pubmed-article:16380379 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16380379 | lifeskim:mentions | umls-concept:C0029246 | lld:lifeskim |
pubmed-article:16380379 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
pubmed-article:16380379 | lifeskim:mentions | umls-concept:C0001721 | lld:lifeskim |
pubmed-article:16380379 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:16380379 | lifeskim:mentions | umls-concept:C1336579 | lld:lifeskim |
pubmed-article:16380379 | lifeskim:mentions | umls-concept:C1172070 | lld:lifeskim |
pubmed-article:16380379 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
pubmed-article:16380379 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:16380379 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:16380379 | pubmed:issue | 8 | lld:pubmed |
pubmed-article:16380379 | pubmed:dateCreated | 2006-2-20 | lld:pubmed |
pubmed-article:16380379 | pubmed:abstractText | Virus-induced expression of interferon (IFN)-A genes is regulated by two members of the IFN regulatory factor (IRF) family, IRF-3 and IRF-7, which are activated by phosphorylation during viral infection by the IKK-related serine/threonine kinases TBK1 and IkappaB kinase epsilon (IKKepsilon). In this study, we demonstrate that three IRF-binding sites located in the virus-responsive element mediate the transcriptional activation of the IFN-A4 promoter by IRF-3. The precise arrangement of these IRF elements is required for synergistic activation of the IFN-A4 promoter following Newcastle disease virus infection or activation by TBK1 or IKKepsilon. The ordered assembly of IRF-3 multimers on the promoter also determines cooperative recruitment of IRF-3 and CREB-binding protein and differential virus-induced expression of IFN-A4 gene promoter compared with IFN-A11. Naturally occurring nucleotide substitutions disrupt two of the IRF elements in the IFN-A11 gene promoter, leading to a dramatic decrease in IRF-3 and CREB-binding protein recruitment and in IRF-3-dependent transcription. Transcription of the IFN-A4 promoter by IRF-7 is mediated by two IRF elements; promoter mutants that carry a reversed IRF element retain the ability to respond to IKKepsilon or TBK1 expression in the presence of IRF-7 but lose the capacity to respond to virus or kinase-induced IRF-3. Interestingly, IKKepsilon or TBK1 stimulates the IRF-7-mediated transcription of IFN-A11, although at a lesser extent compared with IFN-A4. Our data indicate that virus-induced expression of IFN-A genes is dictated by the organization of IRF elements within the IFN-A promoters and that the differential IFN-A gene expression, based on the IRF-3 responsiveness, is partially compensated in the presence of IRF-7 when both factors are activated by IKKepsilon or TBK1. | lld:pubmed |
pubmed-article:16380379 | pubmed:language | eng | lld:pubmed |
pubmed-article:16380379 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16380379 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:16380379 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:16380379 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16380379 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16380379 | pubmed:month | Feb | lld:pubmed |
pubmed-article:16380379 | pubmed:issn | 0021-9258 | lld:pubmed |
pubmed-article:16380379 | pubmed:author | pubmed-author:LinRongtuanR | lld:pubmed |
pubmed-article:16380379 | pubmed:author | pubmed-author:MorinPierreP | lld:pubmed |
pubmed-article:16380379 | pubmed:author | pubmed-author:GéninPierreP | lld:pubmed |
pubmed-article:16380379 | pubmed:author | pubmed-author:CivasAhmetA | lld:pubmed |
pubmed-article:16380379 | pubmed:author | pubmed-author:HiscottJohnJ | lld:pubmed |
pubmed-article:16380379 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16380379 | pubmed:day | 24 | lld:pubmed |
pubmed-article:16380379 | pubmed:volume | 281 | lld:pubmed |
pubmed-article:16380379 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16380379 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16380379 | pubmed:pagination | 4856-66 | lld:pubmed |
pubmed-article:16380379 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:16380379 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:16380379 | pubmed:articleTitle | Promoter organization of the interferon-A genes differentially affects virus-induced expression and responsiveness to TBK1 and IKKepsilon. | lld:pubmed |
pubmed-article:16380379 | pubmed:affiliation | UPR 2228-CNRS, Laboratoire de Régulation Transcriptionnelle et Maladies Génétiques, UFR Biomédicale des Saints-Pères, Université Paris V, 45 rue des Saints-Pères, 75270 Paris Cedex 06, France. ahmet.civas@univ-paris5.fr | lld:pubmed |
pubmed-article:16380379 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16380379 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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