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rdf:type |
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lifeskim:mentions |
umls-concept:C0015980,
umls-concept:C0035820,
umls-concept:C0040649,
umls-concept:C0086860,
umls-concept:C0591833,
umls-concept:C0851285,
umls-concept:C1145667,
umls-concept:C1336789,
umls-concept:C1421565,
umls-concept:C1516240,
umls-concept:C1554184
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pubmed:issue |
5
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pubmed:dateCreated |
2003-2-13
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pubmed:abstractText |
The induction of the beta interferon (IFN-beta) gene constitutes one of the first responses of the cell to virus infection. Its regulation is achieved through an intricate combination of virus-induced binding of transcription factors and local chromatin remodeling. In this work, we demonstrate that transcription factor YY1, known to interact with histone deacetylases (HDAC) and histone acetyltransferases, has a dual activator/repressor role during the regulation of the IFN-beta promoter activity. We show that YY1 specifically binds in vitro and in vivo to the murine IFN-beta promoter at positions -90 and -122. Overexpression of YY1 strongly repressed the transcriptional capacity of a stably integrated IFN-beta promoter fused to a chloramphenicol acetyltransferase reporter gene as well as the endogenous IFN activity of murine L929 cells via an HDAC activity. Stably integrated IFN-beta promoters mutated at the -90 site were no longer repressed by YY1, could no longer be activated by trichostatin A, displayed a retarded postinduction turn off, and a reduced virus-induced activity. Introduction of a mutation at the -122 site did not affect YY1-induced repression, but promoters with this mutation displayed a reduced virus-induced activity. Stably integrated full-length promoters (from position -330 to +20) mutated at both YY1-binding sites displayed extremely reduced promoter activities. We conclude that YY1 has a dual activator/repressor role on IFN-beta promoter activity depending on its binding site and time after infection.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-10082546,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-10220385,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-10452940,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-10487761,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-10490658,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-10693811,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-10888618,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-11070172,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-11106736,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-11238870,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-11250139,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-11486036,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-11498590,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-11572775,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-1309593,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-2172963,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-2410861,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-3221389,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-6307693,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-6313211,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-7479833,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-7501470,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-7816599,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-7853498,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-8003102,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-8134108,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-8276234,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-8455616,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-8530432,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-8756632,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-8999850,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-9199306,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-9620779,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-9660935,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-9759489,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-9759497,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-9809067,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12584314-9893272
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0022-538X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
77
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2903-14
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:12584314-Animals,
pubmed-meshheading:12584314-Base Sequence,
pubmed-meshheading:12584314-Binding Sites,
pubmed-meshheading:12584314-Cell Line,
pubmed-meshheading:12584314-Erythroid-Specific DNA-Binding Factors,
pubmed-meshheading:12584314-Gene Expression Regulation,
pubmed-meshheading:12584314-Interferon-beta,
pubmed-meshheading:12584314-Mice,
pubmed-meshheading:12584314-Molecular Sequence Data,
pubmed-meshheading:12584314-Newcastle disease virus,
pubmed-meshheading:12584314-Promoter Regions, Genetic,
pubmed-meshheading:12584314-Repressor Proteins,
pubmed-meshheading:12584314-Trans-Activators,
pubmed-meshheading:12584314-Transcription Factors,
pubmed-meshheading:12584314-Transfection,
pubmed-meshheading:12584314-YY1 Transcription Factor
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pubmed:year |
2003
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pubmed:articleTitle |
Transcription factor YY1 binds to the murine beta interferon promoter and regulates its transcriptional capacity with a dual activator/repressor role.
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pubmed:affiliation |
Régulation de la Transcription et Maladies Génétiques, CNRS UPR2228, UFR Biomédicale, 75270 Paris cedex 06, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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