ArticleThe EMBO journal1997
The essential role of the Walker A motifs of SUR1 in K-ATP channel activation by Mg-ADP and diazoxide.
Article in The EMBO journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.
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Who cites it
136 citing papers in PubMed, 345 citations in OpenAlex.
- Modulation of pain by ketones: a mini-review.American journal of physiology. Cell physiology · 2025Review
- Residue 39 of Kir6.2 drives a difference in ATP sensitivity in human and canine beta-cell KFrontiers in physiology · 2025Article
- Genotype-histotype-phenotype correlations in hyperinsulinemic hypoglycemia.Histology and histopathology · 2024Review
- Antipsychotics impair regulation of glucose metabolism by central glucose.Molecular psychiatry · 2022Article
- Production and purification of ATP-sensitive potassium channel particles for cryo-electron microscopy.Methods in enzymology · 2021Article
- The Ion Channel and GPCR Toolkit of Brain Capillary Pericytes.Frontiers in cellular neuroscience · 2020Review
- Activation mechanism of ATP-sensitive KeLife · 2019Article
- Role of the C-terminus of SUR in the differential regulation of β-cell and cardiac KThe Journal of physiology · 2018Article
- Expression, purification, and electrophysiological characterization of a recombinant, fluorescent Kir6.2 in mammalian cells.Protein expression and purification · 2018Article
- Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men.Physiological reviews · 2018Review
- Article
- KInternal medicine (Tokyo, Japan) · 2017Review
- AnJournal of clinical research in pediatric endocrinology · 2017Article
- Control of Kir channel gating by cytoplasmic domain interface interactions.The Journal of general physiology · 2017Article
- Glucose elicits cephalic-phase insulin release in mice by activating KAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Running out of time: the decline of channel activity and nucleotide activation in adenosine triphosphate-sensitive K-channels.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Review
- KATP Channels in the Cardiovascular System.Physiological reviews · 2016Review
- Hyperinsulinemic Hypoglycemia - The Molecular Mechanisms.Frontiers in endocrinology · 2016Review
- Sensitivity of KATP channels to cellular metabolic disorders and the underlying structural basis.Acta pharmacologica Sinica · 2016Article
- The Nucleotide-Binding Sites of SUR1: A Mechanistic Model.Biophysical journal · 2015Review
76 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The ATP-sensitive K-channel (K-ATP channel) plays a key role in insulin secretion from pancreatic beta-cells. It is closed by glucose metabolism, which stimulates insulin secretion, and opened by the drug diazoxide, which inhibits insulin release. Metabolic regulation is mediated by changes in ATP and Mg-ADP, which inhibit and potentiate channel activity, respectively. The beta-cell K-ATP channel consists of a pore-forming subunit, Kir6.2, and a regulatory subunit, SUR1. We have mutated (independently or together) two lysine residues in the Walker A (W(A)) motifs of the first (K719A) and second (K1384M) nucleotide-binding domains (NBDs) of SUR1. These mutations are expected to inhibit nucleotide hydrolysis. Our results indicate that the W(A) lysine of NBD1 (but not NBD2) is essential for activation of K-ATP currents by diazoxide. The potentiatory effects of Mg-ADP required the presence of the W(A) lysines in both NBDs. Mutant currents were slightly more sensitive to ATP than wild-type currents. Metabolic inhibition led to activation of wild-type and K1384M currents, but not K719A or K719A/K1384M currents, suggesting that there may be a factor in addition to ATP and ADP which regulates K-ATP channel activity.
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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.