Source:http://linkedlifedata.com/resource/pubmed/id/14972535
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2004-2-19
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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.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4,
http://linkedlifedata.com/resource/pubmed/chemical/Gene Products, env,
http://linkedlifedata.com/resource/pubmed/chemical/Glycosphingolipids,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR5,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CXCR4
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0042-6822
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pubmed:author |
pubmed-author:AblanSherimayS,
pubmed-author:BlumenthalRobertR,
pubmed-author:EatonJulieJ,
pubmed-author:GalloStephen ASA,
pubmed-author:KewalRamaniVineet NVN,
pubmed-author:MartinThomas DTD,
pubmed-author:PuriAnuA,
pubmed-author:RatnayakeShashikalaS,
pubmed-author:RawatSatinder SSS,
pubmed-author:ViardMathiasM,
pubmed-author:WangJi MingJM
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pubmed:issnType |
Print
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pubmed:day |
5
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pubmed:volume |
318
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
55-65
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:14972535-Animals,
pubmed-meshheading:14972535-Antigens, CD4,
pubmed-meshheading:14972535-Gene Products, env,
pubmed-meshheading:14972535-Glycosphingolipids,
pubmed-meshheading:14972535-HIV-1,
pubmed-meshheading:14972535-HIV-2,
pubmed-meshheading:14972535-HeLa Cells,
pubmed-meshheading:14972535-Humans,
pubmed-meshheading:14972535-Melanoma,
pubmed-meshheading:14972535-Membrane Fusion,
pubmed-meshheading:14972535-Mice,
pubmed-meshheading:14972535-NIH 3T3 Cells,
pubmed-meshheading:14972535-Receptors, CCR5,
pubmed-meshheading:14972535-Receptors, CXCR4,
pubmed-meshheading:14972535-Tumor Cells, Cultured
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pubmed:year |
2004
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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.
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pubmed:affiliation |
Laboratory of Experimental and Computational Biology, Center for Cancer Research, NCI-Frederick, National Institutes of Health, Frederick, MD 21702-1201, USA.
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pubmed:publicationType |
Journal Article
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