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ISRN Molecular Biology
Volume 2012 (2012), Article ID 691341, 10 pages
http://dx.doi.org/10.5402/2012/691341
Review Article

Molecular Determinants of Cav1.2 Calcium Channel Inactivation

Humgenex Inc., Kensington, MD 20895, USA

Received 24 August 2012; Accepted 13 September 2012

Academic Editors: M. W. Berchtold, E. Caffarelli, and H.-C. Lee

Copyright © 2012 Nikolai M. Soldatov. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Voltage-gated L-type Cav1.2 calcium channels couple membrane depolarization to transient increase in cytoplasmic free Ca2+ concentration that initiates a number of essential cellular functions including cardiac and vascular muscle contraction, gene expression, neuronal plasticity, and exocytosis. Inactivation or spontaneous termination of the calcium current through Cav1.2 is a critical step in regulation of these processes. The pathophysiological significance of this process is manifested in hypertension, heart failure, arrhythmia, and a number of other diseases where acceleration of the calcium current decay should present a benefit function. The central issue of this paper is the inactivation of the Cav1.2 calcium channel mediated by multiple determinants.