HBXIP functions as a cofactor of survivin in apoptosis suppression

被引:382
作者
Marusawa, H
Matsuzawa, S
Welsh, K
Zou, H
Armstrong, R
Tamm, I
Reed, JC [1 ]
机构
[1] Burnham Inst, La Jolla, CA 92037 USA
[2] IDUN Pharmaceut, San Diego, CA 92121 USA
关键词
apoptosis; caspase; hepatitis B virus; hepatitis B X-interacting protein; survivin;
D O I
10.1093/emboj/cdg263
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
Survivin is an anti-apoptotic protein that is overexpressed in most human cancers. We show that survivin forms complexes with a cellular protein, hepatitis B X-interacting protein (HBXIP), which was originally recognized for its association with the X protein of hepatitis B virus (HBX). Survivin-HBXIP complexes, but neither survivin nor HBXIP individually, bind pro-caspase-9, preventing its recruitment to Apaf1, and thereby selectively suppressing apoptosis initiated via the mitochondria/cytochrome c pathway. Viral HBX protein also interacts with the survivin- HBXIP complex and suppresses caspase activation in a survivin-dependent manner. Thus, HBXIP functions as a cofactor for survivin, and serves as a link between the cellular apoptosis machinery and a viral pathogen involved in hepatocellular carcinogenesis.
引用
收藏
页码:2729 / 2740
页数:12
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