pubmed-article:14972535 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:14972535 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:14972535 | lifeskim:mentions | umls-concept:C1522102 | lld:lifeskim |
pubmed-article:14972535 | lifeskim:mentions | umls-concept:C1622204 | lld:lifeskim |
pubmed-article:14972535 | lifeskim:mentions | umls-concept:C0025246 | lld:lifeskim |
pubmed-article:14972535 | lifeskim:mentions | umls-concept:C0205245 | lld:lifeskim |
pubmed-article:14972535 | lifeskim:mentions | umls-concept:C1836230 | lld:lifeskim |
pubmed-article:14972535 | lifeskim:mentions | umls-concept:C1332823 | lld:lifeskim |
pubmed-article:14972535 | lifeskim:mentions | umls-concept:C1332700 | lld:lifeskim |
pubmed-article:14972535 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
pubmed-article:14972535 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:14972535 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:14972535 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:14972535 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:14972535 | pubmed:dateCreated | 2004-2-19 | lld:pubmed |
pubmed-article:14972535 | pubmed:abstractText | We had previously reported that glycosphingolipids (GSL) support human immunodeficiency virus type 1 (HIV-1) entry. In this study, we further examined this issue by expressing HIV-1 receptors in GSL-deficient GM95 cells. GM95 cells expressing low levels of CD4 and CXCR4 or CCR5 did not support HIV-1 Env-mediated fusion. However, higher expression of these receptors rendered GM95 cells highly susceptible to fusion with cells expressing appropriate HIV-1 envelope glycoproteins (HIV-1 Envs). The GM95 cells exhibited a different fusion phenotype when compared with GSL(+) NIH3T3 cells bearing similar receptor levels. Fusion of GM95 targets expressing higher levels of CD4 and coreceptors occurred at 25 degrees C and was sensitive to cholesterol depletion or disruption of the cytoskeleton. In contrast, the fusion threshold of NIH3T3CD4X4/R5 targets was at >/=28 degrees C as previously reported and was insensitive to cholesterol depletion or cytoskeletal network disruption. On the basis of these observations, we propose that target membrane GSLs support HIV-1 Env-mediated fusion at low density of receptors by stabilizing receptor pools in natural targets. | lld:pubmed |
pubmed-article:14972535 | pubmed:language | eng | lld:pubmed |
pubmed-article:14972535 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14972535 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:14972535 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14972535 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14972535 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:14972535 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14972535 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:14972535 | pubmed:month | Jan | lld:pubmed |
pubmed-article:14972535 | pubmed:issn | 0042-6822 | lld:pubmed |
pubmed-article:14972535 | pubmed:author | pubmed-author:GalloStephen... | lld:pubmed |
pubmed-article:14972535 | pubmed:author | pubmed-author:WangJi MingJM | lld:pubmed |
pubmed-article:14972535 | pubmed:author | pubmed-author:MartinThomas... | lld:pubmed |
pubmed-article:14972535 | pubmed:author | pubmed-author:KewalRamaniVi... | lld:pubmed |
pubmed-article:14972535 | pubmed:author | pubmed-author:PuriAnuA | lld:pubmed |
pubmed-article:14972535 | pubmed:author | pubmed-author:BlumenthalRob... | lld:pubmed |
pubmed-article:14972535 | pubmed:author | pubmed-author:ViardMathiasM | lld:pubmed |
pubmed-article:14972535 | pubmed:author | pubmed-author:AblanSherimay... | lld:pubmed |
pubmed-article:14972535 | pubmed:author | pubmed-author:RawatSatinder... | lld:pubmed |
pubmed-article:14972535 | pubmed:author | pubmed-author:EatonJulieJ | lld:pubmed |
pubmed-article:14972535 | pubmed:author | pubmed-author:RatnayakeShas... | lld:pubmed |
pubmed-article:14972535 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:14972535 | pubmed:day | 5 | lld:pubmed |
pubmed-article:14972535 | pubmed:volume | 318 | lld:pubmed |
pubmed-article:14972535 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:14972535 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:14972535 | pubmed:pagination | 55-65 | lld:pubmed |
pubmed-article:14972535 | pubmed:dateRevised | 2004-11-17 | lld:pubmed |
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pubmed-article:14972535 | pubmed:year | 2004 | lld:pubmed |
pubmed-article:14972535 | pubmed:articleTitle | Functional expression of CD4, CXCR4, and CCR5 in glycosphingolipid-deficient mouse melanoma GM95 cells and susceptibility to HIV-1 envelope glycoprotein-triggered membrane fusion. | lld:pubmed |
pubmed-article:14972535 | pubmed:affiliation | Laboratory of Experimental and Computational Biology, Center for Cancer Research, NCI-Frederick, National Institutes of Health, Frederick, MD 21702-1201, USA. | lld:pubmed |
pubmed-article:14972535 | pubmed:publicationType | Journal Article | lld:pubmed |
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