English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Regulators of G protein signaling (RGS) accelerate intrinsic GTP hydrolysis on alpha subunits of trimeric G proteins and play crucial roles in the physiological regulation of G protein-mediated cell signaling. The control mechanisms of the action of RGS proteins per se are poorly clarified, however. We recently showed a physiological mode of action of a RGS protein in cardiac myocytes. The voltage-dependent formation of Ca2+/calmodulin facilitated the GTPase activity of RGS by an unidentified mechanism, which underlay the "relaxation" behavior of G protein-gated K+ (K(G)) channels. Here we report the mechanism which is the reversal by Ca2+/calmodulin of phosphatidylinositol-3,4,5,-trisphosphate (PIP3)-mediated inhibition of RGS. Purified RGS4 protein alone inhibited GTP-induced K(G) channel activity in inside-out patches from atrial myocytes. The inhibitory effect of RGS4 was reduced by PIP3 and restored by addition of Ca2+/calmodulin. The intracellular application of anti-PIP3 antibody abolished the RGS-dependent relaxation behavior of K(G) current in atrial myocytes. This study, therefore, reveals a general physiological control mechanism of RGS proteins by lipid-protein interaction.

proceedings of the national academy of sciences of the united states of america

PIP 3 inhibition of RGS protein and its reversal by Ca 2+ /calmodulin mediate voltage-dependent control of the G protein cycle in a cardiac K + channel