Control of mitochondrial permeability by Bcl-2 family members

被引：329

作者：

Sharpe, JC ^{[1
]}

Arnoult, D ^{[1
]}

Youle, RJ ^{[1
]}

机构：

[1] NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 2004年 / 1644卷 / 2-3期

关键词：

Bax; Bid; mitochondrion; channel;

D O I：

10.1016/j.bbamcr.2003.10.016

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：

Programmed cell death (apoptosis) is regulated by the Bcl-2 family of proteins. Although it remains unclear how these family members control apoptosis, they clearly have the capacity to regulate the permeability of intracellular membranes to ions and proteins. Proapoptotic members of the Bcl-2 family, especially Bax and Bid, have been extensively analyzed for the ability to form channels in membranes and to regulate preexisting channels. Anti-apoptotic members of the family tend to have the opposing effects on membrane channel formation. The molecular mechanisms of the different models for the permeabilization of membranes by the Bcl-2 family members and the regulation of Bcl-2 family member subcellular localizations are discussed. (C) 2003 Elsevier B.V. All rights reserved.

引用

页码：107 / 113

页数：7

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