Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2002-4-17
pubmed:abstractText
We previously reported that viral antigen expression was markedly up-regulated by stimulation with extracellular Nef, similar to the effects of tumor necrosis factor (TNF)-alpha and phorbol myristate acetate, in model cells for HIV-1 latency. In this study, we examined the molecular mechanism of this novel Nef function. Flow cytometry revealed specific binding of Nef on the surface of latently infected cells. Furthermore, activation of Ras in the cells was detected after treatment with Nef, indicating the involvement of Ras in Nef-mediated activation of HIV-1 from latency. This was also confirmed by the observations that HIV-1 long-terminal repeat-luciferase (LTR-Luc) activity was significantly up-regulated by introduction of the active Ras into uninfected cells, and that LTR-Luc activity observed in Nef-treated cells was specifically inhibited by introduction of a dominant negative Ras. In addition, PD98059 inhibited the activation of HIV-1 by Nef, but not by TNF-alpha. Thus, Nef-mediated reactivation of HIV-1 in latent model cells occurs by signal transduction from Ras to mitogen-activated protein kinase cascades.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0889-2229
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
461-7
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Extracellular Nef protein activates signal transduction pathway from Ras to mitogen-activated protein kinase cascades that leads to activation of human immunodeficiency virus from latency.
pubmed:affiliation
Department of Microbiology and Immunology, School of Medicine, Vanderbilt University, Nashville, Tennessee, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't