Protein kinase C enhances plasma membrane expression of cardiac L-type calcium channel, Ca_V1.2.

ABSTRACT: L-type-voltage-dependent Ca²⁺ channels (L-VDCCs; Ca_V1.2, α_1C), crucial in cardiovascular physiology and pathology, are modulated via activation of G-protein-coupled receptors and subsequently protein kinase C (PKC). Despite extensive study, key aspects of the mechanisms leading to PKC-induced Ca²⁺ current increase are unresolved. A notable residue, Ser1928, located in the distal C-terminus (dCT) of α_1C was shown to be phosphorylated by PKC. Ca_V1.2 undergoes posttranslational modifications yielding full-length and proteolytically cleaved CT-truncated forms. We have previously shown that, in Xenopus oocytes, activation of PKC enhances α_1C macroscopic currents. This increase depended on the isoform of α_1C

SUBMITTER: Raifman TK 

PROVIDER: S-EPMC5786194 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature