RGD Reference Report - Isolation of a novel histone deacetylase reveals that class I and class II deacetylases promote SMRT-mediated repression. - Rat Genome Database

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Isolation of a novel histone deacetylase reveals that class I and class II deacetylases promote SMRT-mediated repression.

Authors: Kao, HY  Downes, M  Ordentlich, P  Evans, RM 
Citation: Kao HY, etal., Genes Dev 2000 Jan 1;14(1):55-66.
RGD ID: 708314
Pubmed: PMID:10640276   (View Abstract at PubMed)
PMCID: PMC316336   (View Article at PubMed Central)

The transcriptional corepressor SMRT functions by mediating the repressive effect of transcription factors involved in diverse signaling pathways. The mechanism by which SMRT represses basal transcription has been proposed to involve the indirect recruitment of histone deacetylase HDAC1 via the adaptor mSin3A. In contrast to this model, a two-hybrid screen on SMRT-interacting proteins resulted in the isolation of the recently described HDAC5 and a new family member termed HDAC7. Molecular and biochemical results indicate that this interaction is direct and in vivo evidence colocalizes SMRT, mHDAC5, and mHDAC7 to a distinct nuclear compartment. Surprisingly, HDAC7 can interact with mSin3A in yeast and in mammalian cells, suggesting association of multiple repression complexes. Taken together, our results provide the first evidence that SMRT-mediated repression is promoted by class I and class II histone deacetylases and that SMRT can recruit class II histone deacetylases in a mSin3A-independent fashion.

Objects referenced in this article
Gene HDAC7 histone deacetylase 7 Homo sapiens
Gene Hdac5 histone deacetylase 5 Mus musculus
Gene Hdac7 histone deacetylase 7 Mus musculus
Gene Ncor2 nuclear receptor co-repressor 2 Mus musculus
Gene Hdac5 histone deacetylase 5 Rattus norvegicus
Gene Hdac7 histone deacetylase 7 Rattus norvegicus

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