ArticleThe Biochemical journal2005
Phosphatidylinositol 3,4,5-trisphosphate and Ca2+/calmodulin competitively bind to the regulators of G-protein-signalling (RGS) domain of RGS4 and reciprocally regulate its action.
Article in The Biochemical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 55 citations in OpenAlex.
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- Mixed-solvent molecular dynamics simulation-based discovery of a putative allosteric site on regulator of G protein signaling 4.Journal of computational chemistry · 2021Article
- Impaired regulation of heart rate and sinoatrial node function by the parasympathetic nervous system in type 2 diabetic mice.Scientific reports · 2021Article
- High-resolution structure of RGS17 suggests a role for CaThe Journal of biological chemistry · 2019Article
- Interplay of cysteine exposure and global protein dynamics in small-molecule recognition by a regulator of G-protein signaling protein.Proteins · 2019Article
- Single Platform for Gene and Protein Expression Analyses Using Luminescent Gold Nanoclusters.ACS omega · 2018Article
- Regulator of G Protein Signaling 17 as a Negative Modulator of GPCR Signaling in Multiple Human Cancers.The AAPS journal · 2016Review
- Regulators of G protein signaling 12 promotes osteoclastogenesis in bone remodeling and pathological bone loss.Cell death and differentiation · 2015Article
- Integration of G protein α (Gα) signaling by the regulator of G protein signaling 14 (RGS14).The Journal of biological chemistry · 2015Article
- Regulation of Gβγi-dependent PLC-β3 activity in smooth muscle: inhibitory phosphorylation of PLC-β3 by PKA and PKG and stimulatory phosphorylation of Gαi-GTPase-activating protein RGS2 by PKG.Cell biochemistry and biophysics · 2014Article
- Solution structure of calmodulin bound to the binding domain of the HIV-1 matrix protein.The Journal of biological chemistry · 2014Article
- Role of regulator of G protein signaling proteins in bone.Frontiers in bioscience (Landmark edition) · 2014Review
- Conformational dynamics of a regulator of G-protein signaling protein reveals a mechanism of allosteric inhibition by a small molecule.ACS chemical biology · 2013Article
- The Ras-binding domain region of RGS14 regulates its functional interactions with heterotrimeric G proteins.Journal of cellular biochemistry · 2013Article
- Latest developments in experimental and computational approaches to characterize protein-lipid interactions.Proteomics · 2012Review
- Regulators of G protein signaling (RGS) proteins as drug targets: modulating G-protein-coupled receptor (GPCR) signal transduction.Journal of medicinal chemistry · 2011Article
- Regulators of G-protein signaling and their Gα substrates: promises and challenges in their use as drug discovery targets.Pharmacological reviews · 2011Review
- Regulators of G-protein signaling in the heart and their potential as therapeutic targets.Circulation research · 2011Review
- A nanomolar-potency small molecule inhibitor of regulator of G-protein signaling proteins.Biochemistry · 2011Article
- Thinking outside of the "RGS box": new approaches to therapeutic targeting of regulators of G protein signaling.Molecular pharmacology · 2010Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RGS (regulators of G-protein signalling) are a diverse group of proteins, which accelerate intrinsic GTP hydrolysis on heterotrimeric G-protein a subunits. They are involved in the control of a physiological behaviour known as 'relaxation' of G-protein-gated K+ channels in cardiac myocytes. The GTPase-accelerating activity of cardiac RGS proteins, such as RGS4, is inhibited by PtdIns(3,4,5)P3 (phosphatidylinositol 3,4,5-trisphosphate) and this inhibition is cancelled by Ca2+/calmodulin (CaM) formed during membrane depolarization. G-protein-gated K+ channel activity decreases on depolarization owing to the facilitation of GTPase-activating protein activity by RGS proteins and vice versa on hyperpolarization. The molecular mechanism responsible for this reciprocal control of RGS action by PtdIns(3,4,5)P3 and Ca2+/CaM, however, has not been fully elucidated. Using lipid-protein co-sedimentation assay and surface plasmon resonance measurements, we show in the present study that the control of the GTPase-accelerating activity of the RGS4 protein is achieved through the competitive binding of PtdIns(3,4,5)P3 and Ca2+/CaM within its RGS domain. Competitive binding occurs exclusively within the RGS domain and involves a cluster of positively charged residues located on the surface opposite to the Ga interaction site. In the RGS proteins conserving these residues, the reciprocal regulation by PtdIns(3,4,5)P3 and Ca2+/CaM may be important for their physiological regulation of G-protein signalling.
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