Bax activation by Bim?

被引：82

作者：

Czabotar, P. E. ^{[1
]}

Colman, P. M. ^{[1
]}

Huang, D. C. S. ^{[1
]}

机构：

[1] Walter & Eliza Hall Inst Med Res, Parkville, Vic 3052, Australia

来源：

CELL DEATH AND DIFFERENTIATION | 2009年 / 16卷 / 09期

基金：

澳大利亚国家健康与医学研究理事会;

关键词：

apoptosis; Bcl-2; Bax; Bim; BCL-2; FAMILY-MEMBERS; BH3-ONLY PROTEINS; MEMBRANE PERMEABILIZATION; BH3; DOMAINS; CELL-DEATH; MITOCHONDRIAL APOPTOSIS; X-RAY; BINDING; HELIX; SITE;

D O I：

10.1038/cdd.2009.83

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：

The mechanism by which the cell death mediator Bax becomes activated to cause mitochondrial damage, a key step for the intrinsic pathway to apoptosis, remain highly contentious. Although some data support a role for certain BH3-only proteins, such as Bim or tBid, to directly activate Bax, others have led to the conclusion that BH3-only proteins act indirectly by antagonizing the prosurvival Bcl-2 proteins, thereby allowing Bax activation to proceed. A recent paper in Nature by Gavathiotis et al. provides the first biophysical evidence for a direct interaction between a BH3 domain, that of Bim, with Bax. Here, we review these intriguing observations and discuss their implications for our understanding of how the BH3-only proteins initiate apoptosis. Cell Death and Differentiation (2009) 16, 1187-1191; doi: 10.1038/cdd.2009.83; published online 26 June 2009

引用

页码：1187 / 1191

页数：5

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