Upregulation of Bcl2 inhibits apoptosis-driven BAX insertion but favors BAX relocalization in mitochondria

被引：110

作者：

Teijido, O. ^{[1
]}

Dejean, L. ^{[1
]}

机构：

[1] NYU, Coll Dent, Dept Basic Sci, New York, NY 10010 USA

来源：

FEBS LETTERS | 2010年 / 584卷 / 15期

关键词：

Bcl2; BAX; Mitochondria; Apoptosis; INDUCED CHANNEL; OUTER-MEMBRANE; CYTOCHROME-C; FAMILY; MAC; PERMEABILIZATION; ACTIVATION; ADDICTION; PROTECTOR; COMPONENT;

D O I：

10.1016/j.febslet.2010.07.002

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：

Protein-protein interactions between the Bcl2 family proteins regulate apoptosis. An imbalance of this interaction network due to the upregulation of the proto-oncogene Bcl2 leads to a resistance to apoptosis associated with tumor formation. Bcl2 overexpression inhibits BAX oligomerization and mitochondrial outer membrane (MOM) permeabilization. However, Bcl2 effects on earlier steps of BAX-mediated apoptosis are not fully understood. Bcl2 overexpression inhibits BAX insertion into the MOM but spontaneously increases BAX relocalization to the mitochondria. Also, a physical interaction between BAX and Bcl2 is necessary for these two effects to occur. Taken together, these results suggest upregulated Bcl2 stabilizes BAX loose binding to mitochondrial membranes, inhibiting its insertion into the MOM and consequently cytochrome c release. Structured summary MINT-7945271: BAX (uniprotkb:Q07813) physically interacts (MI:0915) with Bcl-2 (uniprotkb:P10417) by anti bait coimmunoprecipitation (MI:0006) (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：3305 / 3310

页数：6

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