JAX Mice Database - Hypercholesterolemia

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

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
002052	B6.129P2-Apoe^tm1Unc/J	Level 1
	Mice homozygous for the Apoe^tm1Unc 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. Recent 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-Ldlr^tm1Her/J	Level 2
	Mice homozygous for the Ldlr^tm1Her 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.
001927	C57BL/6-Tg(APOA1)1Rub/J	Level 3
	Mice carrying the human apolipoprotein A-I transgene show a two fold increase in total plasma cholesterol levels and greater than a four fold decrease in the levels of mouse apoAI. Homozygous transgenic mice exhibit reduced susceptibility to diet induced fatty streak lesions. Mice homozygous for the transgenic insert are viable, fertile and normal in size. This human apolipoprotein AI transgene is under the control of its natural promoter. The Jackson Laboratory imported mice derived from the founder line A2 as described in Rubin EM, et al., 1991.
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
006952	B6.Cg-Akt2^tm1.1Mbb Ldlr^tm1Her/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-Ins2^Akita Ldlr^tm1Her/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-Ldlr^tm1Her Sod2^tm1Leb/J	Repository- Live
	Independently, mice that are homozygous for this MnSOD mutation (Sod2^tm1Leb) 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-Ldlr^tm1Her 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-K^d promoter functions on this H2-K^b 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-Lep^ob Ldlr^tm1Her/J	Repository- Live
	Independently, the C57BL/6-Lep^ob 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.
004633	B6.Cg-Tg(GFAP-APOE3)37Hol Apoe^tm1Unc*/J	Repository- Live
	These transgenic mice express the human apolipoprotein E3 isoform (APOE3) under the direction of the human glial fibrillary acidic protein (GFAP) promoter and do not express endogenous mouse apolipoprotein E (APOE). The transgenic isoform expression pattern follows the endogenous mouse APOE and GFAP expression patterns in the brain. Human APOE3 is immunodetectable in glia and neuropil in developing and adult mutant mice. Cultured astrocytes from transgenic mice secrete APOE3 in lipoproteins that are similar in size to high-density (HDL) plasma lipoproteins. Detergent-soluble APOE3 protein levels in hemizygous mice forebrain tissue and in adult human cortex tissue are similar. Mice that are hemizygous or homozygous for the transgenic insert and homozygous for the targeted allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain represents a model that may be useful in studies examining the function of APOE3 in t ..... For more information please see the full descriiption on the strain data sheet
004631	B6.Cg-Tg(GFAP-APOE4)1Hol Apoe^tm1Unc*/J	Repository- Live
	These transgenic mice express the human apolipoprotein E4 isoform (APOE4) under the direction of the human glial fibrillary acidic protein (GFAP) promoter and do not express endogenous mouse apolipoprotein E (APOE). The transgenic isoform expression pattern follows the endogenous mouse APOE and GFAP expression patterns in the brain. Human APOE4 is immunodetectable in glia and neuropil in developing and adult mutant mice. Cultured astrocytes from transgenic mice secrete APOE4 in lipoproteins that are similar in size to high-density (HDL) plasma lipoproteins. Detergent-soluble APOE4 protein levels in hemizygous mice forebrain tissue and in adult human cortex tissue are similar. Mice that are hemizygous or homozygous for the transgenic insert and homozygous for the targeted allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain represents a model that may be useful in studies examining the function of APOE4 in t ..... For more information please see the full descriiption on the strain data sheet
003379	B6;129S2-Scarb1^tm1Kri/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 descriiption on the strain data sheet
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.
002077	B6;129S7-Ldlr^tm1Her/J	Repository- Live
	Mice homozygous for the Ldlr^tm1Her 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.
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
005213	129-Slc10a2^tm1Pda/J	Repository-Cryopreserved
	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 descriiption on the strain data sheet
002246	B6.129-Apoe^tm1Unc Ldlr^tm1Her/J	Repository-Cryopreserved
	Mice homozygous for the Apoe^tm1Unc and Ldlr^tm1Hertargeted mutations on a normal chow diet show cholesterol levels corresponding to those seen in the Apoe^tm1Unc targeted mutant strain. The lipoprotein pattern in homozygous mice also resembles that seen in the Apoe^tm1Unc targeted mutant strain (VLDL & chylomicron remnants). The double targeted mice have a marked increase in both APOB48 and APOB100. In addition, APOAIV is increased.
002056	B6.129P2-Lipc^tm1Unc/J	Repository-Cryopreserved
	Mice homozygous for the Lipc^tm1Unc targeted mutation are viable and fertile. They show increased levels of total plasma cholesterol, plasma phospholipids, and high density lipoprotein. Triglyceride levels in the plasma are equivalent to those in wildtype mice. Homozygous mice also show a doubling of plasma HDL in response to a high fat diet.
005681	B6.129S-Lipg^tm1Tq/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.
004185	B6.129S4-Soat2^tm1Far/J	Repository-Cryopreserved
	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.
007224	B6.Cg-Apoe^tm1Unc (D12Mit182-D12Mit2)/Pgn	Repository-Cryopreserved

004632	B6.Cg-Tg(GFAP-APOE2)14Hol Apoe^tm1Unc*/J	Repository-Cryopreserved
	These transgenic mice express the human apolipoprotein E2 isoform (APOE2) under the direction of the human glial fibrillary acidic protein (GFAP) promoter and do not express endogenous mouse apolipoprotein E (APOE). The transgenic isoform expression pattern follows the endogenous mouse APOE and GFAP expression patterns in the brain. Human APOE2 is immunodetectable in glia and neuropil in developing and adult mutant mice. Cultured astrocytes from transgenic mice secrete APOE2 in lipoproteins that are similar in size to high-density (HDL) plasma lipoproteins. Detergent-soluble APOE2 protein levels in hemizygous mice forebrain tissue and in adult human cortex tissue are similar. Mice that are hemizygous or homozygous for the transgenic insert and homozygous for the targeted allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain represents a model that may be useful in studies examining the function of APOE2 in t ..... For more information please see the full descriiption on the strain data sheet
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.
002245	B6;129-Apoe^tm1Unc Ldlr^tm1Her/J	Repository-Cryopreserved
	Mice homozygous for the Apoe^tm1Unc and Ldlr^tm1Hertargeted mutations on a normal chow diet show cholesterol levels corresponding to those seen in the Apoe^tm1Unc targeted mutant strain. The lipoprotein pattern in homozygous mice also resembles that seen in the Apoe^tm1Unc targeted mutant strain (VLDL & chylomicron remnants). The double targeted mice have a marked increase in both APOB48 and APOB100. In addition, APOAIV is increased.
004362	B6;129-Scarb1^tm1Kri Apoe^tm1Unc/J	Repository-Cryopreserved
	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.
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).
002465	B6;129S-Ldlr^tm1Her Lrpap1^tm1Her/J	Repository-Cryopreserved
	Mice homozygous for both the Ldlr^tm1Her and Lrpap1^tm1Her 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.
005212	B6;129S-Ldlrap1^tm1Her/J	Repository-Cryopreserved
	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 (protein) is detected by Western blot analysis of liver tissue. Low density lipoproteins (LDL) plasma levels are elevated in homozygous mutant mice. Mice homozygous for the mutant allele exhibit mild hypercholesterolemia when fed a chow diet. Low density lipoprotein-cholesterol, LDL-C, plasma levels are elevated 11 fold when homozygous mutant mice are fed the Paigen high cholesterol diet (1.25% cholesterol, 7.5% cocoa butter, 7.5% casein, 0.5% cholic acid) and 4.7 fold when fed the Western diet (0.2% cholesterol). The circulation clearance rate of radiolabeled LDL is reduced by half in mice homozygous for the mutant allele. Immunofluorescence microscopic analysis of liver tissue reveals abnormal LDLR localization to the sinsusoidal membrane. This mutant mouse strain may be useful in studies of autosomal recessive hyper ..... For more information please see the full descriiption on the strain data sheet
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.
002924	B6;CBA-Tg(APOC1)1Bres/J	Repository-Cryopreserved
	Mice carrying the human apolipoprotein CI transgene are viable and fertile. They show elevated plasma triglycerides in both fasted and fed states. They also have elevated plasma cholesterol, increased VLDL, increased LDL, increased plasma APOB, and slowed clearance of both VLDL triglycerides and postlipolysis lipoprotein remnants. This strain serves as a model of decreased clearance of postprandial triglycerides and lipoprotein remnants.
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.
003311	B6;SJL-Tg(rPEPCKSREBF2)788Reh/J	Repository-Cryopreserved
	Transgenic mice overexpress a dominant-positive truncated form of human sterol regulatory element-binding protein-2 (SREBF2) in liver and adipose tissue. Livers from transgenic mice have increased mRNA levels for genes encoding multiple enzymes of cholesterol and fatty acid biosynthesis as well as the LDL receptor. In vivo cholesterol and fatty acid synthetic rates in livers from transgenic mice are increased 28- and 4-fold, respectively.
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
005691	C57BL/6J-Hlb280/J	Repository-Cryopreserved
	For information on Hlb280 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
005495	C57BL/6J-Hlb398/J	Repository-Cryopreserved
	For information on Hlb398 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
008509	C57BL/6J-Hlb446/J	Repository-Cryopreserved
	For information on Hlb446 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
008263	C57BL/6J-Hlb476/J	Repository-Cryopreserved

008504	C57BL/6J-Hlb477/J	Repository-Cryopreserved
	For information on Hlb477 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
008506	C57BL/6J-Hlb529/J	Repository-Cryopreserved
	Mice homozygous for this ENU induced mutation exhibit elevated HDL cholesterol.
008505	C57BL/6J-Hlb561/J	Repository-Cryopreserved
	Mice homozygous for this ENU induced mutation exhibit elevated HDL cholesterol.
008499	C57BL/6J-Hlb589/J	Repository-Cryopreserved
	Mice homozygous for this ENU induced mutation exhibit elevated HDL cholesterol.
008262	C57BL/6J-Hlb594/J	Repository-Cryopreserved

005061	C57BL/6J-Ldlr^Hlb301/J	Repository-Cryopreserved
	For information on Ldlr^hlb301 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
007231	C57BL/6J-hlb243/J	Repository-Cryopreserved
	For information on hlb243 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
005580	C57BL/6J-hlb388/J	Repository-Cryopreserved
	For information on hlb388 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site.
005863	C57BL/6J-Tg(ACTB-DDAH1)1Jpck/J	Repository-Cryopreserved
	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.
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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Stock Number	Strain Name Strain Description	Standard Supply
007069	AKR.129P2(B6)-Apoe^tm1Unc/J	Under Development for Production
Mice homozygous for the Apoe^tm1Unc 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. Recent studies indicate that APOE deficient mice have altered responses to stress, impaired spatial learning and memory, altered long term potentiation, and synaptic damage. In an attempt to offer alleles on well-characteriz > ..... For more information please see the full description on the strain data sheet
007070	AKR.129S7(B6)-Ldlr^tm1Her/J	Under Development for Production
Mice homozygous for the Ldlr^tm1Her 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.
008355	B6.129(Cg)-Slc6a4^tm1Kpl/J	Under Development for Production
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 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
008525	B6.Cg-Tg(Cyp21a1-Apoe)619Fet/J	Under Development for Production
These transgenic mice express the mouse apolipoprotein E gene, Apoe, under the control of the mouse Cyp21a1, cytochrome P450, family 21, subfamily a, polypeptide 1, promoter. Transgene expression is specific to the adrenal gland. When crossed to B6.129P2-Apoe^tm1Unc/J (Stock No. 002052), transgene mRNA is not detected in the liver, testes or peritoneal macrophages. Founder line 619 mice, hemizygous for the transgene and homozygous for the Apoe^tm1Unc allele, express 1.6 pg Apoe mRNA per mg total RNA in the adrenal gland. This transgenic strain carries only the transgene. This mutant mouse strain may be useful in studies of atherosclerosis and hypercholesterolemia.
007067	D2.129P2(B6)-Apoe^tm1Unc/J	Under Development for Production
Mice homozygous for the Apoe^tm1Unc 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. Recent studies indicate that APOE deficient mice have altered responses to stress, impaired spatial learning and memory, altered long term potentiation, and synaptic damage. In an attempt to offer alleles on well-charac ..... For more information please see the full description on the strain data sheet
007068	D2.129S7(B6)-Ldlr^tm1Her/J	Under Development for Production
Mice homozygous for the Ldlr^tm1Her 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.

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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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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.
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