice is described below. In mutant mice of a mixed BALB/c, C57BL/6, and 129S6 background, murine pulmonary microvascular endothelial cells (MPMEC) isolated from homozygotes express no endogenous protein. MPMEC show impaired ephrin-A1-induced vascular assembly and defective migration both in vitro and in vivo. In addition, MPMEC from homozygous mice exhibit decreased angiogenesis and fail to activate Rac1 in response to ephrin-A1 in vivo. Mutant mice crossed to BALB/c for 7 generations are protected from tumor progression, angiogenesis and metastasis following metastatic mammary adenocarcinoma cell transplantation. These mutant mice may be useful in studies of postnatal angiogenesis (endothelial cell migra
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| 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. | ||
| 006208 | B6;129S6-Pdzk1tm1Dls/J | Repository- Live |
| 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. | ||
| 002529 | B6;129S7-Vldlrtm1Her/J | Repository- Live |
| Mice homozygous for the Vldlrtm1Her targeted mutation are viable and fertile. They are smaller and leaner than normal wildtype siblings. The high level of expression in muscle and adipose tissue suggests a role in VLDL triacylglycerol delivery. Plasma levels of cholesterol, triacylglycerol, and lipoproteins were normal when mice were fed normal, high-carbohydrate or high fat diets. However, homozygous mice do show a modest decrease in body weight, body mass index, and adipose tissue mass as determined by the weights of epididymal fat pads. Many homozygous pups in the colony at the Jackson Lab have patchy fur (hair loss) at weaning but look normal at about 6 weeks of age. In a segregation analysis crossing homozygous females with normal "C57BL6/2J" mice, offspring that were homozygous for this Vldlrtm1Her mutation are associated with subretinal neovascularization and were found to have a neovascularization process similar to a type seen in patients wi
..... For more information please see the full descriiption on the strain data sheet | ||
| 007744 | C57BL/6-Tg(APOE-DGAT2)24Far/J | Repository- Live |
| 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 descriiption on the strain data sheet | ||
| 006781 | C57BL/6-Tg(Ckm-DGAT2)10Far/J | Repository- Live |
| 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. | ||
| 006699 | C57BL/6J-Pcsk1N222D/J | Repository- Live |
| 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. | ||
| 007683 | CByJ.129X1(Cg)-Apobtm1.1Zc/J | Repository- Live |
| 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 descriiption 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 descriiption on the strain data sheet | ||
| 006578 | STOCK Myoz2tm1Eno/J | Repository- Live |
| Mice homozygous for this calsarcin-1 mutant allele are viable and fertile. Immunoblot of homozygous cardiac tissue shows no endogenous protein expression. Strong lacZ expression throughout all cardiac chambers mirrors the expression pattern of the endogenous gene, and marked skeletal muscles known to contain a high proportion of type I (slow) fibers. Homozygotes have skeletal muscle abnormalities in type I (slow) fibers and calcineurin activity. Echocardiography of homozygous mice reveals abnormal heart performance. Absence of gene function activates a cardiac hypertrophic fetal gene program (despite the absence of hypertrophy) and enhanced the cardiac growth response to pressure overload. These mutant mice may be useful in studying growth and gene expression of cardiac and skeletal muscle, as well as the pathogenesis of human cardiomyopathies. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic bac
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| 006473 | STOCK Smyd1tm1Dsr/J | Repository- Live |
| Mice heterozygous for this targeted mutation are viable and fertile. Mice homozygous for this targeted allele, however, die between embryonic day (E) 9.5 and 10.5 due to cardiomyocyte maturation defects, including an enlarged heart, single left-side ventricular chamber with tremendous extra cellular matrix expansion between the myocardial and endocardial layers, and defective Hand2 expression. No mRNA transcripts from the targeted mutant gene are detected in cardiac tissue from E9.5 homozygotes. These mutant mice may be useful in studying cardiomyocyte differentiation and cardiac morphogenesis. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 007679 | SWR.129X1(B6)-Apobtm1.1Zc/J | Repository- Live |
| 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 descriiption on the strain data sheet | ||
| 002387 | 129-Asgr2tm1Her/J | Repository-Cryopreserved |
| 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. | ||
| 007005 | 129S-Scg5tm1Led/J | Repository-Cryopreserved |
| The following text reflects the phenotype reported by the donating investigator on a "129Sv" genetic background (probably "Taconic Sv129" (129S6/SvEvJ)). While heterozygotes are viable and fertile, mice homozygous for this mutation (7B2-null) die in prepubertal or pubertal ages (5 weeks) with severe cardio-respiratory failure, convulsions, and hypothermia. No transcripts are detected in brain tissue from the targeted gene. 7B2 null mice are unable to make an active form of prohormone convertase 2 (PC2) and have high circulating corticosterone. Homozygotes on the 129S genetic background exhibit Cushing's-like disease pathologies of liver, pancreas, and pituitary; including pituitary-dependent hyperadrenocorticosteronism, severe hypoglycemia, hyperproinsulinemia, adrenal hypertrophy, pituitary hypotrophy, and altered islet cell morphology. 7B2-null mice develop the disease from intermediate lobe ACTH hypersecretion (rather than from pituitary adenomas). Other abnormalities include thinni
..... For more information please see the full descriiption on the strain data sheet | ||
| 005951 | B6.129-Dgat2tm1Rvf/J | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 006156 | B6.129-Sceltm1Hba/J | Repository-Cryopreserved |
| Homozygous mice are viable and have no overt morphological or developmental abnormalities. The donating investigator reports that fertility may be impaired in homozygous mice (limited number of litters possible). No endogenous gene expression is observed in skin or stratified squamous epithelia. These mutant mice may be useful in dermatological studies, such as cornified envelope formation, organization of the intima, as well as structural distinctions between arteries and veins, and respiratory structure and function. | ||
| 007453 | B6.129P2(Cg)-Dhcr7tm1Gst/J | Repository-Cryopreserved |
| 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 involved
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..... For more information please see the full descriiption on the strain data sheet | ||
| 005429 | B6.129S-Gpamtm1Rcol/J | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 005681 | B6.129S-Lipgtm1Tq/J | Repository-Cryopreserved |
| Homozygous mice are viable and do not display any behavioral or histological defects. Although homozygotes are fertile, the donating investigator reports decreased fecundity. Northern blot analysis showed no endogenous gene expression in lung, liver, kidney, spleen, or aorta. Homozygotes have increased fasting plasma levels of total cholesterol, high-density lipoprotein (HDL) cholesterol, and phospholipids compared to wild type. Mutant mouse plasma apoA-I is increased while heparin-releasable phospholipase activity is impaired. Homozygous null mice have decreased arterial endothelium monocyte adhesion. This mutant can be used in studies of lipoprotein metabolism, atherosclerotic vascular disease, and other cholesterol-related studies. | ||
| 005897 | B6.129S4-Ppardtm1Rev/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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. | ||
| 002987 | B6.129S7-Lrpap1tm1Her/J | Repository-Cryopreserved |
| Mice homozygous for the Lrpap1tm1Her targeted mutation (commonly referred to as RAP) are viable and fertile. They have a functional deficiency of the low density lipoprotein receptor-related protein (LRP) with reduced amounts of LRP seen in both the liver and the brain of homozygotes. | ||
| 002465 | B6;129S-Ldlrtm1Her Lrpap1tm1Her/J | Repository-Cryopreserved |
| 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. | ||
| 006258 | B6;129S4-Apoa2tm1Bres/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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. | ||
| 005937 | B6;129S4-Ucp3tm1Lowl/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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. | ||
| 004365 | B6;129S6-Srebf1tm1Mbr/J | Repository-Cryopreserved |
| 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. | ||
| 002361 | B6;129S7-Asgr2tm1Her/J | Repository-Cryopreserved |
| 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. | ||
| 002751 | B6;129S7-Cyp7a1tm1Rus/J | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 002464 | B6;129S7-Lrpap1tm1Her/J | Repository-Cryopreserved |
| Mice homozygous for the Lrpap1tm1Her targeted mutation (commonly referred to as RAP) are viable and fertile. They have a functional deficiency of the low density lipoprotein receptor-related protein (LRP) with reduced amounts of LRP seen in both the liver and the brain of homozygotes. | ||
| 006907 | B6;CBA-Tg(APOC3)3707Bres/J | Repository-Cryopreserved |
| 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. | ||
| 004583 | B6SJL-Tg(ABCG5/ABCG8)14-2Hobb/J | Repository-Cryopreserved |
| These transgenic mice over-express the human ABCG5 and ABCG8 genes under the direction of their endogenous regulatory sequences. Copy number of the transgene was estimated using Southern blot analysis to compare transgenic mouse genomic DNA to human genomic DNA. These transgenic mice have approximately ten copies of the transgene. Northern blot analysis revealed the human transgene is expressed in the liver and small intestine. RT-PCR showed trace levels of transgene transcript in ovary tissue. Absorption of dietary cholesterol in transgenic mice is reduced by 50%. Mean fasting plasma cholesterol levels are significantly lower in female transgenic mice. Excretion of neutral sterols in feces is elevated to three times higher above normal in male transgenic mice and six times higher in female transgenic mice. Bile from transgenic animals is opaque as compared to the clear bile of wildtype animals. Cholesterol in the bile is elevated to levels five times higher than normal in male transge
..... For more information please see the full descriiption on the strain data sheet | ||
| 002084 | C57BL/6-Tg(APOA2)3Rub/J | Repository-Cryopreserved |
| Mice carrying this transgene express a dimeric form of human apolipoprotein A-II. Human APOA2 mRNA is found only in the liver of transgenic mice. Levels of murine HDL, APOA1, and APOA2 in transgenic mice were comparable to those found in normal wildtype siblings. Small HDL particles comprised of the human APOA2 are present in these mice. | ||
| 006402 | FVB/N-Adrb3tm1Lowl/J | Repository-Cryopreserved |
| Homozygous mice are viable and fertile. No gene product (mRNA) is detected by Northern blot analysis from homozygous brown or white adipose tissue. Homozygous mice have modest increases in fat stores (female more than male). In contrast to control animals, homozygous mice are unresponsive to beta-3 adrenergic receptor (beta3-AR) agonist treatment (no effect on adenylate cyclase activity, lipolysis, or gastro-intestinal motility). These mutant mice may be useful in studies of energy balance, obesity, fat metabolism, cholesterol homeostasis, diabetes, and pharmacological screening of beta3-AR agonists for potential drug treatment. | ||
| 005994 | STOCK Mbtps1tm1Jdh/J | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
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How to Register Interest
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 Under Development
Select the strain name to link to the strain data sheet.
New Strains Under DevelopmentThe 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. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
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It is VERY IMPORTANT that you register interest in strains Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.
- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
These strains are designated as: "Under Development for Distribution Colony"- Strains that will be made available through the Cryopreservation Repository.
These strains are designated as: "Under Development for Cryopreservation Repository"
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