ArticleProceedings of the National Academy of Sciences of the United States of America2003
Agonist unbinding from receptor dictates the nature of deactivation kinetics of G protein-gated K+ channels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 37 citations in OpenAlex.
- GPCR-Mediated Cell Intelligence: A Potential Mechanism for Survival and Long-Term Health.Current issues in molecular biology · 2026Review
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- A nanoluciferase complementation-based assay for monitoring β-arrestin2 recruitment to the dopamine DBiochemistry and biophysics reports · 2025Article
- In Vitro Comparison of Ulotaront (SEP-363856) and Ralmitaront (RO6889450): Two TAAR1 Agonist Candidate Antipsychotics.The international journal of neuropsychopharmacology · 2023Article
- Differential voltage-dependent modulation of the ACh-gated K+ current by adenosine and acetylcholine.PloS one · 2022Article
- Dopamine DInternational journal of molecular sciences · 2021Article
- Notch enhances CaAmerican journal of physiology. Cell physiology · 2020Article
- Voltage-Dependent Dopamine Potency at DFrontiers in pharmacology · 2020Article
- Differential effects of inhibitory G protein isoforms on G protein-gated inwardly rectifying KAmerican journal of physiology. Cell physiology · 2018Article
- The agonist-specific voltage dependence of M2 muscarinic receptors modulates the deactivation of the acetylcholine-gated K(+) current (I KACh).Pflugers Archiv : European journal of physiology · 2016Article
- Absence of the Regulator of G-protein Signaling, RGS4, Predisposes to Atrial Fibrillation and Is Associated with Abnormal Calcium Handling.The Journal of biological chemistry · 2015Article
- Article
- Do caveolae have a role in the fidelity and dynamics of receptor activation of G-protein-gated inwardly rectifying potassium channels?The Journal of biological chemistry · 2010Article
- HL-1 cells express an inwardly rectifying K+ current activated via muscarinic receptors comparable to that in mouse atrial myocytes.Pflugers Archiv : European journal of physiology · 2010Article
- 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
- Turning G proteins on and off using peptide ligands.ACS chemical biology · 2006Article
- Heterotrimeric G proteins precouple with G protein-coupled receptors in living cells.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
G protein-gated inwardly rectifying K(+) (Kir) channels are found in neurones, atrial myocytes, and endocrine cells and are involved in generating late inhibitory postsynaptic potentials, slowing the heart rate and inhibiting hormone release. They are activated by G protein-coupled receptors (GPCRs) via the inhibitory family of G protein, G(i/o), in a membrane-delimited fashion by the direct binding of Gbetagamma dimers to the channel complex. In this study we are concerned with the kinetics of deactivation of the cloned neuronal G protein-gated K(+) channel, Kir3.1 + 3.2A, after stimulation of a number of GPCRs. Termination of the channel activity on agonist removal is thought to solely depend on the intrinsic hydrolysis rate of the G protein alpha subunit. In this study we present data that illustrate a more complex behavior. We hypothesize that there are two processes that account for channel deactivation: agonist unbinding from the GPCR and GTP hydrolysis by the G protein alpha subunit. With some combinations of agonist/GPCR, the rate of agonist unbinding is slow and rate-limiting, and deactivation kinetics are not modulated by regulators of G protein-signaling proteins. In another group, channel deactivation is generally faster and limited by the hydrolysis rate of the G protein alpha subunit. G protein isoform and interaction with G protein-signaling proteins play a significant role with this group of GPCRs.
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