RGD Reference Report - CaM kinase II selectively signals to histone deacetylase 4 during cardiomyocyte hypertrophy. - Rat Genome Database

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CaM kinase II selectively signals to histone deacetylase 4 during cardiomyocyte hypertrophy.

Authors: Backs, J  Song, K  Bezprozvannaya, S  Chang, S  Olson, EN 
Citation: Backs J, etal., J Clin Invest. 2006 Jul;116(7):1853-64. Epub 2006 Jun 8.
RGD ID: 2306455
Pubmed: PMID:16767219   (View Abstract at PubMed)
PMCID: PMC1474817   (View Article at PubMed Central)
DOI: DOI:10.1172/JCI27438   (Journal Full-text)

Class IIa histone deacetylases (HDACs) regulate a variety of cellular processes, including cardiac growth, bone development, and specification of skeletal muscle fiber type. Multiple serine/threonine kinases control the subcellular localization of these HDACs by phosphorylation of common serine residues, but whether certain class IIa HDACs respond selectively to specific kinases has not been determined. Here we show that calcium/calmodulin-dependent kinase II (CaMKII) signals specifically to HDAC4 by binding to a unique docking site that is absent in other class IIa HDACs. Phosphorylation of HDAC4 by CaMKII promotes nuclear export and prevents nuclear import of HDAC4, with consequent derepression of HDAC target genes. In cardiomyocytes, CaMKII phosphorylation of HDAC4 results in hypertrophic growth, which can be blocked by a signal-resistant HDAC4 mutant. These findings reveal a central role for HDAC4 in CaMKII signaling pathways and have implications for the control of gene expression by calcium signaling in a variety of cell types.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
response to xenobiotic stimulus  IDA 2306455; 2306455phenylephrineRGD 

Objects Annotated

Genes (Rattus norvegicus)
Hdac4  (histone deacetylase 4)
Hdac5  (histone deacetylase 5)


Additional Information