Human hepatitis B virus X protein induces apoptosis in HepG2 cells: Role of BH3 domain
- School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive 05N-10, Singapore 637551 (Singapore)
- School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive 05N-10, Singapore 637551 (Singapore)School of Chemical and Biomedical Engineering, Nanyang Technological University, 16 Nanyang Drive Unit 100, Singapore 637722 (Singapore)
The smallest protein of hepatitis B virus, HBX, has been implicated in the development of liver diseases by interfering with normal cellular processes. Its role in cell proliferation has been unclear as both pro-apoptotic and anti-apoptotic activities have been reported. We showed molecular evidence that HBX induced apoptosis in HepG2 cells. A Bcl-2 Homology Domain 3 was identified in HBX, which interacted with anti-apoptotic but not pro-apoptotic members of the Bcl-2 family of proteins. HBX induced apoptosis when transfected into HepG2 cells, as demonstrated by both flow cytometry and caspase-3 activity. However, HBX protein may not be stable in apoptotic cells triggered by its own expression as only its mRNA or the fusion protein with the glutathione-S-transferase was detected in transfected cells. Our results suggested that HBX behaved as a pro-apoptotic protein and was able to induce apoptosis.
- OSTI ID:
- 20793237
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 338, Issue 3; Other Information: DOI: 10.1016/j.bbrc.2005.10.117; PII: S0006-291X(05)02363-6; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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