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- W1592493313 abstract "Oncoprotein p28 GANK , overexpressed in hepatocellular carcinomas (HCC), binds to RelA and retains NF‐κB in the cytoplasm to suppress NF‐κB transactivation. However, the mechanism has not yet been elucidated. In this study, we clarified the mechanism of NF‐κB regulated by p28 GANK . p28 GANK reduced TNF‐α‐induced nuclear translocation of RelA/NF‐κB independent of HDAC3. p28 GANK interacted with p300 to attenuate assembly of RelA with p300, which lessened acetylation of RelA on the lysine 310 sites. Moreover, overexpression of p28 GANK attenuated the capability of NF‐κB binding to the target gene IκBα promoter, but also weakened adriamycin‐induced NF‐κB pro‐apoptotic gene Fas and FasL expression, which subsequently made p53‐deficient tumor cells resistance to adriamycin. These results present mechanistic insight into the key role of p28 GANK in post‐translational regulation of RelA/NF‐κB. © 2014 Wiley Periodicals, Inc." @default.
- W1592493313 created "2016-06-24" @default.
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- W1592493313 date "2014-11-14" @default.
- W1592493313 modified "2023-10-09" @default.
- W1592493313 title "p28<sup>GANK</sup>associates with p300 to attenuate the acetylation of RelA" @default.
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- W1592493313 doi "https://doi.org/10.1002/mc.22235" @default.
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