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- aggregation classification "A1".
- aggregation creator B617882.
- aggregation creator person.
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- aggregation date "2012".
- aggregation format "application/pdf".
- aggregation hasFormat 2983518.bibtex.
- aggregation hasFormat 2983518.csv.
- aggregation hasFormat 2983518.dc.
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- aggregation hasFormat 2983518.yaml.
- aggregation isPartOf urn:issn:0027-8424.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "The Sin3a repressor complex is a master regulator of STAT transcriptional activity".
- aggregation abstract "Tyrosine phosphorylation is a hallmark for activation of STAT proteins, but their transcriptional activity also depends on other secondary modifications. Type I IFNs can activate both the ISGF3 (STAT1:STAT2:IRF9) complex and STAT3, but with cell-specific, selective triggering of only the ISGF3 transcriptional program. Following a genome-wide RNAi screen, we identified the SIN3 transcription regulator homolog A (Sin3a) as an important mediator of this STAT3-targeted transcriptional repression. Sin3a directly interacts with STAT3 and promotes its deacetylation. SIN3A silencing results in a prolonged nuclear retention of activated STAT3 and enhances its recruitment to the SOCS3 promoter, concomitant with histone hyperacetylation and enhanced STAT3-dependent transcription. Conversely, Sin3a is required for ISGF3-dependent gene transcription and for an efficient IFN-mediated antiviral protection against influenza A and hepatitis C viruses. The Sin3a complex therefore acts as a context-dependent ISGF3/STAT3 transcriptional switch.".
- aggregation authorList BK977726.
- aggregation endPage "12063".
- aggregation issue "30".
- aggregation startPage "12058".
- aggregation volume "109".
- aggregation aggregates 4381294.
- aggregation isDescribedBy 2983518.
- aggregation similarTo pnas.1206458109.
- aggregation similarTo LU-2983518.