Derepression of pathological cardiac genes by members of the CaM kinase superfamily.
In response to pathologic stresses such as hypertension or myocardial infarction, the heart undergoes a remodeling process that is characterized by myocyte hypertrophy, myocyte death and fibrosis, resulting in impaired cardiac function and heart failure. Cardiac remodeling is associated with derepression of genes that contribute to disease progression. This review focuses on evidence linking members of the Ca(2+)/calmodulin-dependent protein kinase (CaMK) superfamily, specifically CaMKII, protein kinase D (PKD) and microtubule associated kinase (MARK), to stress-induced derepression of pathological cardiac gene expression through their effects on class IIa histone deacetylases (HDACs).
McKinsey
Timothy A
TA
Myogen, Inc./Gilead Colorado, Inc., 7575 West 103rd Ave., Westminster, Colorado 80021, USA. timothy.mckinsey@gilead.com
D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000502:physiology*; D006332:Cardiomegaly / Q000201:enzymology*; D015971:Gene Expression Regulation, Enzymologic / Q000502:physiology*; D006655:Histone Deacetylases / Q000378:metabolism; D006801:Humans; D009206:Myocardium / Q000201:enzymology*; D011493:Protein Kinase C / Q000378:metabolism; D020257:Ventricular Remodeling
C089212:protein kinase D; D011493:Protein Kinase C; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D006655:Histone Deacetylases