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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0019704,
umls-concept:C0024432,
umls-concept:C0037083,
umls-concept:C0085862,
umls-concept:C0333348,
umls-concept:C0524914,
umls-concept:C0542341,
umls-concept:C1299583,
umls-concept:C1332700,
umls-concept:C1549571,
umls-concept:C1550548,
umls-concept:C1555714,
umls-concept:C1608386,
umls-concept:C1705654,
umls-concept:C1710082
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pubmed:issue |
11
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pubmed:dateCreated |
1997-4-17
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pubmed:abstractText |
The human immunodeficiency virus type 1 (HIV-1) requires the presence of specific chemokine receptors in addition to CD4 to enter its target cell. The chemokine receptor CCR5 is used by macrophage-tropic strains of HIV-1, which predominate during the asymptomatic stages of infection. Here we investigate whether the ability of CCR5 to signal in response to its beta-chemokine ligands is necessary or sufficient for viral entry. Three CCR5 mutants with little or no ability to mobilize calcium in response to macrophage inflammatory protein-1beta could nonetheless support HIV-1 entry and the early steps in the virus life cycle with efficiencies comparable with those of wild-type CCR5. Conversely, a chimeric receptor with the N terminus of CCR2 replacing that of CCR5 responded to macrophage inflammatory protein-1beta and MCP-1 but did not efficiently support viral entry. These results demonstrate that chemokine signaling and HIV-1 entry are separable functions of CCR5 and that only viral entry requires the N-terminal domain of CCR5.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL4,
http://linkedlifedata.com/resource/pubmed/chemical/Macrophage Inflammatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR5,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytokine,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, HIV
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0021-9258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
14
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pubmed:volume |
272
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6854-7
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:9054370-Animals,
pubmed-meshheading:9054370-Cell Line,
pubmed-meshheading:9054370-Chemokine CCL4,
pubmed-meshheading:9054370-Dogs,
pubmed-meshheading:9054370-HIV-1,
pubmed-meshheading:9054370-Humans,
pubmed-meshheading:9054370-Macrophage Inflammatory Proteins,
pubmed-meshheading:9054370-Macrophages,
pubmed-meshheading:9054370-Mutation,
pubmed-meshheading:9054370-Receptors, CCR5,
pubmed-meshheading:9054370-Receptors, Cytokine,
pubmed-meshheading:9054370-Receptors, HIV,
pubmed-meshheading:9054370-Signal Transduction,
pubmed-meshheading:9054370-Virus Replication
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pubmed:year |
1997
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pubmed:articleTitle |
HIV-1 entry and macrophage inflammatory protein-1beta-mediated signaling are independent functions of the chemokine receptor CCR5.
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pubmed:affiliation |
Division of Human Retrovirology, Dana-Farber Cancer Institute, Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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