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The coactivator role of histone deacetylase 3 in IL-1-signaling involves deacetylation of p65 NF-kappaB

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Date
2012
Author
Ziesché, Elisabeth
Kettner-Buhrow, Daniela
Weber, Axel
Wittwer, Tobias
Jurida, Liane
Soelch, Johanna
Müller, Helmut
Newel, Doris
Kronich, Petra
Schneider, Heike
Dittrich-Breiholz, Oliver
Bhaskara, Srividya
Hiebert, Scott W.
Hottiger, Michael O.
Li, Haiying
Burstein, Ezra
Schmitz, M. Lienhard
Kracht, Michael
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http://dx.doi.org/10.22029/jlupub-9052
Abstract

Histone deacetylase (HDAC) 3, as a cofactor in co-repressor complexes containing silencing mediator for retinoid or thyroid-hormone receptors (SMRT) and nuclear receptor co-repressor (N-CoR), has been shown to repress gene transcription in a variety of contexts. Here, we reveal a novel role for HDAC3 as a positive regulator of IL-1-induced gene ... expression. Various experimental approaches involving RNAi-mediated knockdown, conditional gene deletion or small molecule inhibitors indicate a positive role of HDAC3 for transcription of the majority of IL-1-induced human or murine genes. This effect was independent from the gene regulatory effects mediated by the broad-spectrum HDAC inhibitor trichostatin A (TSA) and thus suggests IL-1-specific functions for HDAC3. The stimulatory function of HDAC3 for inflammatory gene expression involves a mechanism that uses binding to NF-?B p65 and its deacetylation at various lysines. NF-?B p65-deficient cells stably reconstituted to express acetylation mimicking forms of p65 (p65 K/Q) had largely lost their potential to stimulate IL-1-triggered gene expression, implying that the co-activating property of HDAC3 involves the removal of inhibitory NF-?B p65 acetylations at K122, 123, 314 and 315. These data describe a novel function for HDAC3 as a co-activator in inflammatory signaling pathways and help to explain the anti-inflammatory effects frequently observed for HDAC inhibitors in (pre)clinical use.

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https://doi.org/10.1093/nar/gks916
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