Modulation of distinct isoforms of L-type calcium channels by G(q)-coupled receptors in Xenopus oocytes: antagonistic effects of Gβγ and protein kinase C.

ABSTRACT: L-type voltage dependent Ca(2+) channels (L-VDCCs; Ca(v)1.2) are crucial in cardiovascular physiology. In heart and smooth muscle, hormones and transmitters operating via G(q) enhance L-VDCC currents via essential protein kinase C (PKC) involvement. Heterologous reconstitution studies in Xenopus oocytes suggested that PKC and G(q)-coupled receptors increased L-VDCC currents only in cardiac long N-terminus (NT) isoforms of α(1C), whereas known smooth muscle short-NT isoforms were inhibited by PKC and G(q) activators. We report a novel regulation of the long-NT α(1C) isoform by Gβγ. Gβγ inhibited whereas a Gβγ scavenger protein augmented the G(q)--but not phorbol ester-mediated enhancement of channel activity, suggesting that Gβγ acts upstream from PKC. In vitro binding experiments reveal bi

SUBMITTER: Weiss S 

PROVIDER: S-EPMC3536727 | biostudies-literature | 2012 Nov-Dec

REPOSITORIES: biostudies-literature