Search Criteria: Research Area is "Mouse/Human Gene Homologs: hypobetalipoproteinemia, familial"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002053 | B6.129P2-Apobtm1Unc/J | Repository- Live |
| The Apobtm1Unc targeted mutation produces a truncated form of the apolipoprotein B protein (APOB70)and no apoB100 that is similar to human familial hypobetalipoproteinemia condition. Expression of apoB48 is not altered. Homozygous mice show greatly reduced levels of plasma APOB, beta-lipoproteins, and total cholesterol. They also have reduced plasma triglyceride concentrations, fasting chylomicronemia, and reduced high density lipoprotein (HDL) cholesterol. Homozygotes also have a high incidence of exencephaly and hydrocephaly. Heterozygous mice show a slight increase over wildtype in the incidence of hydrocephaly. | ||
| 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 | ||
| 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 | ||
| 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 | ||
| 002878 | B6;129-Apobtm1Sgy Apoetm1Unc/J | Repository-Cryopreserved |
| Mice homozygous for the Apobtm1Sgy and Apoetm1Unc targeted mutations do not express the apolipoproteins B100 or E. They do retain the ability to express apolipoprotein B48. They have the highest total cholesterol (392 mg/dl vs 341 for Apobtm1Unc/Apoetm1Unc); highest LDL cholesterol (APOB48 is not a ligand for LDLR), and atherosclerotic lesions more extensive than Apoetm1Unc/Apoetm1Unc homozygotes. The extent of atherosclerosis correlated significantly with plasma cholesterol levels. | ||
| 002879 | B6;129-Apobtm2Sgy Apoetm1Unc/J | Repository-Cryopreserved |
| Mice homozygous for the Apobtm2Sgy and Apoetm1Unc targeted mutations do not express the apolipoproteins B48 or E, they do express APOB100. Homozygotes are viable and fertile with no overt abnormalities. Compared to the APOB48 APOE deficient mice and the APOE deficient mice, they have the lowest total cholesterol (247mg/dl), lowest LDL cholesterol, and the least extensive Atherosclerotic lesions. The extent of atherosclerosis correlated significantly with plasma cholesterol levels. | ||
| 002876 | B6;129S-Apobtm1Sgy/J | Repository-Cryopreserved |
| Mice homozygous for the Apob tm1Sgy targeted mutation are viable and fertile. They show normal expression of APOB48 in the gut but have no expression of APOB100. Homozygous mice show no developmental defects indicating that APOB100 synthesis in the yolk sac is not necessary for normal development. Homozygotes have lower serum LDL cholesterol levels compared to wildtype and APOB100 expressing mice (B6,129-Apob tm2Sgy, Stock No. 002877). | ||
| 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). | ||
| 002877 | B6;129S7-Apobtm2Sgy/J | Repository-Cryopreserved |
| Mice homozygous for the Apobtm2Sgy targeted mutation express only the APOB100 protein; development is normal and there are no intestinal abnormalities. LDL cholesterol is normal. These homozygoous mice have the lowest HDL cholesterol compared to wildtype and APOB48 expressing mice (B6,129-Apobtm1Sgy/J, Stock No. 002876). | ||
| 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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