Hepatitis B virus X protein induces apoptosis by enhancing translocation of Bax to mitochondria.
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 14-3-3epsilon 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.
Kim
Hye Jin
HJ
Department of Microbiology, School of Bioscience and Biotechnology, Chungnam National University, Daejeon 305-764, Korea.
Kim
Sang Yong
SY
Kim
Jinchul
J
Lee
Heemin
H
Choi
Misun
M
Kim
Jeong Ki
JK
Ahn
Jeong Keun
JK
D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism; D002454:Cell Differentiation; D002460:Cell Line; D045744:Cell Line, Tumor; D053938:DNA Fragmentation; D006801:Humans; D008564:Membrane Potentials; D008928:Mitochondria / Q000378:metabolism*; D008954:Models, Biological; D010957:Plasmids / Q000378:metabolism; D021381:Protein Transport; D015534:Trans-Activators / Q000378:metabolism / Q000502:physiology*; D014162:Transfection; D054334:Viral Regulatory and Accessory Proteins; D051028:bcl-2-Associated X Protein / Q000378:metabolism*
D015534:Trans-Activators; D054334:Viral Regulatory and Accessory Proteins; D051028:bcl-2-Associated X Protein; C057628:hepatitis B virus X protein; D053148:Caspase 3