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Cited by 511

The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.

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

Open access
Backs, J.·2006·Journal of Clinical Investigation

Abstract

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.

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Metadata

Authors
Backs, J.
Venue
Journal of Clinical Investigation
Published
2006-07-03
Volume
116
Issue
7
Pages
1853-1864
ISSN
0021-9738 (ISSN-L)
OpenAlex
W2113111385
Cited by
511
References
49
FWCI
8.60
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: CaM kinase II selectively signals to histone deacetylase 4 during cardiomyocyte hypertrophy. https://app.cochat.ai/papers/10.1172/jci27438
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Backs, J. (2006). CaM kinase II selectively signals to histone deacetylase 4 during cardiomyocyte hypertrophy. Journal of Clinical Investigation. https://doi.org/10.1172/jci27438

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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