title: Molecular Determinants of Cav1.2 Calcium Channel Inactivation.
abstract: Voltage-gated L-type Cav1.2 calcium channels couple membrane depolarization to transient increase in cytoplasmic free Ca(2+) 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.
authors.affiliation: Humgenex Inc., Kensington, MD 20895, USA.
authors.forename: Nikolai M
authors.initials: NM
authors.lastname: Soldatov