| pubmed-article:1995951 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1995951 | lifeskim:mentions | umls-concept:C0019682 | lld:lifeskim |
| pubmed-article:1995951 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:1995951 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:1995951 | lifeskim:mentions | umls-concept:C0205145 | lld:lifeskim |
| pubmed-article:1995951 | lifeskim:mentions | umls-concept:C0042774 | lld:lifeskim |
| pubmed-article:1995951 | lifeskim:mentions | umls-concept:C0023978 | lld:lifeskim |
| pubmed-article:1995951 | lifeskim:mentions | umls-concept:C0439828 | lld:lifeskim |
| pubmed-article:1995951 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:1995951 | pubmed:dateCreated | 1991-3-27 | lld:pubmed |
| pubmed-article:1995951 | pubmed:abstractText | The long terminal repeat (LTR) of the human immunodeficiency virus (HIV) contains three binding sites for the transcriptional factor Sp1. In order to investigate the role that the Sp1-binding sites play in regulation of HIV replication, we have introduced a deletion of all three Sp1-binding sites into the LTR of an infectious molecular clone of HIV. Viral stocks have been prepared from this mutant virus, designated dl-Sp, and these stocks have been used to study its replicative ability in human T cells. The dl-Sp virus replicated efficiently in MT4 cells and in phytohemagglutinin-stimulated human peripheral blood lymphocytes, but it replicated poorly and with delayed kinetics in A3.01 (CEM) T cells unless those cells had been treated with the cytokine tumor necrosis factor alpha. Gel retardation assays to study the levels of DNA-binding proteins present in these cells showed that NF-kappa B activity could be detected in the nuclei of MT4 cells but not in A3.01 cells unless they had been treated with tumor necrosis factor alpha. Thus, the presence of NF-kappa B activity appeared to be required for efficient replication of an HIV whose LTR Sp1-binding sites had been deleted. This suggests that NF-kappa B can functionally compensate for Sp1 in activating HIV replication. The HIV LTR is therefore similar to the promoter-enhancer units of other viruses in that it is composed of multiple functional elements that may contribute differently to viral replication depending on the levels of DNA-binding proteins present in the target cells. | lld:pubmed |
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| pubmed-article:1995951 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1995951 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1995951 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1995951 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1995951 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:1995951 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1995951 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:1995951 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:1995951 | pubmed:author | pubmed-author:MartinM AMA | lld:pubmed |
| pubmed-article:1995951 | pubmed:author | pubmed-author:LeonardJJ | lld:pubmed |
| pubmed-article:1995951 | pubmed:author | pubmed-author:TheodoreT STS | lld:pubmed |
| pubmed-article:1995951 | pubmed:author | pubmed-author:RabsonA BAB | lld:pubmed |
| pubmed-article:1995951 | pubmed:author | pubmed-author:ParrottCC | lld:pubmed |
| pubmed-article:1995951 | pubmed:author | pubmed-author:DumNN | lld:pubmed |
| pubmed-article:1995951 | pubmed:author | pubmed-author:Buckler-White... | lld:pubmed |
| pubmed-article:1995951 | pubmed:author | pubmed-author:SeidnerTT | lld:pubmed |
| pubmed-article:1995951 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1995951 | pubmed:volume | 65 | lld:pubmed |
| pubmed-article:1995951 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1995951 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1995951 | pubmed:pagination | 1414-9 | lld:pubmed |
| pubmed-article:1995951 | pubmed:dateRevised | 2010-9-9 | lld:pubmed |
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