This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Chen, J.
Right arrow Articles by Siddiqui, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chen, J.
Right arrow Articles by Siddiqui, A.

 Previous Article  |  Next Article 

Journal of Virology, June 2007, p. 6757-6760, Vol. 81, No. 12
0022-538X/07/$08.00+0     doi:10.1128/JVI.00172-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Hepatitis B Virus X Protein Stimulates the Mitochondrial Translocation of Raf-1 via Oxidative Stress{triangledown}

Jun Chen1,2 and Aleem Siddiqui1*

Department of Medicine, Division of Infectious Diseases, University of California—San Diego, SCRB, MC0711, 9500 Gilman Dr., La Jolla, California 92093,1 Liver Disease Research Center, Second Xiangya Hospital, Central South University, Changsha 410011, China2

Received 25 January 2007/ Accepted 30 March 2007

The human hepatitis B virus (HBV) X protein (HBx) plays a crucial role(s) in the viral life cycle and contributes to the onset of hepatocellular carcinoma (HCC). HBx caused the mitochondrial translocation of Raf-1 kinase either alone or in the context of whole-viral-genome transfections. Mitochondrial translocation of Raf-1 is mediated by HBx-induced oxidative stress and was dependent upon the phosphorylation of Raf-1 at the serine338/339 and Y340/341 residues by p21-activated protein kinase 1 and Src kinase, respectively. These studies provide an insight into the mechanisms by which HBV induces intracellular events relevant to liver disease pathogenesis, including HCC.

* Corresponding author. Mailing address: Department of Medicine, SCRB 409, University of California—San Diego, 9500 Gilman Drive, MC0711, La Jolla, CA 92093. Phone: (858) 822-1750. Fax: (858) 822-1749. E-mail: asiddiqui{at}ucsd.edu

{triangledown} Published ahead of print on 11 April 2007.

Journal of Virology, June 2007, p. 6757-6760, Vol. 81, No. 12
0022-538X/07/$08.00+0     doi:10.1128/JVI.00172-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Clippinger, A. J., Bouchard, M. J. (2008). Hepatitis B Virus HBx Protein Localizes to Mitochondria in Primary Rat Hepatocytes and Modulates Mitochondrial Membrane Potential. J. Virol. 82: 6798-6811 [Abstract] [Full Text]  
  • Tremellen, K. (2008). Oxidative stress and male infertility--a clinical perspective. Hum Reprod Update 14: 243-258 [Abstract] [Full Text]  
  • Fosslien, E. (2008). Cancer Morphogenesis: Role of Mitochondrial Failure. Annals of Clinical & Laboratory Science 38: 307-330 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»