| pubmed-article:8207805 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8207805 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
| pubmed-article:8207805 | lifeskim:mentions | umls-concept:C0080055 | lld:lifeskim |
| pubmed-article:8207805 | lifeskim:mentions | umls-concept:C0598312 | lld:lifeskim |
| pubmed-article:8207805 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:8207805 | pubmed:dateCreated | 1994-7-13 | lld:pubmed |
| pubmed-article:8207805 | pubmed:abstractText | The p53 tumor suppressor gene product, a sequence-specific DNA-binding protein, has been shown to act as a transcriptional activator and repressor both in vitro and in vivo. Consistent with its role in regulating transcription are recent observations that the N-terminal acidic domain of p53 binds directly to the TATA box-binding protein subunit of the general transcription factor, TF IID. It is now demonstrated that wild-type p53 (wt-p53) inhibits human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR)-directed chloramphenicol acetyltransferase activity in a cotransfection assay system. Importantly, this effect of wt-p53 on the HIV-1 LTR was also demonstrated by in vitro transcription assays. In addition, the Sp1 sites and the TATA box of the HIV-1 LTR are demonstrated to be the primary sites involved with p53-induced effects on this viral promoter. The upstream elements of the HIV-1 LTR, including the nuclear factor kappa B (NF-kappa B) binding sites, decrease the p53-induced inhibitory effects on viral transcription. In the presence of the HIV-1 TAR sequence and Tat protein, the HIV-1 LTR also becomes less sensitive to wt-p53-induced inhibition. By using a retroviral vector delivery system, mutant forms of p53 genes were expressed in two HIV-1 latently infected cell lines, ACH-2 and U1. In the ACH-2 cell line, which is now demonstrated to contain an endogenous mutant form of p53 (amino acid 248, Arg to Gln), additional mutant p53 proteins did not alter HIV-1 replication. In U1 cells, which completely lack endogenous p53, overexpression of mutant p53 led to an increase in HIV-1 replication. Thus, these data indicate a possible functional role for wt-p53 and mutant p53 proteins in the control of HIV-1 replication patterns and proviral latency. | lld:pubmed |
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| pubmed-article:8207805 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8207805 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8207805 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8207805 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:8207805 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8207805 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:8207805 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:8207805 | pubmed:author | pubmed-author:TaylorJ PJP | lld:pubmed |
| pubmed-article:8207805 | pubmed:author | pubmed-author:PomerantzR... | lld:pubmed |
| pubmed-article:8207805 | pubmed:author | pubmed-author:OakesJ WJW | lld:pubmed |
| pubmed-article:8207805 | pubmed:author | pubmed-author:OzakiII | lld:pubmed |
| pubmed-article:8207805 | pubmed:author | pubmed-author:KhaliliKK | lld:pubmed |
| pubmed-article:8207805 | pubmed:author | pubmed-author:FurrS JSJ | lld:pubmed |
| pubmed-article:8207805 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8207805 | pubmed:volume | 68 | lld:pubmed |
| pubmed-article:8207805 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8207805 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8207805 | pubmed:pagination | 4302-13 | lld:pubmed |
| pubmed-article:8207805 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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