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Hepatitis B virus X protein induces apoptosis by enhancing translocation of Bax to mitochondria
Author(s) -
Kim Hye Jin,
Kim Sang Yong,
Kim Jinchul,
Lee Heemin,
Choi Misun,
Kim Jeong Ki,
Ahn Jeong Keun
Publication year - 2008
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.68
Subject(s) - hbx , apoptosis , mitochondrion , microbiology and biotechnology , cytochrome c , biology , chromosomal translocation , signal transduction , dna fragmentation , chemistry , programmed cell death , virus , hepatitis b virus , virology , gene , biochemistry
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 14‐3‐3ε 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. © 2008 IUBMB IUBMB Life, 60(7): 473–480, 2008