Hepatitis B virus X protein induces apoptosis by enhancing translocation of Bax to mitochondria

被引：53

作者：

Kim, Hye Jin ^{[1
]}

Kim, Sang Yong ^{[1
]}

Kim, Jinchul ^{[1
]}

Lee, Heemin ^{[1
]}

Choi, Misun ^{[1
]}

Kim, Jeong Ki ^{[1
]}

Ahn, Jeong Keun ^{[1
]}

机构：

[1] Chungnam Natl Univ, Dept Microbiol, Sch Biosci & Biotechnol, Taejon 305764, South Korea

来源：

IUBMB LIFE | 2008年 / 60卷 / 07期

关键词：

HBV; HBx; Bax; 14-3-3; mitochondria;

D O I：

10.1002/iub.68

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：

Hepatitis B virus X protein (HBx) is essential for viral replication and plays an important role in viral pathogenesis. HBx transactivates many viral and cellular genes and participates In cellular signal transduction pathways, proliferation, and apoptosis. In the present study, we report that HBx induces apoptosis by enhancing the translocation of Bax to mitochondria, followed by inducing the loss of mitochondrial membrane potential and release of cytochrome C. In addition, Bcl-2, inhibitor of Bax, rescues the disruption of mitochondrial membrane potential and DNA fragmentation induced by serum starvation in HepG2-X cells expressing HBx. We also found that HBx binds directly to Bax and interferes with the interaction between Bax and 14-3-3 epsilon to enhance the translocation of Bax to mitochondria. Taken together, our data suggest that HBx induces apoptosis by interacting with Bax and enhancing its translocation to mitochondria. (c) 2008 IUBMB.

引用

页码：473 / 480

页数：8

共 28 条

[11] Pro-apoptotic function of HBV X protein is mediated by interaction with c-FLIP and enhancement of death-inducing signal [J].