The regulation and turnover of mitochondrial uncoupling proteins

被引：106

作者：

Azzu, Vian ^{[2
]}

Jastroch, Martin ^{[1
]}

Divakaruni, Ajit S. ^{[1
,2
]}

Brand, Martin D. ^{[1
]}

机构：

[1] Buck Inst Age Res, Novato, CA 94945 USA

[2] MRC, Mitochondrial Biol Unit, Cambridge CB2 0XY, England

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS | 2010年 / 1797卷 / 6-7期

基金：

英国医学研究理事会;

关键词：

Mitochondria; Uncoupling protein; UCP1; UCP2; UCP3; Turnover; Degradation; Regulation; SKELETAL-MUSCLE MITOCHONDRIA; FATTY-ACID OXIDATION; BASAL PROTON CONDUCTANCE; BETA-CELL DYSFUNCTION; INSULIN-SECRETION; EVOLUTIONARY HISTORY; PHYSIOLOGICAL LEVELS; BROWN ADIPOCYTES; THYROID-HORMONE; HIGH GLUCOSE;

D O I：

10.1016/j.bbabio.2010.02.035

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：

Uncoupling proteins (UCP1, UCP2 and UCP3) are important in regulating cellular fuel metabolism and as attenuators of reactive oxygen species production through strong or mild uncoupling. The generic function and broad tissue distribution of the uncoupling protein family means that they are increasingly implicated in a range of pathophysiological processes including obesity, insulin resistance and diabetes mellitus, neurodegeneration, cardiovascular disease, immunity and cancer. The significant recent progress describing the turnover of novel uncoupling proteins, as well as current views on the physiological roles and regulation of UCPs, is outlined. (C) 2010 Elsevier B.V. All rights reserved.

引用

收藏

页码：785 / 791

页数：7

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