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Identification and characterization of a novel nuclear factor of activated T-cells-1 isoform expressed in mouse brain 总被引:5,自引:0,他引:5
Plyte S Boncristiano M Fattori E Galvagni F Paccani SR Majolini MB Oliviero S Ciliberto G Telford JL Baldari CT 《The Journal of biological chemistry》2001,276(17):14350-14358
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Reovirus-induced apoptosis requires activation of transcription factor NF-kappaB 总被引:5,自引:0,他引:5
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Connolly JL Rodgers SE Clarke P Ballard DW Kerr LD Tyler KL Dermody TS 《Journal of virology》2000,74(7):2981-2989
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Activation and repression by the C-terminal domain of Dorsal 总被引:6,自引:0,他引:6
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The p65 (RelA) subunit of NF-kappaB interacts with the histone deacetylase (HDAC) corepressors HDAC1 and HDAC2 to negatively regulate gene expression 总被引:1,自引:0,他引:1
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Regulation of NF-kappaB transactivation function is controlled at several levels, including interactions with coactivator proteins. Here we show that the transactivation function of NF-kappaB is also regulated through interaction of the p65 (RelA) subunit with histone deacetylase (HDAC) corepressor proteins. Our results show that inhibition of HDAC activity with trichostatin A (TSA) results in an increase in both basal and induced expression of an integrated NF-kappaB-dependent reporter gene. Chromatin immunoprecipitation (ChIP) assays show that TSA treatment causes hyperacetylation of the wild-type integrated NF-kappaB-dependent reporter but not of a mutant version in which the NF-kappaB binding sites were mutated. Expression of HDAC1 and HDAC2 repressed tumor necrosis factor (TNF)-induced NF-kappaB-dependent gene expression. Consistent with this, we show that HDAC1 and HDAC2 target NF-kappaB through a direct association of HDAC1 with the Rel homology domain of p65. HDAC2 does not interact with NF-kappaB directly but can regulate NF-kappaB activity through its association with HDAC1. Finally, we show that inhibition of HDAC activity with TSA causes an increase in both basal and TNF-induced expression of the NF-kappaB-regulated interleukin-8 (IL-8) gene. Similar to the wild-type integrated NF-kappaB-dependent reporter, ChIP assays showed that TSA treatment resulted in hyperacetylation of the IL-8 promoter. These data indicate that the transactivation function of NF-kappaB is regulated in part through its association with HDAC corepressor proteins. Moreover, it suggests that the association of NF-kappaB with the HDAC1 and HDAC2 corepressor proteins functions to repress expression of NF-kappaB-regulated genes as well as to control the induced level of expression of these genes. 相似文献