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胆固醇代谢平衡调控的分子机理 被引量:11

Molecular Mechanisms in the Regulation of Cholesterol Metabolic Homeostasis
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摘要 胆固醇代谢平衡调控的分子机理李伯良,段治军(中国科学院上海生物化学研究所上海200031)前言胆固醇在生物体内起着重要而又神秘的作用,特别在哺乳类细胞生命过程中是不可缺少的。由于胆固醇及其类似物的绝大部分分布在细胞膜上,目前一般认为胆固醇可起影响生物... Although the roles of cholesterol in higher eukaryotic cells remain mysterious, it has been proventhat cholesterol balance is essential for higher organisms to lead routine lives. The mechanisms thatgovern regulation of cholesterol metabolism in mammmalian cells provide an example of how metabolicregulation has evolved to establish growth and nutritional control in a multicellular environment. Actually, the honieostatic regulatory mechanisms include the regulation of de novo cholesterol synthesis, receptor-mediated cholesterol uptake, and esterification of cholesterol with long-chain fatty acid to formcholesteryl esters. The former two pathways are responsible for the acquisition of cholesterol for thecell; Whereas the latter is responsible for the transportation and storage of cholesterol. Metabolic homeostasis is achieved by regulating the levels of key proteins involved in the acquisition and storage ofcholesterol. LDL receptor(LDL-R), HMG-CoA synthase(HMG-CoA-S) and reductase(HMG-CoA-R),and acylCoA: cholesterol acyltransferase (ACAT ) are regarded as key proteins and the isolation of thesekey genes threw great light in understanding the mechanisms. Feedback regulation by cholesterol is thedominant regulation form in the cholesterol acquisition pathways; on the other hand, cholesterol is anactiviator of ACAT. SRE (ets-acting elements) and SREBPs(trans-acting proteins), mediate the transcription regulation by cholesterol in the gene expression of LDL-R, HMG-CoA-S and HMG-CoA-R.
出处 《生物工程进展》 CSCD 1996年第5期27-33,共7页 Progress in Biotechnology
关键词 胆固醇 代谢平衡调控 分子机理 Metabolic homeostasis Key proteins SRE SREBPs
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参考文献4

  • 1Cheng Dong,J Biol Chem,1995年,270卷,685页
  • 2Wang Xiaodong,Cell,1994年,77卷,53页
  • 3Chang C C,J Biol Chem,1993年,268卷,2074页
  • 4Hua Xiangxin,Proc Natl Acad Sci USA,1993年,90卷,11603页

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