| pubmed-article:12501250 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12501250 | lifeskim:mentions | umls-concept:C0019682 | lld:lifeskim |
| pubmed-article:12501250 | lifeskim:mentions | umls-concept:C0001068 | lld:lifeskim |
| pubmed-article:12501250 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
| pubmed-article:12501250 | lifeskim:mentions | umls-concept:C0001038 | lld:lifeskim |
| pubmed-article:12501250 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:12501250 | lifeskim:mentions | umls-concept:C0961954 | lld:lifeskim |
| pubmed-article:12501250 | lifeskim:mentions | umls-concept:C1100939 | lld:lifeskim |
| pubmed-article:12501250 | pubmed:issue | 14 | lld:pubmed |
| pubmed-article:12501250 | pubmed:dateCreated | 2003-3-31 | lld:pubmed |
| pubmed-article:12501250 | pubmed:abstractText | Patients with AIDS are at increased risk for developing various neoplasms, including Hodgkin's and non-Hodgkin's lymphomas, Kaposi's sarcomas, and anal-rectal carcinomas, suggestive that human immunodeficiency virus type-1 infection might promote establishment of AIDS-related cancers. Tat, the viral trans-activator, can be endocytosed by uninfected cells and has been shown to inhibit p53 functions, providing a candidate mechanism through which the human immunodeficiency virus type-1 might contribute to malignant transformation. Because Tat has been shown to interact with histone acetyltransferase domains of p300/cAMP-responsive element-binding protein (CREB)-binding protein and p300/CREB-binding protein-associated factor, we have investigated whether Tat might alter p53 acetylation and tumor suppressor-responsive transcription. Here, we demonstrate that both Tat and p53 co-localize with p300/CREB-binding protein-associated factor and p300 in nuclei of IMR-32 human neuroblastoma cells and in PC-12 pheochromocytoma cells. Further, p53 trans-activation of the 14-3-3varsigma promoter was markedly repressed by Tat-histone acetyltransferase interactions, and p53 acetylation by p300/CREB-binding protein-associated factor on residue Lys(320) was diminished as a result of Tat-histone acetyltransferase binding in vivo and in vitro. Tat also inhibited p53 acetylation by p300 in a dosage-dependent manner in vitro. Finally, HIV-1-infected Molt-4 cells displayed reduced p53 acetylation on lysines 320 and 373 in response to UV irradiation. Our results allude to a mechanism whereby the human immunodeficiency virus type-1 trans-activator might impair tumor suppressor functions in immune/neuronal-derived cells, thus favoring the establishment of neoplasia during AIDS. | lld:pubmed |
| pubmed-article:12501250 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12501250 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12501250 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12501250 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12501250 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:12501250 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:12501250 | pubmed:author | pubmed-author:NacsaJanosJ | lld:pubmed |
| pubmed-article:12501250 | pubmed:author | pubmed-author:FranchiniGeno... | lld:pubmed |
| pubmed-article:12501250 | pubmed:author | pubmed-author:Van... | lld:pubmed |
| pubmed-article:12501250 | pubmed:author | pubmed-author:HarrodRobertR | lld:pubmed |
| pubmed-article:12501250 | pubmed:author | pubmed-author:KarpovaTatian... | lld:pubmed |
| pubmed-article:12501250 | pubmed:author | pubmed-author:McNallyJamesJ | lld:pubmed |
| pubmed-article:12501250 | pubmed:author | pubmed-author:HansenJeremyJ | lld:pubmed |
| pubmed-article:12501250 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12501250 | pubmed:day | 4 | lld:pubmed |
| pubmed-article:12501250 | pubmed:volume | 278 | lld:pubmed |
| pubmed-article:12501250 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12501250 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12501250 | pubmed:pagination | 12310-8 | lld:pubmed |
| pubmed-article:12501250 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:12501250 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12501250 | pubmed:articleTitle | Human immunodeficiency virus type-1 Tat/co-activator acetyltransferase interactions inhibit p53Lys-320 acetylation and p53-responsive transcription. | lld:pubmed |
| pubmed-article:12501250 | pubmed:affiliation | Laboratory of Molecular Virology, Department of Biological Sciences, Southern Methodist University, Dallas, Texas 75275-0376, USA. rharrod@mail.smu.edu | lld:pubmed |
| pubmed-article:12501250 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12501250 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12501250 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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