Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-12-12
pubmed:abstractText
Chemokine receptors are not only able to bind chemokines but, together with CD4, they serve as an entry door for the human immunodeficiency virus type 1 (HIV-1). The signalling capacity of chemokine receptors, which is of fundamental importance for chemokine-induced chemotaxis, is not used by HIV-1 to enter a target cell, nor by chemokines or chemokine-derived ligands to inhibit viral entry. In addition, an ill-defined signal triggered by chemokines can, under some circumstances, lead to an increase in HIV-1 expression. We show here that, in infected cells, exposure to SDF-1 leads to an increased expression of a X4 strain of HIV-1. A similar increase can be induced by an N-terminal peptide of SDF-1 which had previously been shown to elicit an intracellular calcium response and to inhibit the entry of X4 strains of HIV-1. We demonstrate the involvement of extracellular signal-regulated kinases (ERK) in this phenomenon. SDF-1 activates ERK-1 and ERK-2 in Jurkat cells. In HeLa cells, ERK-2 only is activated by SDF-1 or by a SDF-derived peptide. This ERK activation can be blocked by pertussis toxin and by the MEK inhibitor U0126. Most importantly, SDF-1-dependent HIV-1 expression is abolished by pretreating the cells with pertussis toxin or with U0126. The consequences of this SDF-1-induced, ERK-dependent modulation of HIV-1 expression in infected cells may have a clinical relevance for eradicating latent viruses.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Anti-HIV Agents, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4, http://linkedlifedata.com/resource/pubmed/chemical/Butadienes, http://linkedlifedata.com/resource/pubmed/chemical/CXCL12 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Calcium, http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL12, http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CXC, http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Nitriles, http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CXCR4, http://linkedlifedata.com/resource/pubmed/chemical/U 0126
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1148-5493
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
470-7
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11022134-Anti-HIV Agents, pubmed-meshheading:11022134-Antigens, CD4, pubmed-meshheading:11022134-Butadienes, pubmed-meshheading:11022134-Calcium, pubmed-meshheading:11022134-Cell Cycle, pubmed-meshheading:11022134-Chemokine CXCL12, pubmed-meshheading:11022134-Chemokines, CXC, pubmed-meshheading:11022134-Enzyme Activation, pubmed-meshheading:11022134-Enzyme Inhibitors, pubmed-meshheading:11022134-HIV Long Terminal Repeat, pubmed-meshheading:11022134-HIV-1, pubmed-meshheading:11022134-HeLa Cells, pubmed-meshheading:11022134-Humans, pubmed-meshheading:11022134-Jurkat Cells, pubmed-meshheading:11022134-Mitogen-Activated Protein Kinases, pubmed-meshheading:11022134-Nitriles, pubmed-meshheading:11022134-Peptide Fragments, pubmed-meshheading:11022134-Receptors, CXCR4, pubmed-meshheading:11022134-Transcription, Genetic, pubmed-meshheading:11022134-Transfection, pubmed-meshheading:11022134-Virus Replication
pubmed:year
2000
pubmed:articleTitle
SDF-1-induced activation of ERK enhances HIV-1 expression.
pubmed:affiliation
CNRS UMR 7627, CERVI, CHU Pitié-Salpêtrière, 75013 Paris, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't