BAIT
HDAC4
AHO3, BDMR, HA6116, HD4, HDAC-4, HDAC-A, HDACA
histone deacetylase 4
GO Process (24)
GO Function (12)
GO Component (5)
Gene Ontology Biological Process
- B cell activation [TAS]
- B cell differentiation [TAS]
- cardiac muscle hypertrophy in response to stress [TAS]
- chromatin remodeling [IDA]
- histone H3 deacetylation [IDA]
- histone H4 deacetylation [IDA]
- histone deacetylation [IDA, IMP]
- inflammatory response [TAS]
- negative regulation of glycolytic process [ISS]
- negative regulation of myotube differentiation [IMP]
- negative regulation of sequence-specific DNA binding transcription factor activity [IMP]
- negative regulation of transcription from RNA polymerase II promoter [IDA, IMP]
- negative regulation of transcription, DNA-templated [IDA, IMP]
- nervous system development [TAS]
- peptidyl-lysine deacetylation [IDA]
- positive regulation of cell proliferation [IMP]
- positive regulation of protein sumoylation [IDA]
- positive regulation of sequence-specific DNA binding transcription factor activity [IMP]
- positive regulation of transcription from RNA polymerase II promoter [IMP, ISS]
- positive regulation of transcription, DNA-templated [ISS]
- regulation of gene expression, epigenetic [IMP]
- regulation of protein binding [IMP]
- response to denervation involved in regulation of muscle adaptation [ISS]
- response to interleukin-1 [IMP]
Gene Ontology Molecular Function- activating transcription factor binding [IPI]
- core promoter binding [IDA]
- histone deacetylase activity [IDA]
- histone deacetylase binding [IPI]
- potassium ion binding [IDA]
- protein binding [IPI]
- protein deacetylase activity [IDA]
- repressing transcription factor binding [IPI]
- sequence-specific DNA binding [IDA]
- transcription factor binding [IPI]
- transcription regulatory region DNA binding [IDA]
- zinc ion binding [IDA]
- activating transcription factor binding [IPI]
- core promoter binding [IDA]
- histone deacetylase activity [IDA]
- histone deacetylase binding [IPI]
- potassium ion binding [IDA]
- protein binding [IPI]
- protein deacetylase activity [IDA]
- repressing transcription factor binding [IPI]
- sequence-specific DNA binding [IDA]
- transcription factor binding [IPI]
- transcription regulatory region DNA binding [IDA]
- zinc ion binding [IDA]
Gene Ontology Cellular Component
Homo sapiens
PREY
CTBP1
BARS
C-terminal binding protein 1
GO Process (11)
GO Function (7)
GO Component (3)
Gene Ontology Biological Process
- chromatin organization involved in regulation of transcription [IMP]
- negative regulation of cell proliferation [TAS]
- negative regulation of histone H4 acetylation [IMP]
- negative regulation of histone acetylation [IMP]
- negative regulation of transcription from RNA polymerase II promoter [IMP]
- negative regulation of transcription, DNA-templated [ISS]
- positive regulation of histone deacetylation [IMP]
- protein phosphorylation [TAS]
- regulation of cell cycle [IMP]
- viral genome replication [TAS]
- white fat cell differentiation [ISS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
Reconstituted Complex
An interaction is detected between purified proteins in vitro.
Publication
Association of COOH-terminal-binding protein (CtBP) and MEF2-interacting transcription repressor (MITR) contributes to transcriptional repression of the MEF2 transcription factor.
The class II histone deacetylases (HDACs) 4, 5, and 7 share a common structural organization, with a carboxyl-terminal catalytic domain and an amino-terminal extension that mediates interactions with members of the myocyte enhancer factor-2 (MEF2) family of transcription factors. Association of these HDACs with MEF2 factors represses transcription of MEF2 target genes. MEF2-interacting transcription repressor (MITR) shares homology with the ... [more]
J. Biol. Chem. Jan. 05, 2001; 276(1);35-9 [Pubmed: 11022042]
Throughput
- Low Throughput
Additional Notes
- Through a CtBP-binding motif (P-X-D-L-R) conserved in MITR and HDACs 4, 5, and 7. Mutation of this sequence in MITR abolishes interaction with CtBP and impairs, but does not eliminate, the ability of MITR to inhibit MEF2-dependent transcription
Curated By
- BioGRID