| pubmed-article:9054370 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9054370 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
| pubmed-article:9054370 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
| pubmed-article:9054370 | lifeskim:mentions | umls-concept:C0524914 | lld:lifeskim |
| pubmed-article:9054370 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:9054370 | lifeskim:mentions | umls-concept:C0085862 | lld:lifeskim |
| pubmed-article:9054370 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
| pubmed-article:9054370 | lifeskim:mentions | umls-concept:C1299583 | lld:lifeskim |
| pubmed-article:9054370 | lifeskim:mentions | umls-concept:C1332700 | lld:lifeskim |
| pubmed-article:9054370 | lifeskim:mentions | umls-concept:C0333348 | lld:lifeskim |
| pubmed-article:9054370 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:9054370 | lifeskim:mentions | umls-concept:C1550548 | lld:lifeskim |
| pubmed-article:9054370 | lifeskim:mentions | umls-concept:C1555714 | lld:lifeskim |
| pubmed-article:9054370 | lifeskim:mentions | umls-concept:C1608386 | lld:lifeskim |
| pubmed-article:9054370 | lifeskim:mentions | umls-concept:C1549571 | lld:lifeskim |
| pubmed-article:9054370 | lifeskim:mentions | umls-concept:C1705654 | lld:lifeskim |
| pubmed-article:9054370 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:9054370 | pubmed:dateCreated | 1997-4-17 | lld:pubmed |
| pubmed-article:9054370 | 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. | lld:pubmed |
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| pubmed-article:9054370 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9054370 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9054370 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9054370 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9054370 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9054370 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9054370 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9054370 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9054370 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:9054370 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:9054370 | pubmed:author | pubmed-author:GerardCC | lld:pubmed |
| pubmed-article:9054370 | pubmed:author | pubmed-author:SunYY | lld:pubmed |
| pubmed-article:9054370 | pubmed:author | pubmed-author:MartinK AKA | lld:pubmed |
| pubmed-article:9054370 | pubmed:author | pubmed-author:SodroskiJJ | lld:pubmed |
| pubmed-article:9054370 | pubmed:author | pubmed-author:MackayC RCR | lld:pubmed |
| pubmed-article:9054370 | pubmed:author | pubmed-author:GerardN PNP | lld:pubmed |
| pubmed-article:9054370 | pubmed:author | pubmed-author:ChoiLL | lld:pubmed |
| pubmed-article:9054370 | pubmed:author | pubmed-author:FarzanMM | lld:pubmed |
| pubmed-article:9054370 | pubmed:author | pubmed-author:SidelkoMM | lld:pubmed |
| pubmed-article:9054370 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9054370 | pubmed:day | 14 | lld:pubmed |
| pubmed-article:9054370 | pubmed:volume | 272 | lld:pubmed |
| pubmed-article:9054370 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9054370 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9054370 | pubmed:pagination | 6854-7 | lld:pubmed |
| pubmed-article:9054370 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
| pubmed-article:9054370 | pubmed:meshHeading | pubmed-meshheading:9054370-... | lld:pubmed |
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| pubmed-article:9054370 | pubmed:meshHeading | pubmed-meshheading:9054370-... | lld:pubmed |
| pubmed-article:9054370 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9054370 | pubmed:articleTitle | HIV-1 entry and macrophage inflammatory protein-1beta-mediated signaling are independent functions of the chemokine receptor CCR5. | lld:pubmed |
| pubmed-article:9054370 | pubmed:affiliation | Division of Human Retrovirology, Dana-Farber Cancer Institute, Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA. | lld:pubmed |
| pubmed-article:9054370 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9054370 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9054370 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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