ArticleThe Journal of general physiology2002
Open state destabilization by ATP occupancy is mechanism speeding burst exit underlying KATP channel inhibition by ATP.
Article in The Journal of general physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- A fluorescent probe for the enzymatic activity of KbioRxiv : the preprint server for biology · 2025Article
- Molecular structure of an open human KProceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Genetic and Molecular Mechanisms of Congenital Hyperinsulinism.Frontiers in endocrinology · 2019Review
- Role of the C-terminus of SUR in the differential regulation of β-cell and cardiac KThe Journal of physiology · 2018Article
- Cryo-electron microscopy structures and progress toward a dynamic understanding of KThe Journal of general physiology · 2018Review
- Hyperinsulinemic Hypoglycemia - The Molecular Mechanisms.Frontiers in endocrinology · 2016Review
- Molecular action of sulphonylureas on KATP channels: a real partnership between drugs and nucleotides.Biochemical Society transactions · 2015Review
- A Conserved Residue Cluster That Governs Kinetics of ATP-dependent Gating of Kir6.2 Potassium Channels.The Journal of biological chemistry · 2015Article
- 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
- Measuring and evaluating the role of ATP-sensitive K+ channels in cardiac muscle.Journal of molecular and cellular cardiology · 2012Review
- Mechanisms underlying stage-1 TRPL channel translocation in Drosophila photoreceptors.PloS one · 2012Article
- Activation of the K(ATP) channel by Mg-nucleotide interaction with SUR1.The Journal of general physiology · 2010Article
- Voltage-dependent gating in a "voltage sensor-less" ion channel.PLoS biology · 2010Article
- DEND mutation in Kir6.2 (KCNJ11) reveals a flexible N-terminal region critical for ATP-sensing of the KATP channel.Biophysical journal · 2008Article
- How ATP inhibits the open K(ATP) channel.The Journal of general physiology · 2008Article
- Ligand-dependent linkage of the ATP site to inhibition gate closure in the KATP channel.The Journal of general physiology · 2005Article
- 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
- The pore helix is involved in stabilizing the open state of inwardly rectifying K+ channels.Biophysical journal · 2003Article
- Molecular basis for Kir6.2 channel inhibition by adenine nucleotides.Biophysical journal · 2003Article
Corrections and comments
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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
The ATP-sensitive potassium (K(ATP)) channel is named after its characteristic inhibition by intracellular ATP. The inhibition is a centerpiece of how the K(ATP) channel sets electrical signaling to the energy state of the cell. In the beta cell of the endocrine pancreas, for example, ATP inhibition results from high blood glucose levels and turns on electrical activity leading to insulin release. The underlying gating mechanism (ATP inhibition gating) includes ATP stabilization of closed states, but the action of ATP on the open state of the channel is disputed. The original models of ATP inhibition gating proposed that ATP directly binds the open state, whereas recent models indicate a prerequisite transition from the open to a closed state before ATP binds and inhibits activity. We tested these two classes of models by using kinetic analysis of single-channel currents from the cloned mouse pancreatic K(ATP) channel expressed in Xenopus oocytes. In particular, we combined gating models based on fundamental rate law and burst gating kinetic considerations. The results demonstrate open-state ATP dependence as the major mechanism by which ATP speeds exit from the active burst state underlying inhibition of the K(ATP) channel by ATP.
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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.