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10.15252/embr.201438990 http://scihub22266oqcxt.onion/10.15252/embr.201438990 C4253493!4253493!25269644     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EMBO+Rep 2014 ; 15 (11): 1192-201 Nephropedia Template TP {{tp|p=25269644|t=2014. Gcn5 and PCAF negatively regulate interferon-? production through HAT-independent inhibition of TBK1 |pdf=|usr=}}{{25269644}} gab.com Text Gcn5 and PCAF negatively regulate interferon- production through HAT-independent inhibition of TBK1 JO: EMBO Rep http://www.kidney.de/pget.php?&tw=1&pmid=25269644 #FOAvip Viral infection triggers innate immune signaling, which in turn induces interferon-? (IFN-?) production to establish innate antiviral immunity. Previous studies showed that Gcn5 (Kat2a), a histone acetyltransferase (HAT) with partial functional redundancy with PCAF (Kat2b), and Gcn5/PCAF-mediated histone H3K9 acetylation (H3K9ac) are enriched on the active IFNB gene promoter. However, whether Gcn5/PCAF and H3K9ac regulate IFN-? production is unknown. Here, we show that Gcn5/PCAF-mediated H3K9ac correlates well with, but is surprisingly dispensable for, the expression of endogenous IFNB and the vast majority of active genes in fibroblasts. Instead, Gcn5/PCAF repress IFN-? production and innate antiviral immunity in several cell types in a HAT-independent and non-transcriptional manner: by inhibiting the innate immune signaling kinase TBK1 in the cytoplasm. Our results thus identify Gcn5 and PCAF as negative regulators of IFN-? production and innate immune signaling. Twit Text FOAVip Gcn5 and PCAF negatively regulate interferon- production through HAT-independent inhibition of TBK1 ????EMBO Rep http://www.kidney.de/pget.php?&tw=1&pmid=25269644 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25269644 #FOAvip English Wikipedia <ref>{{Cite pmid|25269644}}</ref> Gcn5 and PCAF negatively regulate interferon-? production through HAT-independent inhibition of TBK1 #MMPMID25269644 Jin Q; Zhuang L; Lai B; Wang C; Li W; Dolan B; Lu Y; Wang Z; Zhao K; Peng W; Dent SY; Ge K EMBO Rep 2014[Nov]; 15 (11): 1192-201 PMID25269644show ga Viral infection triggers innate immune signaling, which in turn induces interferon-? (IFN-?) production to establish innate antiviral immunity. Previous studies showed that Gcn5 (Kat2a), a histone acetyltransferase (HAT) with partial functional redundancy with PCAF (Kat2b), and Gcn5/PCAF-mediated histone H3K9 acetylation (H3K9ac) are enriched on the active IFNB gene promoter. However, whether Gcn5/PCAF and H3K9ac regulate IFN-? production is unknown. Here, we show that Gcn5/PCAF-mediated H3K9ac correlates well with, but is surprisingly dispensable for, the expression of endogenous IFNB and the vast majority of active genes in fibroblasts. Instead, Gcn5/PCAF repress IFN-? production and innate antiviral immunity in several cell types in a HAT-independent and non-transcriptional manner: by inhibiting the innate immune signaling kinase TBK1 in the cytoplasm. Our results thus identify Gcn5 and PCAF as negative regulators of IFN-? production and innate immune signaling. äGcn5 and PCAF negatively regulate interferon-? production through HAT-(epmc).pdf DeepDyve Pubget Overpricing