ArticleProceedings of the National Academy of Sciences of the United States of America1999
Cooperative binding of ATP and MgADP in the sulfonylurea receptor is modulated by glibenclamide.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 153 citations in OpenAlex.
- Structure and mechanism of a mycobacterial isoniazid efflux pump MsRv1273c/72c with a degenerate nucleotide-binding site.Nature communications · 2025Article
- Expression of SUR1 isoforms in the brain and heart after ischemia/reperfusion.Frontiers in molecular neuroscience · 2025Article
- Dynamic duo: Kir6 and SUR in KChannels (Austin, Tex.) · 2024Review
- Prognostic value ofFrontiers in genetics · 2022Article
- The role of the degenerate nucleotide binding site in type I ABC exporters.FEBS letters · 2020Review
- Nucleotide inhibition of the pancreatic ATP-sensitive K+ channel explored with patch-clamp fluorometry.eLife · 2020Article
- Activation mechanism of ATP-sensitive KeLife · 2019Article
- Computational Identification of Novel Kir6 Channel Inhibitors.Frontiers in pharmacology · 2019Article
- Ligand binding and conformational changes of SUR1 subunit in pancreatic ATP-sensitive potassium channels.Protein & cell · 2018Article
- Cryo-electron microscopy structures and progress toward a dynamic understanding of KThe Journal of general physiology · 2018Review
- Cantu syndrome-associated SUR2 (ABCC9) mutations in distinct structural domains result in KThe Journal of biological chemistry · 2018Article
- Ameliorative potential of conditioning on ischemia-reperfusion injury in diabetes.Conditioning medicine · 2018Article
- ATP sensitive potassium channel openers: A new class of ocular hypotensive agents.Experimental eye research · 2017Review
- 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
- Phosphorylation-dependent changes in nucleotide binding, conformation, and dynamics of the first nucleotide binding domain (NBD1) of the sulfonylurea receptor 2B (SUR2B).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
- Nonequilibrium gating of CFTR on an equilibrium theme.Physiology (Bethesda, Md.) · 2012Review
- Mechanism of KATP hyperactivity and sulfonylurea tolerance due to a diabetogenic mutation in L0 helix of sulfonylurea receptor 1 (ABCC8).FEBS letters · 2011Article
- Syntaxin-1A interacts with distinct domains within nucleotide-binding folds of sulfonylurea receptor 1 to inhibit beta-cell ATP-sensitive potassium channels.The Journal of biological chemistry · 2011Article
- K(ATP) channels process nucleotide signals in muscle thermogenic response.Critical reviews in biochemistry and molecular biology · 2010Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ATP-sensitive potassium (KATP) channels in pancreatic beta cells are critical in the regulation of glucose-induced insulin secretion. Although electrophysiological studies provide clues to the complex control of KATP channels by ATP, MgADP, and pharmacological agents, the molecular mechanism of KATP-channel regulation remains unclear. The KATP channel is a heterooligomeric complex of SUR1 subunits of the ATP-binding-cassette superfamily with two nucleotide-binding folds (NBF1 and NBF2) and the pore-forming Kir6.2 subunits. Here, we report that MgATP and MgADP, but not the Mg salt of gamma-thio-ATP, stabilize the binding of prebound 8-azido-[alpha-32P]ATP to SUR1. Mutation in the Walker A and B motifs of NBF2 of SUR1 abolished this stabilizing effect of MgADP. These results suggest that SUR1 binds 8-azido-ATP strongly at NBF1 and that MgADP, either by direct binding to NBF2 or by hydrolysis of bound MgATP at NBF2, stabilizes prebound 8-azido-ATP binding at NBF1. The sulfonylurea glibenclamide caused release of prebound 8-azido-[alpha-32P]ATP from SUR1 in the presence of MgADP or MgATP in a concentration-dependent manner. This direct biochemical evidence of cooperative interaction in nucleotide binding of the two NBFs of SUR1 suggests that glibenclamide both blocks this cooperative binding of ATP and MgADP and, in cooperation with the MgADP bound at NBF2, causes ATP to be released from NBF1.
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