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Regulation of cardiac L‐type Ca 2+ channel by coexpression of G αs in Xenopus oocytes
Author(s) -
Blumenstein Yakov,
Ivanina Tatiana,
Shistik Elena,
Bossi Elena,
Peres Antonio,
Dascal Nathan
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)00035-6
Subject(s) - xenopus , receptor , protein subunit , phosphorylation , protein kinase a , gene knockdown , biology , microbiology and biotechnology , g protein , adrenergic receptor , endogeny , endocrinology , chemistry , biophysics , gene , biochemistry
Activation of G αs via β‐adrenergic receptors enhances the activity of cardiac voltage‐dependent Ca 2+ 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 α 2 /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 Ca 2+ channel via a PKA‐independent effect on the α 1C subunit.