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Raf-1 and protein kinase B regulate cell survival through the activation of NF-kappaB in hepatitis B virus X-expressing cells.

Authors
Um, HR; Lim, WC; Chae, SY; Park, S; Park, JH; Cho, H
Citation
Virus research, 125(1):1-8, 2007
Journal Title
Virus research
ISSN
0168-17021872-7492
Abstract
We previously demonstrated that activation of NF-kappaB by the hepatitis B virus X (HBx) gene plays an important role in cell survival. In the present study, we explored the upstream mediators of NF-kappaB activation and their correlations with cell survival. XTT assays and colony generation assays revealed that inhibition of NF-kappaB activation indeed increased cell death in HBx-expressing cells. Utilizing inactivating mutants of signal transducers, we showed that dominant negative mutants of stress-activated protein kinase/extracellular signal-regulated kinase (SEK1) or PKCalpha significantly diminished the HBx-mediated NF-kappaB activation. However, neither of these mutants significantly affected the cell survival in colony generation assays. In contrast, inactivating mutants of Raf-1 or PKB (protein kinase B)/Akt abrogated the HBx-mediated NF-kappaB activation and also suppressed the cell survival. Our results suggest that the Raf-1 or PKB-mediated NF-kappaB activation promotes cell survival in HBx-expressing cells.
MeSH terms
AnimalsCell Survival/physiology*Hepatitis B virus/geneticsHepatitis B virus/physiology*HumansNF-kappa B/metabolism*Proto-Oncogene Proteins c-akt/physiology*Proto-Oncogene Proteins c-raf/physiology*RabbitsTrans-Activators/geneticsTrans-Activators/metabolismTrans-Activators/pharmacology*Transcription, Genetic
DOI
10.1016/j.virusres.2006.11.007
PMID
17188775
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
Journal Papers > School of Medicine / Graduate School of Medicine > Microbiology
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