pubmed-article:8985415 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8985415 | lifeskim:mentions | umls-concept:C0079082 | lld:lifeskim |
pubmed-article:8985415 | lifeskim:mentions | umls-concept:C1335872 | lld:lifeskim |
pubmed-article:8985415 | lifeskim:mentions | umls-concept:C0026473 | lld:lifeskim |
pubmed-article:8985415 | lifeskim:mentions | umls-concept:C0023978 | lld:lifeskim |
pubmed-article:8985415 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
pubmed-article:8985415 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
pubmed-article:8985415 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
pubmed-article:8985415 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:8985415 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:8985415 | pubmed:dateCreated | 1997-1-31 | lld:pubmed |
pubmed-article:8985415 | pubmed:abstractText | The caprine arthritis-encephalitis virus (CAEV) long terminal repeat (LTR) is activated by gamma interferon (IFN-gamma) in promonocytic cells. We have previously shown that a 70-bp element is necessary and sufficient for the response of the CAEV LTR to this cytokine. At the 5' end, this 70-bp IFN-gamma response element contains sequence similarity to the gamma activated site (GAS). Here we demonstrate that the putative GAS element in the CAEV LTR binds specifically to a cellular factor induced by IFN-gamma in promonocytic cells. Substitution mutations in this consensus sequence eliminate binding of the inducible factor. The GAS element from the 70-bp motif is sufficient to confer responsiveness to IFN-gamma using a heterologous minimal promoter. Consistent with the binding data, the same mutations in the GAS element eliminate responsiveness to IFN-gamma in the context of both a functional CAEV LTR and a heterologous promoter. The cellular factor that binds to the GAS element is present from 5 min to 14 h after stimulation with IFN-gamma. Binding of the nuclear factor to the GAS element in the CAEV LTR is inhibited by antibody directed against STAT1 (p91/84). Thus, the GAS sequence in the CAEV LTR is essential for the response to IFN-gamma and a STAT1-like factor binds to this site. The STAT-1 signaling pathway provides at least one mechanism for activation of the CAEV LTR by IFN-gamma in monocytes. These data are the first demonstration of a role for a STAT family member in the regulation of a viral promoter. | lld:pubmed |
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pubmed-article:8985415 | pubmed:language | eng | lld:pubmed |
pubmed-article:8985415 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8985415 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:8985415 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8985415 | pubmed:month | Jan | lld:pubmed |
pubmed-article:8985415 | pubmed:issn | 0022-538X | lld:pubmed |
pubmed-article:8985415 | pubmed:author | pubmed-author:SepeAA | lld:pubmed |
pubmed-article:8985415 | pubmed:author | pubmed-author:Tong-Starksen... | lld:pubmed |
pubmed-article:8985415 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8985415 | pubmed:volume | 71 | lld:pubmed |
pubmed-article:8985415 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8985415 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8985415 | pubmed:pagination | 771-7 | lld:pubmed |
pubmed-article:8985415 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:8985415 | pubmed:meshHeading | pubmed-meshheading:8985415-... | lld:pubmed |
pubmed-article:8985415 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:8985415 | pubmed:articleTitle | STAT1 pathway is involved in activation of caprine arthritis-encephalitis virus long terminal repeat in monocytes. | lld:pubmed |
pubmed-article:8985415 | pubmed:affiliation | Department of Medicine, University of California-San Francisco, 94121, USA. | lld:pubmed |
pubmed-article:8985415 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8985415 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:8985415 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
pubmed-article:8985415 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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