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TRANSCRIPTIONAL REGULATION

The p65 (RelA) Subunit of NF-κB Interacts with the Histone Deacetylase (HDAC) Corepressors HDAC1 and HDAC2 To Negatively Regulate Gene Expression

Brian P. Ashburner, Sandy D. Westerheide, Albert S. Baldwin Jr.
Brian P. Ashburner
Lineberger Comprehensive Cancer Center,
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Sandy D. Westerheide
Lineberger Comprehensive Cancer Center,
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Albert S. Baldwin Jr.
Lineberger Comprehensive Cancer Center,
Curriculum in Genetics and Molecular Biology, and
Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599
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DOI: 10.1128/MCB.21.20.7065-7077.2001
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ABSTRACT

Regulation of NF-κB transactivation function is controlled at several levels, including interactions with coactivator proteins. Here we show that the transactivation function of NF-κB 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-κB-dependent reporter gene. Chromatin immunoprecipitation (ChIP) assays show that TSA treatment causes hyperacetylation of the wild-type integrated NF-κB-dependent reporter but not of a mutant version in which the NF-κB binding sites were mutated. Expression of HDAC1 and HDAC2 repressed tumor necrosis factor (TNF)-induced NF-κB-dependent gene expression. Consistent with this, we show that HDAC1 and HDAC2 target NF-κB through a direct association of HDAC1 with the Rel homology domain of p65. HDAC2 does not interact with NF-κB directly but can regulate NF-κB 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-κB-regulated interleukin-8 (IL-8) gene. Similar to the wild-type integrated NF-κB-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-κB is regulated in part through its association with HDAC corepressor proteins. Moreover, it suggests that the association of NF-κB with the HDAC1 and HDAC2 corepressor proteins functions to repress expression of NF-κB-regulated genes as well as to control the induced level of expression of these genes.

  • Copyright © 2001 American Society for Microbiology
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The p65 (RelA) Subunit of NF-κB Interacts with the Histone Deacetylase (HDAC) Corepressors HDAC1 and HDAC2 To Negatively Regulate Gene Expression
Brian P. Ashburner, Sandy D. Westerheide, Albert S. Baldwin Jr.
Molecular and Cellular Biology Oct 2001, 21 (20) 7065-7077; DOI: 10.1128/MCB.21.20.7065-7077.2001

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The p65 (RelA) Subunit of NF-κB Interacts with the Histone Deacetylase (HDAC) Corepressors HDAC1 and HDAC2 To Negatively Regulate Gene Expression
Brian P. Ashburner, Sandy D. Westerheide, Albert S. Baldwin Jr.
Molecular and Cellular Biology Oct 2001, 21 (20) 7065-7077; DOI: 10.1128/MCB.21.20.7065-7077.2001
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KEYWORDS

Down-Regulation
Gene Expression Regulation, Enzymologic
Histone Deacetylases
NF-kappa B
Repressor Proteins

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