ArticleThe Journal of general physiology1996
Na+ activation of the muscarinic K+ channel by a G-protein-independent mechanism.
Article in The Journal of general physiology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
48 citing papers in PubMed, 129 citations in OpenAlex.
- Molecular mechanism of GIRK2 channel gating modulated by cholesteryl hemisuccinate.Frontiers in physiology · 2024Article
- From Crosstalk to Synergism: The Combined Effect of Cholesterol and PI(4,5)PAdvances in experimental medicine and biology · 2023Review
- Oxidation Driven Reversal of PIPFunction (Oxford, England) · 2023Article
- PI(4,5)PAdvances in experimental medicine and biology · 2023Article
- Neuronal G protein-gated KAmerican journal of physiology. Cell physiology · 2022Review
- Insight into the Phospholipid-Binding Preferences of Kir3.4.Biochemistry · 2021Article
- Kir Channel Molecular Physiology, Pharmacology, and Therapeutic Implications.Handbook of experimental pharmacology · 2021Review
- Sodium ions allosterically modulate the M2 muscarinic receptor.Scientific reports · 2020Article
- The small molecule GAT1508 activates brain-specific GIRK1/2 channel heteromers and facilitates conditioned fear extinction in rodents.The Journal of biological chemistry · 2020Article
- Sodium Fluctuations in Astroglia and Their Potential Impact on Astrocyte Function.Frontiers in physiology · 2020Review
- On the mechanism of GIRK2 channel gating by phosphatidylinositol bisphosphate, sodium, and the Gβγ dimer.The Journal of biological chemistry · 2019Article
- International Union of Basic and Clinical Pharmacology. C. Nomenclature and Properties of Calcium-Activated and Sodium-Activated Potassium Channels.Pharmacological reviews · 2017Review
- The ICl,swell inhibitor DCPIB blocks Kir channels that possess weak affinity for PIP2.Pflugers Archiv : European journal of physiology · 2016Article
- Article
- Mechanisms underlying the activation of G-protein-gated inwardly rectifying K+ (GIRK) channels by the novel anxiolytic drug, ML297.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Dual regulation of G proteins and the G-protein-activated K+ channels by lithium.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Molecular mechanism underlying ethanol activation of G-protein-gated inwardly rectifying potassium channels.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- A computational model predicts that Gβγ acts at a cleft between channel subunits to activate GIRK1 channels.Science signaling · 2013Article
- Article
- Slack, Slick and Sodium-Activated Potassium Channels.ISRN neuroscience · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Muscarinic potassium channels (KACh) are composed of two subunits, GIRK1 and GIRK4 (or CIR), and are directly gated by G proteins. We have identified a novel gating mechanism of KACh, independent of G-protein activation. This mechanism involved functional modification of KACh which required hydrolysis of physiological levels of intracellular ATP and was manifested by an increase in the channel mean open time. The ATP-modified channels could in turn be gated by intracellular Na+, starting at approximately 3 mM with an EC50 of approximately 40 mM. The Na(+)-gating of KACh was operative both in native atrial cells and in a heterologous system expressing recombinant channel subunits. Block of the Na+/K+ pump (e.g., by cardiac glycosides) caused significant activation of KACh in atrial cells, with a time course similar to that of Na+ accumulation and in a manner indistinguishable from that of Na(+)-mediated activation of the channel, suggesting that cardiac glycosides activated KACh by increasing intracellular Na+ levels. These results demonstrate for the first time a direct effect of cardiac glycosides on atrial myocytes involving ion channels which are critical in the regulation of cardiac rhythm.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.