Exclusion of alternative exon 33 of Ca_V1.2 calcium channels in heart is proarrhythmogenic.

ABSTRACT: Alternative splicing changes the Ca_V1.2 calcium channel electrophysiological property, but the in vivo significance of such altered channel function is lacking. Structure-function studies of heterologously expressed Ca_V1.2 channels could not recapitulate channel function in the native milieu of the cardiomyocyte. To address this gap in knowledge, we investigated the role of alternative exon 33 of the Ca_V1.2 calcium channel in heart function. Exclusion of exon 33 in Ca_V1.2 channels has been reported to shift the activation potential -10.4 mV to the hyperpolarized direction, and increased expression of Ca_V1.2_Δ33 channels was observed in rat myocardial infarcted hearts. However, how a change in Ca_V1.2 channel electro

SUBMITTER: Li G 

PROVIDER: S-EPMC5448171 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature