Linked Life Data

8814265

Source:http://linkedlifedata.com/resource/pubmed/id/8814265

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1996-10-24
pubmed:abstractText
The CD4 co-receptor interacts with nonpolymorphic regions of major histocompatibility complex class II molecules on antigen-presenting cells. This interaction results in the mobilization of a number of signaling mediators shared by the T cell receptor (TcR) signaling pathway and thus amplifies TcR-generated signals. We have investigated the outcome of CD4 engagement on the activation of both cellular transcription factors and the HIV-1 long terminal repeat (LTR). We show that CD4 triggering activates different pathways of HIV LTR activation which can be identified by their sensitivity to the immunosuppressant cyclosporin A. The response of the inducible cellular transcription factors involved in HIVLTR activation shows that both nuclear factor (NF)-kappa B and NF-AT mediate a cyclosporin A-sensitive response to CD4, while AP-1 is at least in part responsible for the cyclosporin A-insensitive response. Both pathways can, however, be blocked by a kinase-defective dominant negative p56lck mutant, supporting an essential role for p56lck kinase activity in CD4-dependent signal transduction. A functional analysis of different CD4 epitopes using either anti-CD4 mAb or HIV-1 gp120 reveals a common epitope-specific activation of both the LTR and of the transcription factors NF-kappa B and NF-AT.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0014-2980
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2181-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Cyclosporin A sensitivity of the HIV-1 long terminal repeat identifies distinct p56lck-dependent pathways activated by CD4 triggering.
pubmed:affiliation
Department of Evolutionary Biology, University of Siena, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't