Search Criteria: Research Area is "Mouse/Human Gene Homologs: hypercholesterolemia, familial"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 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. | ||
| 006952 | B6.Cg-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. | ||
| 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. | ||
| 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. | ||
| 002246 | B6.129-Apoetm1Unc Ldlrtm1Her/J | Repository-Cryopreserved |
| 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. | ||
| 002245 | B6;129-Apoetm1Unc Ldlrtm1Her/J | Repository-Cryopreserved |
| 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. | ||
| 003000 | B6;129S-Apobtm2Sgy Ldlrtm1Her/J | Repository-Cryopreserved |
| 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-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. | ||
| 004192 | STOCK Mttptm2Sgy Ldlrtm1Her Apobtm2Sgy Tg(Mx1-cre)1Cgn/J | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
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