JAX Mice Database - Hypocholesterolemia

Search Criteria: Research Area is "Cardiovascular Research: Hypocholesterolemia"

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
002055	B6.129P2-Apoa1^tm1Unc/J	Repository- Live
	Mice homozygous for the Apoa1^tm1Unc targeted mutation have no APOA1 protein in their plasma. They have severely reduced levels of plasma cholesterol and HDL-cholesterol after overnight fasting. They also show a deficiency in alpha-migrating HDL particles. The Apoa1^tm1Unc mutant mice appear to develop normally.
002053	B6.129P2-Apob^tm1Unc/J	Repository- Live
	The Apob^tm1Unc 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-Apob^tm1.1Zc/J	Repository- Live
	Mice homozygous for this apoB38.9 allele (apoB^38.9/38.9) 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
005323	B6;129P2 Pemt^tm1J-tnyw/J	Repository- Live

005939	B6;129S6-Insig1^tm1Mbjg Insig2^tm1Mbjg/J	Repository- Live
	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. Double homozygous mutant 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.
005993	B6;129S6-Pcsk9^tm1Jdh/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.
007683	CByJ.129X1(Cg)-Apob^tm1.1Zc/J	Repository- Live
	Mice homozygous for this apoB38.9 allele (apoB^38.9/38.9) 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 (Acads^del-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)-Apob^tm1.1Zc/J	Repository- Live
	Mice homozygous for this apoB38.9 allele (apoB^38.9/38.9) 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
002057	B6.129-Apoc3^tm1Unc/J	Repository-Cryopreserved
	Mice homozygous for the Apoc3^tm1Unc show fasted plasma triglyceride levels that are 70% that present in normal wildtype siblings. Levels of total plasma cholesterol and HDL in homozygous mice are slightly reduced compared to normal wildtype silbings. Homozygotes also show hypotriglyceridemia when given the "fat meal test", and are able to clear chylomicrons faster than normal wildtype silbings. Heterozygous mice show fasted plasma triglyceride levels that are reduced compared to normal wildtype mice, though not as severely as in homozygous mice.
003918	B6.129P2-Pltp^tm1Jia/J	Repository-Cryopreserved
	Mice that are homozygous null for the Pltp gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Pltp mRNA is detected in the tissues that normally express Pltp (lung and liver). No plasma Pltp activity is detected. Marked decreases in plasma HDL phospholipid (66%), cholesteryl ester (69%), free cholesterol (70%) and apoAI are observed. When mice are maintained on a high fat/high cholesterol diet, similar reductions are observed, as are increases in VLDL and LDL phospholipid, free cholesterol and cholesteryl ester. This mutant strain offers a model useful in studies related to cholesterol metabolism and atherosclerosis.
002878	B6;129-Apob^tm1Sgy Apoe^tm1Unc/J	Repository-Cryopreserved
	Mice homozygous for the Apob^tm1Sgy and Apoe^tm1Unc 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 Apob^tm1Unc/Apoe^tm1Unc); highest LDL cholesterol (APOB48 is not a ligand for LDLR), and atherosclerotic lesions more extensive than Apoe^tm1Unc/Apoe^tm1Unc homozygotes. The extent of atherosclerosis correlated significantly with plasma cholesterol levels.
002879	B6;129-Apob^tm2Sgy Apoe^tm1Unc/J	Repository-Cryopreserved
	Mice homozygous for the Apob^tm2Sgy and Apoe^tm1Unc 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.
003187	B6;129P2-Pemt^tm1J/J	Repository-Cryopreserved
	Mice homozygous for the Pemt^tm1J 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.
002876	B6;129S-Apob^tm1Sgy/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-Apob^tm2Sgy Ldlr^tm1Her/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 (Ldlr^tm1Her/Ldlr^tm1Her).
002227	B6;129S-Apoc3^tm1Unc/J	Repository-Cryopreserved
	Mice homozygous for the Apoc3^tm1Unc show fasted plasma triglyceride levels that are 70% that present in normal wildtype siblings. Levels of total plasma cholesterol and HDL in homozygous mice are slightly reduced compared to normal wildtype silbings. Homozygotes also show hypotriglyceridemia when given the "fat meal test", and are able to clear chylomicrons faster than normal wildtype silbings. Heterozygous mice show fasted plasma triglyceride levels that are reduced compared to normal wildtype mice, though not as severely as in homozygous mice.
006258	B6;129S4-Apoa2^tm1Bres/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-Apoa4^tm1Bres/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.
004670	B6;129S6-Abcg5/Abcg8^tm1Hobb/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.
002877	B6;129S7-Apob^tm2Sgy/J	Repository-Cryopreserved
	Mice homozygous for the Apob^tm2Sgy 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-Apob^tm1Sgy/J, Stock No. 002876).
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
003285	C57BL/6-Tg(LIPC)6784His/J	Repository-Cryopreserved
	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 descriiption on the strain data sheet
008507	C57BL/6J-Hlb320/J	Repository-Cryopreserved
	For information on Hlb320 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
008508	C57BL/6J-hlb218/J	Repository-Cryopreserved
	For information on hlb218 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
002882	C57BL/6J-Tg(PLTP)1Pgn/J	Repository-Cryopreserved
	Transgenic mice overexpressing the human PLTP gene (Line A) show mRNA transcripts in adipose tissue, lung, heart, and spleen. The PLTP expression in the liver was low and plasma phospholipid transfer activity did not significantly vary between transgenic and control mice. However, transgene expression did alter lipoprotein levels in mice fed a standard chow diet. Non-HDL cholesterol was significantly lowered and the HDL cholesterol/non-HDL cholesterol ratio raised in transgenic mice compared to controls. Overall, the expression of human PLTP in mice altered the lipoprotein profile in a manner that suggests enhanced expression of PLTP could potentially retard atherosclerosis.
003897	DBA/1-Abca1^tm1Jdm/J	Repository-Cryopreserved
	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 descriiption on the strain data sheet
004192	STOCK Mttp^tm2Sgy Ldlr^tm1Her Apob^tm2Sgy 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 Ldlr^tm1Sgy and Apob^tm1Sgy 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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New Strains Under Development

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Stock Number	Strain Name Strain Description	Standard Supply
008763	B6.129-Abcg8^tm1Elk/J	Under Development for Production
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 description on the strain data sheet
008235	B6.129P2-Abcg5^tm1Plo/J	Under Development for Production
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 description on the strain data sheet

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New Strains Under Development
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The 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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