| pubmed-article:7988553 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7988553 | lifeskim:mentions | umls-concept:C0019693 | lld:lifeskim |
| pubmed-article:7988553 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:7988553 | lifeskim:mentions | umls-concept:C1511625 | lld:lifeskim |
| pubmed-article:7988553 | lifeskim:mentions | umls-concept:C0032214 | lld:lifeskim |
| pubmed-article:7988553 | lifeskim:mentions | umls-concept:C0600138 | lld:lifeskim |
| pubmed-article:7988553 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
| pubmed-article:7988553 | lifeskim:mentions | umls-concept:C1306673 | lld:lifeskim |
| pubmed-article:7988553 | lifeskim:mentions | umls-concept:C1511545 | lld:lifeskim |
| pubmed-article:7988553 | pubmed:issue | 23 | lld:pubmed |
| pubmed-article:7988553 | pubmed:dateCreated | 1995-1-9 | lld:pubmed |
| pubmed-article:7988553 | pubmed:abstractText | The role played by the cytoplasmic domain of the CD4 molecule in the process of HIV infection was investigated, using A2.01 cells which express different forms of the CD4 gene. A delay in HIV production was consistently observed in cells expressing a truncated CD4 which lacks the cytoplasmic domain (CD4.401) compared with cells expressing the wild type CD4. The delay was much less in cells expressing a hybrid CD4-CD8 molecule (amino acids 1-177 of CD4 fused to the hinge, transmembrane and cytoplasmic domains of CD8). Yet the extent of viral entry and reverse transcription, monitored by semi-quantitative PCR, was similar in each cell type studied. For further study of the mechanism responsible for delayed HIV replication in the A2.01/CD4.401 cell line, cells were treated with phytohaemagglutinin (PHA), 24 h after HIV infection. Under such experimental conditions HIV production was detected at the same time in the culture supernatants of A2.01/CD4 and A2.01/CD4.401 cells. Moreover, we found that CD4 oligomerization by HIV-1 induced NF-kappa B translocation in A2.01/CD4 and A2.01/CD4-CD8 but not in A2.01/CD4.401 cells. This was consistent with CAT assay experiments which provided evidence for Tat-independent NF-kappa B mediated activation of HIV-1 LTR promoter after HIV binding to CD4 in A2.01/CD4 and A2.01/CD4-CD8 but not in A2.01/CD4.401 cells. In contrast to results published recently by Tremblay et al. (1994, EMBO J., 13, 774-783), we propose that a positive cellular signal initiated following oligomerization of the CD4 by the virus itself is involved in NF-kappa B-dependent early HIV transcription in A2.01/CD4 cells. | lld:pubmed |
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| pubmed-article:7988553 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7988553 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7988553 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:7988553 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:7988553 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7988553 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:7988553 | pubmed:issn | 0261-4189 | lld:pubmed |
| pubmed-article:7988553 | pubmed:author | pubmed-author:DevauxCC | lld:pubmed |
| pubmed-article:7988553 | pubmed:author | pubmed-author:BenkiraneMM | lld:pubmed |
| pubmed-article:7988553 | pubmed:author | pubmed-author:JeangK TKT | lld:pubmed |
| pubmed-article:7988553 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7988553 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:7988553 | pubmed:volume | 13 | lld:pubmed |
| pubmed-article:7988553 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7988553 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7988553 | pubmed:pagination | 5559-69 | lld:pubmed |
| pubmed-article:7988553 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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