Associated Papers
LRRC8 channel complexes counterbalance KATP channels to mediate swell-secretion coupling in mouse pancreatic β cells.
Abd El-Aziz TM et al.
Jci Insight, 2025
Personalized Therapeutics for KATP-Dependent Pathologies.
Nichols CG
Annual Review of Pharmacology and Toxicology, 2023
Blocking Kir6.2 channels with SpTx1 potentiates glucose-stimulated insulin secretion from murine pancreatic β cells and lowers blood glucose in diabetic mice.
Ramu Y et al.
Elife, 2022
Cognitive deficits and impaired hippocampal long-term potentiation in KATP-induced DEND syndrome.
Yahil S et al.
Proceedings of the National Academy of Sciences of the United States of America, 2021
Continuous spectrum of glucose dysmetabolism due to the KCNJ11 gene mutation-Case reports and review of the literature.
He B et al.
Journal of Diabetes, 2021
Molecular Genetics, Clinical Characteristics, and Treatment Outcomes of KATP-Channel Neonatal Diabetes Mellitus in Vietnam National Children's Hospital.
Ngoc CTB et al.
Frontiers in Endocrinology, 2021
Neonatal diabetes due to potassium channel mutation: Response to sulfonylurea according to the genotype.
Garcin L et al.
Pediatric Diabetes, 2020
New insights into KATP channel gene mutations and neonatal diabetes mellitus.
Pipatpolkai T et al.
Nature Reviews. Endocrinology, 2020
Beta-cell excitability and excitability-driven diabetes in adult Zebrafish islets.
Emfinger CH et al.
Physiological Reports, 2019
Contribution of systemic inflammation to permanence of KATP-induced neonatal diabetes in mice.
Emfinger CH et al.
American Journal of Physiology. Endocrinology and Metabolism, 2018
ATP-Sensitive Potassium Channels and Their Physiological and Pathophysiological Roles.
Tinker A et al.
Comprehensive Physiology, 2018
New Understanding of β-Cell Heterogeneity and In Situ Islet Function.
Benninger RKP et al.
Diabetes, 2018
Decreases in Gap Junction Coupling Recovers Ca2+ and Insulin Secretion in Neonatal Diabetes Mellitus, Dependent on Beta Cell Heterogeneity and Noise.
Notary AM et al.
Plos Computational Biology, 2016
Neonatal diabetes caused by a homozygous KCNJ11 mutation demonstrates that tiny changes in ATP sensitivity markedly affect diabetes risk.
Vedovato N et al.
Diabetologia, 2016
Decreasing cx36 gap junction coupling compensates for overactive KATP channels to restore insulin secretion and prevent hyperglycemia in a mouse model of neonatal diabetes.
Nguyen LM et al.
Diabetes, 2014
Mouse Models of β-cell KATP Channel Dysfunction.
Brereton MF et al.
Drug Discovery Today. Disease Models, 2013
Cardiac specific ATP-sensitive K+ channel (KATP) overexpression results in embryonic lethality.
Toib A et al.
Journal of Molecular and Cellular Cardiology, 2012
Mice expressing a human K(ATP) channel mutation have altered channel ATP sensitivity but no cardiac abnormalities.
Clark R et al.
Diabetologia, 2012
Promoter DNA methylation regulates murine SUR1 (Abcc8) and SUR2 (Abcc9) expression in HL-1 cardiomyocytes.
Fatima N et al.
Plos One, 2012
Acute sulfonylurea therapy at disease onset can cause permanent remission of KATP-induced diabetes.
Remedi MS et al.
Diabetes, 2011
Defects in beta cell Ca²+ signalling, glucose metabolism and insulin secretion in a murine model of K(ATP) channel-induced neonatal diabetes mellitus.
Benninger RK et al.
Diabetologia, 2011
Central venous hypoxemia is a determinant of human atrial ATP-sensitive potassium channel expression: evidence for a novel hypoxia-inducible factor 1alpha-Forkhead box class O signaling pathway.
Raeis V et al.
Hypertension (dallas, Tex. : 1979), 2010
The first clinical case of a mutation at residue K185 of Kir6.2 (KCNJ11): a major ATP-binding residue.
Shimomura K et al.
Diabetic Medicine : a Journal of the British Diabetic Association, 2010
Cardiac sarcolemmal K(ATP) channels: Latest twists in a questing tale!
Zhang H et al.
Journal of Molecular and Cellular Cardiology, 2010
ATP-sensitive potassium channels in health and disease.
Clark R et al.
Advances in Experimental Medicine and Biology, 2010
Secondary consequences of beta cell inexcitability: identification and prevention in a murine model of K(ATP)-induced neonatal diabetes mellitus.
Remedi MS et al.
Cell Metabolism, 2009
Glucose sensing by POMC neurons regulates glucose homeostasis and is impaired in obesity.
Parton LE et al.
Nature, 2007
Transgenic overexpression of SUR1 in the heart suppresses sarcolemmal K(ATP).
Flagg TP et al.
Journal of Molecular and Cellular Cardiology, 2005
Regulation of the ATP-sensitive K channel Kir6.2 by ATP and PIP(2).
Ribalet B et al.
Journal of Molecular and Cellular Cardiology, 2005
Activation of adenosine triphosphate-sensitive potassium channels by acyl coenzyme A esters involves multiple phosphatidylinositol 4,5-bisphosphate-interacting residues.
Manning Fox JE et al.
Molecular Endocrinology (baltimore, Md.), 2004
Sur domains that associate with and gate KATP pores define a novel gatekeeper.
Babenko AP et al.
The Journal of Biological Chemistry, 2003
Molecular mechanism for ATP-dependent closure of the K+ channel Kir6.2.
John SA et al.
The Journal of Physiology, 2003
Pyridine nucleotide regulation of the KATP channel Kir6.2/SUR1 expressed in Xenopus oocytes.
Dabrowski M et al.
The Journal of Physiology, 2003
Identification of residues contributing to the ATP binding site of Kir6.2.
Trapp S et al.
The Embo Journal, 2003
Physiological and pathophysiological roles of ATP-sensitive K+ channels.
Seino S et al.
Progress in Biophysics and Molecular Biology, 2003
Molecular basis for Kir6.2 channel inhibition by adenine nucleotides.
Ribalet B et al.
Biophysical Journal, 2003
Multiple sites of interaction between the intracellular domains of an inwardly rectifying potassium channel, Kir6.2.
Jones PA et al.
Febs Letters, 2001
Structural determinants of PIP(2) regulation of inward rectifier K(ATP) channels.
Shyng SL et al.
The Journal of General Physiology, 2000
Targeted overactivity of beta cell K(ATP) channels induces profound neonatal diabetes.
Koster JC et al.
Cell, 2000
Mapping of the physical interaction between the intracellular domains of an inwardly rectifying potassium channel, Kir6.2.
Tucker SJ et al.
The Journal of Biological Chemistry, 1999
The role of lysine 185 in the kir6.2 subunit of the ATP-sensitive channel in channel inhibition by ATP.
Reimann F et al.
The Journal of Physiology, 1999
Sulfonylurea and K(+)-channel opener sensitivity of K(ATP) channels. Functional coupling of Kir6.2 and SUR1 subunits.
Koster JC et al.
The Journal of General Physiology, 1999
ATP inhibition of KATP channels: control of nucleotide sensitivity by the N-terminal domain of the Kir6.2 subunit.
Koster JC et al.
The Journal of Physiology, 1999
Involvement of the N-terminus of Kir6.2 in the inhibition of the KATP channel by ATP.
Proks P et al.
The Journal of Physiology, 1999
Cytoplasmic terminus domains of Kir6.x confer different nucleotide-dependent gating on the ATP-sensitive K+ channel.
Takano M et al.
The Journal of Physiology, 1998
Molecular determinants of KATP channel inhibition by ATP.
Tucker SJ et al.
The Embo Journal, 1998
Phentolamine block of KATP channels is mediated by Kir6.2.
Proks P et al.
Proceedings of the National Academy of Sciences of the United States of America, 1997
Truncation of Kir6.2 produces ATP-sensitive K+ channels in the absence of the sulphonylurea receptor.
Tucker SJ et al.
Nature, 1997