ArticleProceedings of the National Academy of Sciences of the United States of America2002
PIP3 inhibition of RGS protein and its reversal by Ca2+/calmodulin mediate voltage-dependent control of the G protein cycle in a cardiac K+ channel.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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33 citing papers in PubMed, 80 citations in OpenAlex.
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- Transmembrane Membrane Readers form a Novel Class of Proteins That Include Peripheral Phosphoinositide Recognition Domains and Viral Spikes.Membranes · 2022Review
- Structural and Electrical Remodeling of the Sinoatrial Node in Diabetes: New Dimensions and Perspectives.Frontiers in endocrinology · 2022Review
- Mixed-solvent molecular dynamics simulation-based discovery of a putative allosteric site on regulator of G protein signaling 4.Journal of computational chemistry · 2021Article
- RGS4-Deficiency Alters Intracellular Calcium and PKA-Mediated Control of Insulin Secretion in Glucose-Stimulated Beta Islets.Biomedicines · 2021Article
- Impaired regulation of heart rate and sinoatrial node function by the parasympathetic nervous system in type 2 diabetic mice.Scientific reports · 2021Article
- A model for time interval learning in the Purkinje cell.PLoS computational biology · 2020Article
- Short-term desensitization of muscarinic K+ current in the heart.Biophysical journal · 2013Article
- Controlling Parasympathetic Regulation of Heart Rate: A Gatekeeper Role for RGS Proteins in the Sinoatrial Node.Frontiers in physiology · 2012Article
- Regulators of G-protein signaling and their Gα substrates: promises and challenges in their use as drug discovery targets.Pharmacological reviews · 2011Review
- Thinking outside of the "RGS box": new approaches to therapeutic targeting of regulators of G protein signaling.Molecular pharmacology · 2010Review
- Cardiac strong inward rectifier potassium channels.Journal of molecular and cellular cardiology · 2010Review
- PI(3,4,5)P3 potentiates phospholipase C-beta activity.Journal of receptor and signal transduction research · 2009Article
- Coordinating speed and amplitude in G-protein signaling.Current biology : CB · 2008Review
- A role for RGS10 in beta-adrenergic modulation of G-protein-activated K+ (GIRK) channel current in rat atrial myocytes.The Journal of physiology · 2008Article
- R4 RGS proteins: regulation of G-protein signaling and beyond.Pharmacology & therapeutics · 2007Review
- Generation of a constitutive Na+-dependent inward-rectifier current in rat adult atrial myocytes by overexpression of Kir3.4.The Journal of physiology · 2007Article
- Specificity of RGS10A as a key component in the RANKL signaling mechanism for osteoclast differentiation.Journal of cell science · 2007Article
- RGS10-null mutation impairs osteoclast differentiation resulting from the loss of [Ca2+]i oscillation regulation.Genes & development · 2007Article
- Calmodulin potentiates G beta gamma activation of phospholipase C-beta3.Biochemical pharmacology · 2007Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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