Cholesterol homeostasis: How do cells sense sterol excess?

被引：51

作者：

Howe, Vicky ^{[1
]}

Sharpe, Laura J. ^{[1
]}

Alexopoulos, Stephanie J. ^{[1
]}

Kunze, Sarah V. ^{[1
]}

Chua, Ngee Kiat ^{[1
]}

Li, Dianfan ^{[2
]}

Brown, Andrew J. ^{[1
]}

机构：

[1] Univ New South Wales, Sch Biotechnol & Biomol Sci, Sydney, NSW 2052, Australia

[2] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, Natl Ctr Prot Sci,State Key Lab Mol Biol, Shanghai, Peoples R China

来源：

CHEMISTRY AND PHYSICS OF LIPIDS | 2016年 / 199卷

关键词：

Cholesterol; Oxysterols; Cholesterol sensing; Membranes; Homeostasis; ENDOPLASMIC-RETICULUM CHOLESTEROL; NUCLEAR RECEPTOR LXR; SQUALENE MONOOXYGENASE; PLASMA-MEMBRANE; REGULATED UBIQUITINATION; SCAP PROTEIN; LOOP; BINDING; DEGRADATION; TRANSPORT;

D O I：

10.1016/j.chemphyslip.2016.02.011

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Cholesterol is vital in mammals, but toxic in excess. Consequently, elaborate molecular mechanisms have evolved to maintain this sterol within narrow limits. How cells sense excess cholesterol is an intriguing area of research. Cells sense cholesterol, and other related sterols such as oxysterols or cholesterol synthesis intermediates, and respond to changing levels through several elegant mechanisms of feedback regulation. Cholesterol sensing involves both direct binding of sterols to the homeostatic machinery located in the endoplasmic reticulum (ER), and indirect effects elicited by sterol-dependent alteration of the physical properties of membranes. Here, we examine the mechanisms employed by cells to maintain cholesterol homeostasis. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

引用

页码：170 / 178

页数：9

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