Open AccessNeurohormonal Regulation of Cardiac Histone Deacetylase 5 Nuclear Localization by Phosphorylation-Dependent and Phosphorylation-Independent Mechanisms
Author(s) -
Robert S. Haworth,
Κωνσταντίνα Σταθοπούλου,
Alexandra J. Candasamy,
Metin Avkiran
Publication year - 2012
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/circresaha.111.263665
Subject(s) - mef2 , histone deacetylase 5 , phosphorylation , nuclear export signal , microbiology and biotechnology , histone deacetylase , biology , nuclear transport , signal transduction , nuclear localization sequence , transcription factor , histone , cell nucleus , enhancer , biochemistry , gene , nucleus , cytoplasm
Myocyte enhancer factor 2 (MEF2) transcription factors drive the genetic reprogramming that precipitates pathological cardiac hypertrophy and remodeling. Class II histone deacetylase (HDAC) isoforms, such as HDAC5, act as signal-responsive repressors of MEF2 activity in cardiac myocytes and their nuclear export provides a key mechanism for the neurohormonal induction of such activity.
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