Review

Oncogene (2007) 26, 5439–5449; doi:10.1038/sj.onc.1210612

HDAC3: taking the SMRT-N-CoRrect road to repression

P Karagianni1 and J Wong1,2

1Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, USA

Correspondence: Dr J Wong, Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA. E-mail: jmweng@bio.ecnu.edu.cn

2Current address: Institute of Biomedical Sciences, College of Life Science, East China Normal University, Dongchuan Road 500, Shanghai 200241, China.

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Abstract

Known histone deacetylases (HDACs) are divided into different classes, and HDAC3 belongs to Class I. Through forming multiprotein complexes with the corepressors SMRT and N-CoR, HDAC3 regulates the transcription of a plethora of genes. A growing list of nonhistone substrates extends the role of HDAC3 beyond transcriptional repression. Here, we review data on the composition, regulation and mechanism of action of the SMRT/N-CoR-HDAC3 complexes and provide several examples of nontranscriptional functions, to illustrate the wide variety of physiological processes affected by this deacetylase. Furthermore, we discuss the implication of HDAC3 in cancer, focusing on leukemia. We conclude with some thoughts about the potential therapeutic efficacies of HDAC3 activity modulation.

Keywords:

HDAC3, SMRT, N-CoR, corepressor complex, histone deacetylation, repression and cancer

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