Strain Name:

B6.Cg-Lepob Ldlrtm1Her/J

Stock Number:

006906

Availability:

Repository- Live
The mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, and hypercholesterolemia.

Description

Strain Information

Type Congenic; Mutant Strain; Spontaneous Mutation; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Mating SystemSee Colony Maintenance
Specieslaboratory mouse
GenerationF?+N1F2 (16-JUL-08)
 
Donating Investigator Jan Breslow,   Rockefeller University

Description
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.

Development
The Ldlrtm1Her mutation was made by Dr. Robert Hammer and Joachim Herz (HHMI, University of Texas Southwestern Medical Center). Briefly, a targeting vector was used to insert a neo cassette into exon 4. The vector was electroporated into 129S7/SvEvBrd-derived AB1 embryonic stem (ES) cells. Chimeric mice were bred to C57BL/6J, and the strain was made congenic on a C57BL/6J genetic background at The Jackson Laboratory (Stock No. 002207). The ob spontaneous mutation in the leptin gene is maintained on a congenic C57BL/6J genetic background at The Jackson Laboratory (Stock No. 000632). To generate the double mutant strain, Stock No. 002207 mice were bred with Stock No. 000632 mice in the laboratory of Dr. Jan Breslow at The Rockefeller University. Double mutant mice were bred as heterozygous for the ob mutation and homozygous for the LDLR mutation for many generations prior to arrival at The Jackson Laboratory.

Control Information

  Control
   Wild-type for Lepob, Homozygous for Ldlrtm1Her
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

View Strains carrying   Ldlrtm1Her     (13 strains)

Strains carrying   Lepob allele
000632   B6.V-Lepob/J
000696   BKS.V-Lepob/J
004824   BTBR.V(B6)-Lepob/WiscJ
View Strains carrying   Lepob     (3 strains)

Strains carrying other alleles of Ldlr
005061   C57BL/6J-LdlrHlb301/J
View Strains carrying other alleles of Ldlr     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms
Hypercholesterolemia, Autosomal Dominant - Models with phenotypic similarity to human disease where etiologies involve orthologs.1
1 Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
View Mammalian Phenotype Terms

Mammalian Phenotype Terms
      assigned by genotype

Ldlrtm1Her/Ldlr+ Lepob/Lepob

        B6.Cg-Lepob Ldlrtm1Her
  • homeostasis/metabolism phenotype
  • increased cholesterol level (MGI Ref ID J:72027)
    • livers exhibit slightly, but significantly, higher levels of cholesterol
    • increased circulating cholesterol level (MGI Ref ID J:72027)
      • age dependent increase in cholesterol levels between 1 and 4 months of age, with maximal values at 3-4 months of age (282 mg/dl vs 81 md/dl in wild-type) that are maintained thereafter
      • increased circulating HDL cholesterol level (MGI Ref ID J:72027)
        • slightly elevated at 3 and 8 months of age
  • increased triglyceride level (MGI Ref ID J:72027)
    • livers exhibit about 10x higher levels of triglyceride, however no icrease in plasma triglyceride levels

Ldlrtm1Her/Ldlrtm1Her Lepob/Lepob

        B6.Cg-Lepob Ldlrtm1Her
  • cardiovascular system phenotype
  • atherosclerotic lesions (MGI Ref ID J:72027)
    • extensive atherosclerotic lesions throughout the aorta by 6 months of age
  • homeostasis/metabolism phenotype
  • abnormal circulating cholesterol level (MGI Ref ID J:72027)
    • plasma contains severely elevated and broadened lipoprotein peak, ranging from VLDL/LDL-sized particles to LDL-sized particles
    • increased circulating cholesterol level (MGI Ref ID J:72027)
      • age dependent increase in cholesterol levels between 1 and 4 months of age, with maximal values at 3-4 months of age (1715 mg/dl vs. 81 mg/dl in wild-type), followed by a gradual decrease by 8 months
      • fasting, diet restriction, and low-level leptin treatment only slightly lowers plasma cholesterol levels
      • increased circulating HDL cholesterol level (MGI Ref ID J:72027)
        • elevated at 3 and 8 months of age
  • hyperlipidemia (MGI Ref ID J:72027)
  • increased cholesterol level (MGI Ref ID J:72027)
    • livers exhibit slightly, but significantly, higher levels of cholesterol
    • increased circulating cholesterol level (MGI Ref ID J:72027)
      • age dependent increase in cholesterol levels between 1 and 4 months of age, with maximal values at 3-4 months of age (1715 mg/dl vs. 81 mg/dl in wild-type), followed by a gradual decrease by 8 months
      • fasting, diet restriction, and low-level leptin treatment only slightly lowers plasma cholesterol levels
      • increased circulating HDL cholesterol level (MGI Ref ID J:72027)
        • elevated at 3 and 8 months of age
  • increased triglyceride level (MGI Ref ID J:72027)
    • livers exhibit about 10x higher levels of triglyceride
    • increased circulating triglyceride level (MGI Ref ID J:72027)
      • age dependent increase in triglyceride levels between 1 and 4 months of age, with maximal values at 3-4 months of age, followed by a gradual decrease by 8 months
      • fasting, diet restriction, and low-level leptin treatment significantly lowers plasma triglyceride levels
View Research Applications

Research Applications
This mouse can be used to support research in many areas including:

Cardiovascular Research
Atherosclerosis
Hypercholesterolemia
Other
      altered fat metabolism

Diabetes and Obesity Research
Hyperglycemia
Hyperinsulinemia

Metabolism Research
Lipid Metabolism

Research Tools
Cardiovascular Research
Diabetes and Obesity Research
Metabolism Research

Ldlrtm1Her related

Cardiovascular Research
Atherosclerosis
Hypercholesterolemia

Metabolism Research
Lipid Metabolism

Mouse/Human Gene Homologs
hypercholesterolemia, familial

Lepob related

Diabetes and Obesity Research
Hyperinsulinemia
Impaired Wound Healing
Insulin Resistance
Obesity With Diabetes

Endocrine Deficiency Research
Adipose Defects
Hypothalamus/Pituitary Defects
Pancreas Defects

Immunology and Inflammation Research
Immunodeficiency Associated with Other Defects

Internal/Organ Research
Adipose Defects

Metabolism Research

Mouse/Human Gene Homologs
obesity, severe, due to leptin deficiency (rare)

Reproductive Biology Research
Fertility Defects

Genes & Alleles

Gene & Allele Information

 
Allele Symbol Ldlrtm1Her
Allele Name targeted mutation 1, Joachim Herz
Allele Type Targeted (knock-out)
Common Name(s) LDLR KO; LDLR-; LDLr0; LDLrKO; Ldlrtm1Her;
Mutation Made By Joachim Herz,   Univ of Texas Southwest Med Ctr Dallas
Strain of Origin129S7/SvEvBrd-Hprt1<+>
ES Cell Line NameAB1
ES Cell Line Strain129S7/SvEvBrd-Hprt1<+>
Gene Symbol and Name Ldlr, low density lipoprotein receptor
Chromosome 9
Gene Common Name(s) FH; FHC; LDLCQ2; LDLRA;
General Note When used in bone marrow transplant into Ldlrtm1Her homozygous mice, Abca1tm1Jdm Abcg1tm1Dgen homozygous cells accelerate the development of atherosclerosis. (J:130777)
Molecular Note Insertion of a neomycin resistance cassette into exon 4. The authors predict that the targeted allele would encode a truncated non-functional protein that will not bind LDL, and that lacks a membrane spanning segment. Immunoblot analysis of liver membranes detected a truncated protein in homozygous mutant animals. [MGI Ref ID J:37394]
 
Allele Symbol Lepob
Allele Name obese
Allele Type Spontaneous
Common Name(s) ob;
Strain of OriginSTOCK Mlph a Tgfa Cdh23 Ednrb
Gene Symbol and Name Lep, leptin
Chromosome 6
Gene Common Name(s) FLJ94114; OB; OBS; ob; obese;
General Note Homozygous obese mice are first recognizable at about 4 weeks of age. They increase in weight rapidly and may reach three times normal weight (J:13066). In addition to obesity, mutant mice exhibit hyperphagia; a diabetes-like syndrome of hyperglycemia, glucose intolerance, and elevated plasma insulin; subfertility; and increased hormone production from both pituitary and adrenal. They also have difficulty maintaining body temperature under cold conditions (J:7702).

The obesity is characterized by both an increased number of adipocytes and an increase in their size (J:7702); this is in contrast to other genetic obesities in the mouse in which increase in fat depots is due entirely to cell enlargement (J:5253, J:5765).

Hyperphagia may contribute tothe obesity. However, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal lean mice, thus demonstrating an increased metabolic efficiency (J:6236). In parabiosis with normal mice, Lepob homozygotes eat less and lose weight; in parabiosis with Leprdb homozygotes, they cease eating completely and die of starvation. This is taken to mean that they have a normal response to a 'satiety' factor, presumably the leptin protein, but are unable to produce enough of it to maintain normal food intake (J:5401).

Hyperinsulinemia does not develop until after the increase in food intake and is probably the result of it (J:5759). It has been shown, however, that homozygous Lepob mice have an abnormally low threshold for stimulation of pancreatic islet insulin secretion (J:14402), even in very young animals before obesity develops (J:22634). As is the case with the diabetes mutant Leprdb, manifestation of the diabetic syndrome is strikingly dependent on genetic background. On a C57BL/6 background, Lepob homozygotes develop a well compensated diabetes with only temporary and moderate hyperglycemia, marked hyperinsulinemia, and enlarged islets of Langerhans. Onthe C57BLKS background, however, they become severely diabetic with regression of the islets and early death (J:5400).

Lepob homozygous mice have an impaired capacity for non-shivering thermogenesis which can be demonstrated at low temperatures as early as 10 days of age (J:12010). At 4 degrees C they rapidly become hypothermic and die within a few hours (J:5958). It has been suggested that a reduction in the energy requirement normally used for thermoregulatory heat production could be responsible for the increased metabolic efficiency noted above. That is unlikely to be the major cause of the thermoregulatory problems, however, since brief exposure of obese mice to 10 degrees C produces cold adaptation and allows indefinite survival at 4degrees C with maintenance of nearly normal body temperature (J:6756).

Coleman has suggested that the hyperinsulinemia of obese mice, which increases synthetic processes and decreases degradation, might spare the energy normally spent on tissue turnover and account at least in part for the increased efficiency (J:6756). Some contribution to the effect may also come from a low basal Na+,K+ATPase activity, shown to occur in muscle of 14-day old mutants (J:6182).

Heterozygotes (Lepob/+) have normal body weight, blood glucose, and plasma insulin, but can survive a prolonged fast longer than congenic wild-type controls, suggesting that increased metabolic efficiency is expressed to some extent in heterozygotes (J:159).

Female homozygotes are always sterile, although their ovaries respond to exogenous pituitary hormones. About 20% of male homozygotes may be transiently fertile, particularly if maintained on a restricted diet (J:7702).

Cloning of the Lep gene has made possible the production of recombinant leptin. Injection of this protein into Lepob homozygotes sharply reduces body weight, decreases food intake, and increases energy expenditure. There is no effect in diabetic Leprdb homozygotes, who are resistant to effects of the Lepob mutation. Normal mice also decrease food consumption and lose weight, with an accompanying loss in body fat (J:29161). Other investigators have obtained congruent results in normal and in Lepob mice (J:29162, J:29075); leptin also reduces food intake in fasted normal mice (J:28578). Leptin treatment effects on behavior of Lepob mice suggest a direct effect on neuronal networks (J:29160). Interactions of leptin with effects of hypothalamic lesions and of the Lepr gene indicate that Lep is upstream in the pathway of adipose tissue mass regulation (J:27422). Mutant leptin produced by the Lepob mutation fails to self-regulate production of leptin mRNA, which rises to a level 4 times that in normal mice. Lean mice when fasted decrease in leptin mRNA levels, but obese animals do not (J:29081).

There is a vast literature on the biochemical and physiological changes in Lepob mice, which has been reviewed by Herberg and Coleman (J:5759) and more recently by Charlton (J:7702). Many of the studies performed in adult mice may involve secondary effects of obesity rather than primary causes of it.

Increased blood levels of corticosterone occur in Lepob/Lepob mice, and most of the symptoms of the obese syndrome are ameliorated by excision of the adrenal glands. The hypothalamus-pituitary-adrenal axis is dysregulated, with hyperactivity of pituitary synthesis and secretion of adrenocorticotropic hormone (ACTH), as well as hyperresponsiveness of the adrenal cortex to ACTH (J:13151). Adrenal medullary activity, on the other hand, may be decreased; a diminished urinary excretion of epinephrine in obese homozygous mice indicates reduced medullary production, although this may be a secondary effect of the obesity (J:4033). A low serum level of the thyroid hormone triiodothyronine (T3) is also characteristic of obese homozygotes. Early treatment of these mice with T3 increases oxygen consumption and temperature while reducing body fat (J:22025). T3 treatment increases oxidative metabolism in muscle, but not in brown adipose tissue or in liver (J:22377).

Plasma triglyceride levels are elevated in mouse mutants considered models of non-insulin-dependent diabetes,including Lepob mutants. Cholesterol is also elevated, but the increase is primarily in high-density lipoprotein cholesterol (J:18161), so that atherosclerotic lesions are not increased (J:19043).

Molecular Note Sequencing of RT-PCR products revealed a nonsense mutation in codon 105 resulting from a C to T point mutation. The 16 kDa leptin protein, expressed predominantly in adipose tissue of normal mice, is missing from homozygous mutant mice (J:29081). [MGI Ref ID J:20512] [MGI Ref ID J:29081] [MGI Ref ID J:45748]

Genotyping

Genotyping Information

Genotyping Protocols

Ldlr tm1Her, Standard PCR
Lepob, Pyrosequencing
Lepob, Restriction Enzyme Digest

Helpful Links

Genotyping resources and troubleshooting

References

References

Additional References

Ishibashi S; Brown MS; Goldstein JL; Gerard RD; Hammer RE; Herz J. 1993. Hypercholesterolemia in low density lipoprotein receptor knockout mice and its reversal by adenovirus-mediated gene delivery [see comments] J Clin Invest 92(2):883-93. [PubMed: 8349823]  [MGI Ref ID J:37394]

Zhang Y; Proenca R; Maffei M; Barone M; Leopold L; Friedman JM. 1994. Positional cloning of the mouse obese gene and its human homologue [published erratum appears in Nature 1995 Mar 30;374(6521):479] [see comments] Nature 372(6505):425-32. [PubMed: 7984236]  [MGI Ref ID J:20512]

Ldlrtm1Her related

Accad M; Smith SJ; Newland DL; Sanan DA; King LE Jr; Linton MF; Fazio S; Farese RV Jr. 2000. Massive xanthomatosis and altered composition of atherosclerotic lesions in hyperlipidemic mice lacking acyl CoA:cholesterol acyltransferase 1 [see comments] J Clin Invest 105(6):711-9. [PubMed: 10727439]  [MGI Ref ID J:61147]

Afek A; Keren G; Harats D; George J. 2001. Whole body hyperthermia accelerates atherogenesis in low-density lipoprotein receptor deficient mice. Exp Mol Pathol 71(1):63-72. [PubMed: 11502098]  [MGI Ref ID J:106255]

Ait-Oufella H; Kinugawa K; Zoll J; Simon T; Boddaert J; Heeneman S; Blanc-Brude O; Barateau V; Potteaux S; Merval R; Esposito B; Teissier E; Daemen MJ; Leseche G; Boulanger C; Tedgui A; Mallat Z. 2007. Lactadherin deficiency leads to apoptotic cell accumulation and accelerated atherosclerosis in mice. Circulation 115(16):2168-77. [PubMed: 17420351]  [MGI Ref ID J:135906]

Ait-Oufella H; Salomon BL; Potteaux S; Robertson AK; Gourdy P; Zoll J; Merval R; Esposito B; Cohen JL; Fisson S; Flavell RA; Hansson GK; Klatzmann D; Tedgui A; Mallat Z. 2006. Natural regulatory T cells control the development of atherosclerosis in mice. Nat Med 12(2):178-80. [PubMed: 16462800]  [MGI Ref ID J:105800]

Allred KF; Smart EJ; Wilson ME. 2006. Estrogen receptor-alpha mediates gender differences in atherosclerosis induced by HIV protease inhibitors. J Biol Chem 281(3):1419-25. [PubMed: 16299001]  [MGI Ref ID J:107322]

Altenburg M; Arbones-Mainar J; Johnson L; Wilder J; Maeda N. 2008. Human LDL receptor enhances sequestration of ApoE4 and VLDL remnants on the surface of hepatocytes but not their internalization in mice. Arterioscler Thromb Vasc Biol 28(6):1104-10. [PubMed: 18369154]  [MGI Ref ID J:149026]

Angeli V; Llodra J; Rong JX; Satoh K; Ishii S; Shimizu T; Fisher EA; Randolph GJ. 2004. Dyslipidemia associated with atherosclerotic disease systemically alters dendritic cell mobilization. Immunity 21(4):561-74. [PubMed: 15485633]  [MGI Ref ID J:93917]

Arai S; Shelton JM; Chen M; Bradley MN; Castrillo A; Bookout AL; Mak PA; Edwards PA; Mangelsdorf DJ; Tontonoz P; Miyazaki T. 2005. A role for the apoptosis inhibitory factor AIM/Spalpha/Api6 in atherosclerosis development. Cell Metab 1(3):201-13. [PubMed: 16054063]  [MGI Ref ID J:129845]

Aslanian AM; Chapman HA; Charo IF. 2005. Transient role for CD1d-restricted natural killer T cells in the formation of atherosclerotic lesions. Arterioscler Thromb Vasc Biol 25(3):628-32. [PubMed: 15591216]  [MGI Ref ID J:110061]

Aslanian AM; Charo IF. 2006. Targeted disruption of the scavenger receptor and chemokine CXCL16 accelerates atherosclerosis. Circulation 114(6):583-90. [PubMed: 16880330]  [MGI Ref ID J:123851]

Azhar S; Luo Y; Medicherla S; Reaven E. 1999. Upregulation of selective cholesteryl ester uptake pathway in mice with deletion of low-density lipoprotein receptor function. J Cell Physiol 180(2):190-202. [PubMed: 10395289]  [MGI Ref ID J:56099]

Babaev VR; Chew JD; Ding L; Davis S; Breyer MD; Breyer RM; Oates JA; Fazio S; Linton MF. 2008. Macrophage EP4 deficiency increases apoptosis and suppresses early atherosclerosis. Cell Metab 8(6):492-501. [PubMed: 19041765]  [MGI Ref ID J:144376]

Babaev VR; Ding L; Reese J; Morrow JD; Breyer MD; Dey SK; Fazio S; Linton MF. 2006. Cyclooxygenase-1 deficiency in bone marrow cells increases early atherosclerosis in apolipoprotein E- and low-density lipoprotein receptor-null mice. Circulation 113(1):108-17. [PubMed: 16380543]  [MGI Ref ID J:121507]

Babaev VR; Ishiguro H; Ding L; Yancey PG; Dove DE; Kovacs WJ; Semenkovich CF; Fazio S; Linton MF. 2007. Macrophage expression of peroxisome proliferator-activated receptor-alpha reduces atherosclerosis in low-density lipoprotein receptor-deficient mice. Circulation 116(12):1404-12. [PubMed: 17724261]  [MGI Ref ID J:139843]

Babaev VR; Yancey PG; Ryzhov SV; Kon V; Breyer MD; Magnuson MA; Fazio S; Linton MF. 2005. Conditional knockout of macrophage PPARgamma increases atherosclerosis in C57BL/6 and low-density lipoprotein receptor-deficient mice. Arterioscler Thromb Vasc Biol 25(8):1647-53. [PubMed: 15947238]  [MGI Ref ID J:114332]

Baldan A; Pei L; Lee R; Tarr P; Tangirala RK; Weinstein MM; Frank J; Li AC; Tontonoz P; Edwards PA. 2006. Impaired development of atherosclerosis in hyperlipidemic Ldlr-/- and ApoE-/- mice transplanted with Abcg1-/- bone marrow. Arterioscler Thromb Vasc Biol 26(10):2301-7. [PubMed: 16888235]  [MGI Ref ID J:128048]

Barlic J; Murphy PM. 2007. Chemokine regulation of atherosclerosis. J Leukoc Biol 82(2):226-36. [PubMed: 17329566]  [MGI Ref ID J:123530]

Basso F; Amar MJ; Wagner EM; Vaisman B; Paigen B; Santamarina-Fojo S; Remaley AT. 2006. Enhanced ABCG1 expression increases atherosclerosis in LDLr-KO mice on a western diet. Biochem Biophys Res Commun 351(2):398-404. [PubMed: 17070501]  [MGI Ref ID J:116554]

Basso F; Freeman LA; Ko C; Joyce C; Amar MJ; Shamburek RD; Tansey T; Thomas F; Wu J; Paigen B; Remaley AT; Santamarina-Fojo S; Brewer HB Jr. 2007. Hepatic ABCG5/G8 overexpression reduces apoB-lipoproteins and atherosclerosis when cholesterol absorption is inhibited. J Lipid Res 48(1):114-26. [PubMed: 17060690]  [MGI Ref ID J:117682]

Bavendiek U; Zirlik A; LaClair S; MacFarlane L; Libby P; Schonbeck U. 2005. Atherogenesis in mice does not require CD40 ligand from bone marrow-derived cells. Arterioscler Thromb Vasc Biol 25(6):1244-9. [PubMed: 15746436]  [MGI Ref ID J:114293]

Bell TA rd; Kelley K; Wilson MD; Sawyer JK; Rudel LL. 2007. Dietary fat-induced alterations in atherosclerosis are abolished by ACAT2-deficiency in ApoB100 only, LDLr-/- mice. Arterioscler Thromb Vasc Biol 27(6):1396-402. [PubMed: 17431188]  [MGI Ref ID J:134910]

Bernal-Mizrachi C; Weng S; Feng C; Finck BN; Knutsen RH; Leone TC; Coleman T; Mecham RP; Kelly DP; Semenkovich CF. 2003. Dexamethasone induction of hypertension and diabetes is PPAR-alpha dependent in LDL receptor-null mice. Nat Med 9(8):1069-75. [PubMed: 12847522]  [MGI Ref ID J:84844]

Bernhagen J; Krohn R; Lue H; Gregory JL; Zernecke A; Koenen RR; Dewor M; Georgiev I; Schober A; Leng L; Kooistra T; Fingerle-Rowson G; Ghezzi P; Kleemann R; McColl SR; Bucala R; Hickey MJ; Weber C. 2007. MIF is a noncognate ligand of CXC chemokine receptors in inflammatory and atherogenic cell recruitment. Nat Med 13(5):587-596. [PubMed: 17435771]  [MGI Ref ID J:121807]

Bhasin KK; van Nas A; Martin LJ; Davis RC; Devaskar SU; Lusis AJ. 2009. Maternal low-protein diet or hypercholesterolemia reduces circulating essential amino acids and leads to intrauterine growth restriction. Diabetes 58(3):559-66. [PubMed: 19073773]  [MGI Ref ID J:146932]

Bhatia VK; Yun S; Leung V; Grimsditch DC; Benson GM; Botto MB; Boyle JJ; Haskard DO. 2007. Complement C1q reduces early atherosclerosis in low-density lipoprotein receptor-deficient mice. Am J Pathol 170(1):416-26. [PubMed: 17200212]  [MGI Ref ID J:117210]

Billon-Gales A; Fontaine C; Filipe C; Douin-Echinard V; Fouque MJ; Flouriot G; Gourdy P; Lenfant F; Laurell H; Krust A; Chambon P; Arnal JF. 2009. The transactivating function 1 of estrogen receptor alpha is dispensable for the vasculoprotective actions of 17beta-estradiol. Proc Natl Acad Sci U S A 106(6):2053-8. [PubMed: 19188600]  [MGI Ref ID J:144952]

Binder CJ; Hartvigsen K; Chang MK; Miller M; Broide D; Palinski W; Curtiss LK; Corr M; Witztum JL. 2004. IL-5 links adaptive and natural immunity specific for epitopes of oxidized LDL and protects from atherosclerosis. J Clin Invest 114(3):427-37. [PubMed: 15286809]  [MGI Ref ID J:118092]

Binder CJ; Horkko S; Dewan A; Chang MK; Kieu EP; Goodyear CS; Shaw PX; Palinski W; Witztum JL; Silverman GJ. 2003. Pneumococcal vaccination decreases atherosclerotic lesion formation: molecular mimicry between Streptococcus pneumoniae and oxidized LDL. Nat Med 9(6):736-43. [PubMed: 12740573]  [MGI Ref ID J:83726]

Blasiole DA; Oler AT; Attie AD. 2008. Regulation of ApoB secretion by the low density lipoprotein receptor requires exit from the endoplasmic reticulum and interaction with ApoE or ApoB. J Biol Chem 283(17):11374-81. [PubMed: 18272520]  [MGI Ref ID J:136523]

Boisvert WA; Rose DM; Johnson KA; Fuentes ME; Lira SA; Curtiss LK; Terkeltaub RA. 2006. Up-regulated expression of the CXCR2 Ligand KC/GRO-alpha in atherosclerotic lesions plays a central role in macrophage accumulation and lesion progression. Am J Pathol 168(4):1385-95. [PubMed: 16565511]  [MGI Ref ID J:107325]

Boisvert WA; Santiago R; Curtiss LK; Terkeltaub RA. 1998. A leukocyte homologue of the IL-8 receptor CXCR-2 mediates the accumulation of macrophages in atherosclerotic lesions of LDL receptor-deficient mice. J Clin Invest 101(2):353-63. [PubMed: 9435307]  [MGI Ref ID J:45392]

Bostrom MA; Boyanovsky BB; Jordan CT; Wadsworth MP; Taatjes DJ; de Beer FC; Webb NR. 2007. Group v secretory phospholipase A2 promotes atherosclerosis: evidence from genetically altered mice. Arterioscler Thromb Vasc Biol 27(3):600-6. [PubMed: 17204667]  [MGI Ref ID J:149057]

Boucher P; Gotthardt M; Li WP; Anderson RG; Herz J. 2003. LRP: role in vascular wall integrity and protection from atherosclerosis. Science 300(5617):329-32. [PubMed: 12690199]  [MGI Ref ID J:82871]

Boucher P; Li WP; Matz RL; Takayama Y; Auwerx J; Anderson RG; Herz J. 2007. LRP1 functions as an atheroprotective integrator of TGFbeta and PDFG signals in the vascular wall: implications for Marfan syndrome. PLoS ONE 2(5):e448. [PubMed: 17505534]  [MGI Ref ID J:129347]

Bovenschen N; Mertens K; Hu L; Havekes LM; van Vlijmen BJ. 2005. LDL receptor cooperates with LDL receptor-related protein in regulating plasma levels of coagulation factor VIII in vivo. Blood 106(3):906-12. [PubMed: 15840700]  [MGI Ref ID J:117317]

Boyanovsky BB; van der Westhuyzen DR; Webb NR. 2005. Group V secretory phospholipase A2-modified low density lipoprotein promotes foam cell formation by a SR-A- and CD36-independent process that involves cellular proteoglycans. J Biol Chem 280(38):32746-52. [PubMed: 16040605]  [MGI Ref ID J:102157]

Bretillon L; Acar N; Seeliger MW; Santos M; Maire MA; Juaneda P; Martine L; Gregoire S; Joffre C; Bron AM; Creuzot-Garcher C. 2008. ApoB100,LDLR-/- mice exhibit reduced electroretinographic response and cholesteryl esters deposits in the retina. Invest Ophthalmol Vis Sci 49(4):1307-14. [PubMed: 18385042]  [MGI Ref ID J:136142]

Broedl UC; Maugeais C; Millar JS; Jin W; Moore RE; Fuki IV; Marchadier D; Glick JM; Rader DJ. 2004. Endothelial lipase promotes the catabolism of ApoB-containing lipoproteins. Circ Res 94(12):1554-61. [PubMed: 15117821]  [MGI Ref ID J:100064]

Brown JM; Bell TA rd; Alger HM; Sawyer JK; Smith TL; Kelley K; Shah R; Wilson MD; Davis MA; Lee RG; Graham MJ; Crooke RM; Rudel LL. 2008. Targeted depletion of hepatic ACAT2-driven cholesterol esterification reveals a non-biliary route for fecal neutral sterol loss. J Biol Chem 283(16):10522-34. [PubMed: 18281279]  [MGI Ref ID J:136556]

Buga GM; Frank JS; Mottino GA; Hakhamian A; Narasimha A; Watson AD; Yekta B; Navab M; Reddy ST; Anantharamaiah GM; Fogelman AM. 2008. D-4F reduces EO6 immunoreactivity, SREBP-1c mRNA levels, and renal inflammation in LDL receptor-null mice fed a Western diet. J Lipid Res 49(1):192-205. [PubMed: 17925450]  [MGI Ref ID J:130095]

Buga GM; Frank JS; Mottino GA; Hendizadeh M; Hakhamian A; Tillisch JH; Reddy ST; Navab M; Anantharamaiah GM; Ignarro LJ; Fogelman AM. 2006. D-4F decreases brain arteriole inflammation and improves cognitive performance in LDL receptor-null mice on a Western diet. J Lipid Res 47(10):2148-60. [PubMed: 16835442]  [MGI Ref ID J:116493]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX11

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice are bred as heterozygous for the ob mutation and homozygous for the LDLR mutation.
Mating SystemSee above
Diet Information LabDiet® 5K52/5K67

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Pricing for USA, Canada and Mexico shipping destinations View International pricing
Weeks of AgePrice (US dollars $)GenderGenotypes Provided
Individual Mouse $243.50Female or MaleHeterozygous for Lepob, Homozygous for Ldlrtm1Her
$300.70Female or MaleHomozygous for Lepob, Homozygous for Ldlrtm1Her
Pairs /Price (US dollars $)Pair Genotype
$487.00Heterozygous for Lepob, Homozygous for Ldlrtm1Her x Heterozygous for Lepob, Homozygous for Ldlrtm1Her

Additional Supply Details

Pricing for International shipping destinations View USA Canada and Mexico pricing
Weeks of AgePrice (US dollars $)GenderGenotypes Provided
Individual Mouse $316.60Female or MaleHeterozygous for Lepob, Homozygous for Ldlrtm1Her
$391.00Female or MaleHomozygous for Lepob, Homozygous for Ldlrtm1Her
Pairs /Price (US dollars $)Pair Genotype
$633.10Heterozygous for Lepob, Homozygous for Ldlrtm1Her x Heterozygous for Lepob, Homozygous for Ldlrtm1Her

Additional Supply Details

Supply Details

Standard SupplyRepository-Live. A collection of over 1000 strains maintained as live colonies. Individual colonies are sized to meet current customer demand. Delivery for orders of 10 mice or less ranges on average from one to eight weeks; mice are generally shipped between four to six weeks of age with a maximum shipping age of approximately nine weeks. Colony sizes do not generally support stringent age specifications for large volumes of mice; however custom orders and larger quantities of mice are easily arranged. Estimated ship dates for all orders provided within two business days following order placement.
Supply Notes

Control Information

  Control
   Wild-type for Lepob, Homozygous for Ldlrtm1Her
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains.
  International - Control Pricing Information for Genetically Engineered Mutant Strains.

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
Ordering and Purchasing Information

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      Surgical Services

Contact Information
Orders & Technical Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries

Contracts Administration

phone:207-288-6470
fax:207-288-6655

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. In purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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