Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2007-12-17
pubmed:abstractText
Akt1 was revealed to interact with Ki-Ras in the cytoplasm of Ki-Ras-transformed human prostate epithelial cells, 267B1/K-ras. Moreover, p65/RelA in the nucleus was found to interact with both Ki-Ras and Akt1, suggesting the nuclear translocation of Akt1:Ki-Ras complex for NF- kappaB activation. In support of this, compared with wild type Akt1, the dominant negative Akt1 mutant was decreased in its nuclear expression, reducing the Ki-Ras-induced NF-kappaB transcriptional activation. Moreover, inhibitors of Ras (sulindac sulfide and farnesyltransferase inhibitor I) or PI3K/Akt (wortmannin), reduced the amounts of Akt1 and Ki-Ras in the nucleus as well as partial NF-kappaB activity. The complete inhibition of Ki-Ras-induced NF-kappaB activation, however, could only be obtained by combined treatment with wortmannin and proteasome inhibitor-1. Accordingly, clonogenic assay showed Akt1 contribution to IkappaBalpha-mediated NF-kappaB activation for oncogenic cell growth by Ki-Ras. Our data suggest a crucial role of Ki-Ras:Akt1 complex in NF-kappaB transcriptional activation and enhancement of cell survival.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1090-2104
pubmed:author
pubmed:issnType
Electronic
pubmed:day
25
pubmed:volume
365
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
771-6
pubmed:dateRevised
2009-12-10
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Complex formation of p65/RelA with nuclear Akt1 for enhanced transcriptional activation of NF-kappaB.
pubmed:affiliation
Functional Metabolomics Research Center, KRIBB, Yuseong, Daejeon, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't