pubmed-article:11846978 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11846978 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
pubmed-article:11846978 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:11846978 | lifeskim:mentions | umls-concept:C1415906 | lld:lifeskim |
pubmed-article:11846978 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
pubmed-article:11846978 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
pubmed-article:11846978 | lifeskim:mentions | umls-concept:C1709061 | lld:lifeskim |
pubmed-article:11846978 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:11846978 | pubmed:dateCreated | 2002-2-15 | lld:pubmed |
pubmed-article:11846978 | pubmed:abstractText | Maximal activation of murine infection-A4 (IFNA4) gene transcription following viral infection requires the presence of four cooperating DNA sequences (denoted A to D), which make up the virus responsive element VRE-A4. The B, C, and D modules, when tandemized, form binding sites for the virus-induced factor (VIF), a multiprotein complex that is detected early after viral infection in the nuclei of mouse L929 cells. We now demonstrate that IFN regulatory factor-3 (IRF-3) is a component of VIF and that VIF is different from the previously identified virus-activated complexes containing IRF-3 and coactivators of transcription, such as CREB binding protein (CBP) or p300. We also show that the C module is critical for both IRF-3-mediated and virus-induced transcription of the murine IFNA4 gene. Consistently, DNase I footprinting experiments and EMSA performed with increasing amounts of recombinant GST-IRF-3(DBD) fusion proteins demonstrate that cooperativity between the modules facilitate the binding of IRF-3 and recruitment of transcription coactivators on the IFNA4 promoter. These results indicate that VIF differentially recognizes the virus-responsive modules of VRE-A4 and further actualize our previous model concerning the differential expression of murine IFNA genes. | lld:pubmed |
pubmed-article:11846978 | pubmed:language | eng | lld:pubmed |
pubmed-article:11846978 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11846978 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11846978 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11846978 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11846978 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11846978 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11846978 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11846978 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11846978 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11846978 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:11846978 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11846978 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11846978 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11846978 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11846978 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11846978 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11846978 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11846978 | pubmed:month | Jan | lld:pubmed |
pubmed-article:11846978 | pubmed:issn | 1079-9907 | lld:pubmed |
pubmed-article:11846978 | pubmed:author | pubmed-author:MorinPierreP | lld:pubmed |
pubmed-article:11846978 | pubmed:author | pubmed-author:GéninPierreP | lld:pubmed |
pubmed-article:11846978 | pubmed:author | pubmed-author:DolyJanineJ | lld:pubmed |
pubmed-article:11846978 | pubmed:author | pubmed-author:CivasAhmetA | lld:pubmed |
pubmed-article:11846978 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11846978 | pubmed:volume | 22 | lld:pubmed |
pubmed-article:11846978 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11846978 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11846978 | pubmed:pagination | 77-86 | lld:pubmed |
pubmed-article:11846978 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:11846978 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:11846978 | pubmed:articleTitle | The virus-induced factor VIF differentially recognizes the virus-responsive modules of the mouse IFNA4 gene promoter. | lld:pubmed |
pubmed-article:11846978 | pubmed:affiliation | UPR 2228-CNRS, Régulation Transcriptionnelle et Maladies Génétiques, UFR Biomédicale des Saints-Pères, Université Paris V, 75270 Paris Cedex 06, France. | lld:pubmed |
pubmed-article:11846978 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11846978 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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