A bilobal model of Ca²⁺-dependent inactivation to probe the physiology of L-type Ca²⁺ channels.

ABSTRACT: L-type calcium channels (LTCCs) are critical elements of normal cardiac function, playing a major role in orchestrating cardiac electrical activity and initiating downstream signaling processes. LTCCs thus use feedback mechanisms to precisely control calcium (Ca²⁺) entry into cells. Of these, Ca²⁺-dependent inactivation (CDI) is significant because it shapes cardiac action potential duration and is essential for normal cardiac rhythm. This important form of regulation is mediated by a resident Ca²⁺ sensor, calmodulin (CaM), which is comprised of two lobes that are each capable of responding to spatially distinct Ca²⁺ sources. Disruption of CaM-mediated CDI leads to severe forms of long-QT syndrome (LQTS) and life-threatening arrhythmias. Thus, a

SUBMITTER: Limpitikul WB 

PROVIDER: S-EPMC6279366 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature