ArticleThe Journal of general physiology1998
Ligand-insensitive state of cardiac ATP-sensitive K+ channels. Basis for channel opening.
Article in The Journal of general physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 72 citations in OpenAlex.
- Inward and outward currents of native and cloned K(ATP) channels (Kir6.2/SUR1) share single-channel kinetic properties.Biochemistry and biophysics reports · 2022Article
- Uridine treatment prevents myocardial injury in rat models of acute ischemia and ischemia/reperfusion by activating the mitochondrial ATP-dependent potassium channel.Scientific reports · 2021Article
- Control of Kir channel gating by cytoplasmic domain interface interactions.The Journal of general physiology · 2017Article
- KATP Channels in the Cardiovascular System.Physiological reviews · 2016Review
- Sulfonylureas suppress the stimulatory action of Mg-nucleotides on Kir6.2/SUR1 but not Kir6.2/SUR2A KATP channels: a mechanistic study.The Journal of general physiology · 2014Article
- Activation of the K(ATP) channel by Mg-nucleotide interaction with SUR1.The Journal of general physiology · 2010Article
- Cholesterol regulates glucose-stimulated insulin secretion through phosphatidylinositol 4,5-bisphosphate.The Journal of biological chemistry · 2009Article
- Modulation of K(ATP) currents in rat ventricular myocytes by hypoxia and a redox reaction.Acta pharmacologica Sinica · 2009Article
- How ATP inhibits the open K(ATP) channel.The Journal of general physiology · 2008Article
- Role for SUR2A ED domain in allosteric coupling within the K(ATP) channel complex.The Journal of general physiology · 2008Article
- A mutation in the ATP-binding site of the Kir6.2 subunit of the KATP channel alters coupling with the SUR2A subunit.The Journal of physiology · 2007Article
- ATP-sensitive K+ channels: regulation of bursting by the sulphonylurea receptor, PIP2 and regions of Kir6.2.The Journal of physiology · 2006Article
- Ligand-dependent linkage of the ATP site to inhibition gate closure in the KATP channel.The Journal of general physiology · 2005Article
- ATP-sensitive K+ channel channel/enzyme multimer: metabolic gating in the heart.Journal of molecular and cellular cardiology · 2005Review
- Concerted gating mechanism underlying KATP channel inhibition by ATP.Biophysical journal · 2004Article
- Gating mechanism of KATP channels: function fits form.The Journal of general physiology · 2003Review
- Cellular remodeling in heart failure disrupts K(ATP) channel-dependent stress tolerance.The EMBO journal · 2003Article
- Analysis of the differential modulation of sulphonylurea block of beta-cell and cardiac ATP-sensitive K+ (K(ATP)) channels by Mg-nucleotides.The Journal of physiology · 2003Article
- Effect of metabolic inhibition on glimepiride block of native and cloned cardiac sarcolemmal K(ATP) channels.British journal of pharmacology · 2002Article
- Open state destabilization by ATP occupancy is mechanism speeding burst exit underlying KATP channel inhibition by ATP.The Journal of general physiology · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism by which ATP-sensitive K+ (KATP) channels open in the presence of inhibitory concentrations of ATP remains unknown. Herein, using a four-state kinetic model, we found that the nucleotide diphosphate UDP directed cardiac KATP channels to operate within intraburst transitions. These transitions are not targeted by ATP, nor the structurally unrelated sulfonylurea glyburide, which inhibit channel opening by acting on interburst transitions. Therefore, the channel remained insensitive to ATP and glyburide in the presence of UDP. "Rundown" of channel activity decreased the efficacy with which UDP could direct and maintain the channel to operate within intraburst transitions. Under this condition, the channel was sensitive to inhibition by ATP and glyburide despite the presence of UDP. This behavior of the KATP channel could be accounted for by an allosteric model of ligand-channel interaction. Thus, the response of cardiac KATP channels towards inhibitory ligands is determined by the relative lifetime the channel spends in a ligand-sensitive versus -insensitive state. Interconversion between these two conformational states represents a novel basis for KATP channel opening in the presence of inhibitory concentrations of ATP in a cardiac cell.
Indexed as
Identifiers
What OpenQuestion holds
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.