Linked Life Data

17188775

Source:http://linkedlifedata.com/resource/pubmed/id/17188775

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-3-20
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0168-1702
pubmed:author
pubmed:issnType
Print
pubmed:volume
125
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Raf-1 and protein kinase B regulate cell survival through the activation of NF-kappaB in hepatitis B virus X-expressing cells.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, Chronic Inflammatory Disease Research Center, Ajou University School of Medicine, 5 Wonchon-Dong, Yeongtong-Gu, Suwon, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't