Regulation of cardiac L-type Ca2+ channel by coexpression of G(αs) in Xenopus oocytes

Yakov Blumenstein, Tatiana Ivanina, Elena Shistik, Elena Bossi, Antonio Peres, Nathan Dascal*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

16 Scopus citations

Abstract

Activation of G(αs) via β-adrenergic receptors enhances the activity of cardiac voltage-dependent Ca2+ channels of the L-type, mainly via protein kinase A (PKA)-dependent phosphorylation. Contribution of a PKA-independent effect of G(αs) has been proposed but remains controversial. We demonstrate that, in Xenopus oocytes, antisense knockdown of endogenous G(αs) reduced, whereas coexpression of G(αs) enhanced, currents via expressed cardiac L-type channels, independently of the presence of the auxiliary subunits α2/δ or β(2A). Coexpression of G(αs) did not increase the amount of α(1C) protein in whole oocytes or in the plasma membrane (measured immunochemically). Activation of coexpressed β2 adrenergic receptors did not cause a detectable enhancement of channel activity; rather, a small cAMP-dependent decrease was observed. We conclude that coexpression of G(αs), but not its acute activation via β-adrenergic receptors, enhances the activity of the cardiac L-type Ca2+ channel via a PKA-independent effect on the α(1C) subunit.

Original languageEnglish
Pages (from-to)78-84
Number of pages7
JournalFEBS Letters
Volume444
Issue number1
DOIs
StatePublished - 5 Feb 1999

Funding

FundersFunder number
National Institutes of Health
National Institute of General Medical SciencesR01GM056260
Academy of Leisure Sciences

    Keywords

    • Calcium channel
    • G-protein
    • Xenopus ocyte

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