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Apoa1  -  apolipoprotein A-I

Mus musculus

Synonyms: Alp-1, Apo-AI, ApoA-I, Apoa-1, Apolipoprotein A-I, ...
 
 
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Disease relevance of Apoa1

 

High impact information on Apoa1

  • Overexpression of EL in mice reduced plasma concentrations of HDL cholesterol and its major protein apolipoprotein A-I [6].
  • Thus, HDL activates eNOS via SR-BI through a process that requires ApoA-I binding [7].
  • One, Idd-1s, is tightly linked to the H-2K locus on chromosome 17; another, Idd-2s, is localized proximal to the Thy-1/Alp-1 cluster on chromosome 9 [8].
  • Bile acid-activated nuclear receptor FXR suppresses apolipoprotein A-I transcription via a negative FXR response element [9].
  • Studies in mice, hamsters and rats demonstrate that repression of hepatic apolipoprotein-A1 expression by Taurocholic acid in mice is not mediated by the Farnesoid-X-receptor [10].
  • Previous studies showed that transgenic mice overexpressing either apolipoprotein AI (apoAI) or apolipoprotein AII (apoAII), the major proteins of HDL, exhibited elevated levels of HDL cholesterol, but, whereas the apoAI-transgenic mice were protected against atherosclerosis, the apoAII-transgenic mice had increased lesion development [11].
 

Chemical compound and disease context of Apoa1

 

Biological context of Apoa1

  • We also investigated the question of whether the Apoa1 gene is responsible for the cholesterol QTLs (Cq4 and Cq5) that had been identified previously on chromosome 9 in C57BL/6J x KK-Ay/a F2 and in KK x RR F2, but not in C57BL/6J x RR F2 mice [13].
  • The mouse Apoa-1 gene is 1.76 kb in length with four exons and three introns [14].
  • Apolipoprotein AI, the dominant protein component of serum high density lipoprotein, is intimately involved in cholesterol homeostasis [15].
  • Mouse apolipoprotein AI. cDNA-derived primary structure, gene organisation and complete nucleotide sequence [15].
  • Point mutations in apolipoprotein A-I mimic the phenotype observed in patients with classical lecithin:cholesterol acyltransferase deficiency [16].
 

Anatomical context of Apoa1

 

Associations of Apoa1 with chemical compounds

 

Regulatory relationships of Apoa1

  • This article describes bile acid metabolism in apo AI-deficient (Apo AI(-/-)) mice and their C57BL/6 (Apo AI(+/+)) controls fed either a basal rodent diet alone or containing cholesterol or cholestyramine [27].
 

Other interactions of Apoa1

  • Severe insulitis and concomitant high diabetes incidences occurred in all genotypic classes of congenic mice carrying Thy-1/Apoa-1 linkage markers for either NOD or NON alleles at Idd-2 [28].
  • Cultured murine hepatocytes were used to examine the role of hepatic ABCA1 in mediating the lipidation of apolipoprotein A-I (apoA-I) for HDL particle formation [29].
  • This study provides the first estimate of the distances between Es-17, Ups and Alp-1 [30].
  • Characterization of the mouse apolipoprotein Apoa-1/Apoc-3 gene locus: genomic, mRNA, and protein sequences with comparisons to other species [14].
  • LDL receptor-null mice on a Western diet (WD) have inflammation in large arteries and endothelial dysfunction in small arteries, which are improved with the apolipoprotein A-I mimetic D-4F [31].
 

Analytical, diagnostic and therapeutic context of Apoa1

  • Mice homozygous for the disrupted gene have no plasma apolipoprotein A-I detectable by double immunodiffusion; their total plasma cholesterol and HDL-cholesterol levels after overnight fasting are reduced to about one-third and one-fifth of normal levels, and they are grossly deficient in alpha-migrating HDL particles [19].
  • ApoA-I and apoA-I(M) mRNA expression, as assessed by Northern blot analysis and quantitative real time reverse transcription-PCR, did not exhibit significant differences in either liver or intestine [32].
  • OBJECTIVE: Using bone marrow transplantation, we assessed the impact of macrophage-derived phospholipid transfer protein (PLTP) on lesion development in hypercholesterolemic mice that expressed either normal levels of mouse apolipoprotein AI (apoAI) or elevated levels of only human apoAI [33].
  • All monoclonal antibodies were specific for apolipoprotein A-I and bound between 55% and 100% of 125I-labeled high density lipoproteins (HDL) in a fluid phase radioimmunoassay [34].
  • Epitope mapping of the human biliary amphipathic, anionic polypeptide: similarity with a calcium-binding protein isolated from gallstones and bile, and immunologic cross-reactivity with apolipoprotein A-I [35].

 

References

  1. Expression of human apolipoprotein A-I/C-III/A-IV gene cluster in mice reduces atherogenesis in response to a high fat-high cholesterol diet. Baroukh, N., Ostos, M.A., Vergnes, L., Recalde, D., Staels, B., Fruchart, J., Ochoa, A., Castro, G., Zakin, M.M. FEBS Lett. (2001) [Pubmed]
  2. ApoA-I deficiency causes both hypertriglyceridemia and increased atherosclerosis in human apoB transgenic mice. Voyiaziakis, E., Goldberg, I.J., Plump, A.S., Rubin, E.M., Breslow, J.L., Huang, L.S. J. Lipid Res. (1998) [Pubmed]
  3. Role of apolipoprotein A-I in protecting against endotoxin toxicity. Ma, J., Liao, X.L., Lou, B., Wu, M.P. Acta Biochim. Biophys. Sin. (Shanghai) (2004) [Pubmed]
  4. Effects of D-4F on vasodilation and vessel wall thickness in hypercholesterolemic LDL receptor-null and LDL receptor/apolipoprotein A-I double-knockout mice on Western diet. Ou, J., Wang, J., Xu, H., Ou, Z., Sorci-Thomas, M.G., Jones, D.W., Signorino, P., Densmore, J.C., Kaul, S., Oldham, K.T., Pritchard, K.A. Circ. Res. (2005) [Pubmed]
  5. Heteronuclear NMR studies of human serum apolipoprotein A-I. Part I. Secondary structure in lipid-mimetic solution. Okon, M., Frank, P.G., Marcel, Y.L., Cushley, R.J. FEBS Lett. (2002) [Pubmed]
  6. A novel endothelial-derived lipase that modulates HDL metabolism. Jaye, M., Lynch, K.J., Krawiec, J., Marchadier, D., Maugeais, C., Doan, K., South, V., Amin, D., Perrone, M., Rader, D.J. Nat. Genet. (1999) [Pubmed]
  7. High-density lipoprotein binding to scavenger receptor-BI activates endothelial nitric oxide synthase. Yuhanna, I.S., Zhu, Y., Cox, B.E., Hahner, L.D., Osborne-Lawrence, S., Lu, P., Marcel, Y.L., Anderson, R.G., Mendelsohn, M.E., Hobbs, H.H., Shaul, P.W. Nat. Med. (2001) [Pubmed]
  8. Three recessive loci required for insulin-dependent diabetes in nonobese diabetic mice. Prochazka, M., Leiter, E.H., Serreze, D.V., Coleman, D.L. Science (1987) [Pubmed]
  9. Bile acid-activated nuclear receptor FXR suppresses apolipoprotein A-I transcription via a negative FXR response element. Claudel, T., Sturm, E., Duez, H., Torra, I.P., Sirvent, A., Kosykh, V., Fruchart, J.C., Dallongeville, J., Hum, D.W., Kuipers, F., Staels, B. J. Clin. Invest. (2002) [Pubmed]
  10. Studies in mice, hamsters, and rats demonstrate that repression of hepatic apoA-I expression by taurocholic acid in mice is not mediated by the farnesoid-X-receptor. Gardès, C., Blum, D., Bleicher, K., Chaput, E., Ebeling, M., Hartman, P., Handschin, C., Richter, H., Benson, G.M. J. Lipid. Res. (2011) [Pubmed]
  11. Overexpression of apolipoprotein AII in transgenic mice converts high density lipoproteins to proinflammatory particles. Castellani, L.W., Navab, M., Van Lenten, B.J., Hedrick, C.C., Hama, S.Y., Goto, A.M., Fogelman, A.M., Lusis, A.J. J. Clin. Invest. (1997) [Pubmed]
  12. Beneficial effects of ApoA-I on LPS-induced acute lung injury and endotoxemia in mice. Yan, Y.J., Li, Y., Lou, B., Wu, M.P. Life Sci. (2006) [Pubmed]
  13. Quantitative trait locus analysis of plasma cholesterol and triglyceride levels in C57BL/6J x RR F2 mice. Suto, J., Takahashi, Y., Sekikawa, K. Biochem. Genet. (2004) [Pubmed]
  14. Characterization of the mouse apolipoprotein Apoa-1/Apoc-3 gene locus: genomic, mRNA, and protein sequences with comparisons to other species. Januzzi, J.L., Azrolan, N., O'Connell, A., Aalto-Setälä, K., Breslow, J.L. Genomics (1992) [Pubmed]
  15. Mouse apolipoprotein AI. cDNA-derived primary structure, gene organisation and complete nucleotide sequence. Stoffel, W., Müller, R., Binczek, E., Hofmann, K. Biol. Chem. Hoppe-Seyler (1992) [Pubmed]
  16. Point mutations in apolipoprotein A-I mimic the phenotype observed in patients with classical lecithin:cholesterol acyltransferase deficiency. Chroni, A., Duka, A., Kan, H.Y., Liu, T., Zannis, V.I. Biochemistry (2005) [Pubmed]
  17. ApoA-I lipidation in primary mouse hepatocytes. Separate controls for phospholipid and cholesterol transfers. Zheng, H., Kiss, R.S., Franklin, V., Wang, M.D., Haidar, B., Marcel, Y.L. J. Biol. Chem. (2005) [Pubmed]
  18. Hydroxytyrosol administration enhances atherosclerotic lesion development in apo e deficient mice. Acín, S., Navarro, M.A., Arbonés-Mainar, J.M., Guillén, N., Sarría, A.J., Carnicer, R., Surra, J.C., Orman, I., Segovia, J.C., Torre, R.d.e. .L., Covas, M.I., Fernández-Bolaños, J., Ruiz-Gutiérrez, V., Osada, J. J. Biochem. (2006) [Pubmed]
  19. Marked reduction of high density lipoprotein cholesterol in mice genetically modified to lack apolipoprotein A-I. Williamson, R., Lee, D., Hagaman, J., Maeda, N. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
  20. Potential involvement of dissociated apoA-I in the ABCA1-dependent cellular lipid release by HDL. Okuhira, K., Tsujita, M., Yamauchi, Y., Abe-Dohmae, S., Kato, K., Handa, T., Yokoyama, S. J. Lipid Res. (2004) [Pubmed]
  21. Apolipoprotein A-I induces translocation of protein kinase C[alpha] to a cytosolic lipid-protein particle in astrocytes. Ito, J., Li, H., Nagayasu, Y., Kheirollah, A., Yokoyama, S. J. Lipid Res. (2004) [Pubmed]
  22. Lack of apoA-I is not associated with increased susceptibility to atherosclerosis in mice. Li, H., Reddick, R.L., Maeda, N. Arterioscler. Thromb. (1993) [Pubmed]
  23. Apolipoprotein A-I is required for cholesteryl ester accumulation in steroidogenic cells and for normal adrenal steroid production. Plump, A.S., Erickson, S.K., Weng, W., Partin, J.S., Breslow, J.L., Williams, D.L. J. Clin. Invest. (1996) [Pubmed]
  24. High doses of bifendate elevate serum and hepatic triglyceride levels in rabbits and mice: animal models of acute hypertriglyceridemia. Pan, S.Y., Yang, R., Han, Y.F., Dong, H., Feng, X.D., Li, N., Geng, W., Ko, K.M. Acta Pharmacol. Sin. (2006) [Pubmed]
  25. The role of apolipoprotein A-I-containing lipoproteins in atherosclerosis. Forte, T.M., McCall, M.R. Curr. Opin. Lipidol. (1994) [Pubmed]
  26. In vivo regulation of apolipoprotein A-I gene expression by estradiol and testosterone occurs by different mechanisms in inbred strains of mice. Tang, J.J., Srivastava, R.A., Krul, E.S., Baumann, D., Pfleger, B.A., Kitchens, R.T., Schonfeld, G. J. Lipid Res. (1991) [Pubmed]
  27. Induction of bile acid synthesis by cholesterol and cholestyramine feeding is unimpaired in mice deficient in apolipoprotein AI. Jolley, C.D., Dietschy, J.M., Turley, S.D. Hepatology (2000) [Pubmed]
  28. Genetic control of diabetogenesis in NOD/Lt mice. Development and analysis of congenic stocks. Prochazka, M., Serreze, D.V., Worthen, S.M., Leiter, E.H. Diabetes (1989) [Pubmed]
  29. ABCA1-dependent lipid efflux to apolipoprotein A-I mediates HDL particle formation and decreases VLDL secretion from murine hepatocytes. Sahoo, D., Trischuk, T.C., Chan, T., Drover, V.A., Ho, S., Chimini, G., Agellon, L.B., Agnihotri, R., Francis, G.A., Lehner, R. J. Lipid Res. (2004) [Pubmed]
  30. Conserved linkage within a 4-cM region of mouse chromosome 9 and human chromosome 11. Antonucci, T.K., Von Deimling, O.H., Rosenblum, B.B., Skow, L.C., Meisler, M.H. Genetics (1984) [Pubmed]
  31. D-4F decreases brain arteriole inflammation and improves cognitive performance in LDL receptor-null mice on a Western diet. Buga, G.M., Frank, J.S., Mottino, G.A., Hendizadeh, M., Hakhamian, A., Tillisch, J.H., Reddy, S.T., Navab, M., Anantharamaiah, G.M., Ignarro, L.J., Fogelman, A.M. J. Lipid Res. (2006) [Pubmed]
  32. Targeted replacement of mouse apolipoprotein A-I with human ApoA-I or the mutant ApoA-IMilano. Evidence of APOA-IM impaired hepatic secretion. Parolini, C., Chiesa, G., Zhu, Y., Forte, T., Caligari, S., Gianazza, E., Sacco, M.G., Sirtori, C.R., Rubin, E.M. J. Biol. Chem. (2003) [Pubmed]
  33. Atheroprotective potential of macrophage-derived phospholipid transfer protein in low-density lipoprotein receptor-deficient mice is overcome by apolipoprotein AI overexpression. Valenta, D.T., Ogier, N., Bradshaw, G., Black, A.S., Bonnet, D.J., Lagrost, L., Curtiss, L.K., Desrumaux, C.M. Arterioscler. Thromb. Vasc. Biol. (2006) [Pubmed]
  34. Immunochemical characterization of six monoclonal antibodies to human apolipoprotein A-I: epitope mapping and expression. Marcovina, S., Fantappie, S., Zoppo, A., Franceschini, G., Catapano, A.L. J. Lipid Res. (1990) [Pubmed]
  35. Epitope mapping of the human biliary amphipathic, anionic polypeptide: similarity with a calcium-binding protein isolated from gallstones and bile, and immunologic cross-reactivity with apolipoprotein A-I. Domingo, N., Grosclaude, J., Bekaert, E.D., Mège, D., Chapman, M.J., Shimizu, S., Ayrault-Jarrier, M., Ostrow, J.D., Lafont, H. J. Lipid Res. (1992) [Pubmed]
 
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