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The Ca2+-binding protein calmodulin (CaM) and the Ca2+/CaM-sensitive kinase (CaMKII) play an important role in the regulation of cardiac excitation–contraction coupling, regulating ryanodine receptor and phospholamban activity.1 CaM is also known to regulate a variety of ion channels; voltage-dependent Ca2+ channels are the classical example, and CaM has been identified as the mediator of Ca2+-dependent channel inactivation. The discovery that Ca2+-dependent inactivation is associated with a specific region in the C-terminus containing a consensus ‘IQ’ motif2 initiated the pursuance of calcium-dependent regulation of other ion channels.The recognition of the presence of an IQ-like motif within the C-terminus of voltage-gated sodium channels (VGSCs) in mammalian cells3 triggered interest in the possibility that VGSCs may also undergo regulation via this mechanism. In the heart, VGSCs are integral to conduction within the myocardium and maintenance of normal cardiac rhythm, underlying the action potential upstroke and velocity of impulse propagation. Impairment of VGSC function is frequently associated with clinical conditions, including Brugada syndrome, and conditions involving augmented late sodium VGSC current ( I NaL) such as long-QT syndrome (LQT3).4 At present, however, there is limited information regarding the effects of CaM/CaMKII modulation on activity of cardiac VGSCs. The results of a few individual studies that focused on the mechanisms … *Corresponding author. Tel: +44 1225 384471; fax: +44 1225 826 114. E-mail address : s.v.smirnov{at}bath.ac.uk

Calcium-dependent regulation of voltage-gated sodium channels in cardiac myocytes: just the beginning?