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Cardiovascular Research 2007 73(4):641-647; doi:10.1016/j.cardiores.2006.10.019
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Copyright © 2006, European Society of Cardiology

Calmodulin and CaMKII as molecular switches for cardiac ion channels

Geoffrey S. Pitt*

Department of Medicine, Division of Cardiology, College of Physicians and Surgeons of Columbia University, 630 W 168th St, PH 7W 318, New York, NY 10032, USA
Department of Pharmacology, College of Physicians and Surgeons of Columbia University, 630 W 168th St, PH 7W 318, New York, NY 10032, USA

* Department of Pharmacology, College of Physicians and Surgeons of Columbia University, 630 W 168th St, PH 7W 318, New York, NY 10032, USA. Tel.: +1 212 305 1009; fax: +1 212 305 8780. Email address: gp2004{at}columbia.edu

Because changes in intracellular Ca2+ concentration are the final signals of electrical activity in excitable cells, many mechanisms have evolved to regulate Ca2+ influx. Among the most important are those pathways that directly regulate the ion channels responsible for regulating and generating the Ca2+ influx signal. Recent work has demonstrated that the Ca2+ binding protein calmodulin (CaM) and the Ca2+/CaM-sensitive kinase CaMKII are important modulators of cardiac ion channels. Thus, Ca2+ participates in feedback modulation to control electrical activity. This review highlights various mechanisms by which CaM and CaMKII regulate cardiovascular ion channel activity and presents a novel model for CaMKII regulation of CaV1.2 Ca2+ channel function.

KEYWORDS Ion channel; Calcium; Calmodulin; CaMKII; Calcium channel; Sodium channel; Potassium channel; KCNQ1; Subunit assembly

Time for primary review 31 days


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