ArticleThe Biochemical journal1990
The beta-cell glibenclamide receptor is an ADP-binding protein.
Article in The Biochemical journal, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 45 citations in OpenAlex.
- Interaction of sulphonylurea derivatives with vascular ATP-sensitive potassium channels in humans.Diabetologia · 1996Trial
- 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
- Sulphonylurea action revisited: the post-cloning era.Diabetologia · 2003Review
- Characterization of the sensitivity of cardiac outwardly-rectifying K+ channels to class III antiarrhythmics: the influence of inhibitory sulfonamide derivatives.Naunyn-Schmiedeberg's archives of pharmacology · 1995Article
- Distinct modes of blockade in cardiac ATP-sensitive K+ channels suggest multiple targets for inhibitory drug molecules.The Journal of membrane biology · 1994Article
- Continuous versus intermittent sulphonylurea therapy in non-insulin-dependent diabetes mellitus.Drug safety · 1993Review
- Ion channels.Diabetologia · 1992Review
- Adenine nucleotide-induced inhibition of binding of sulphonylureas to their receptor in pancreatic islets.British journal of pharmacology · 1992Article
- Characterization of the solubilized glibenclamide receptor in a hamster pancreatic beta-cell line, HIT T15.The Biochemical journal · 1991Article
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 effects of ADP on [3H]glibenclamide binding to membranes and whole cells, the activity of the ATP-sensitive K+ channel (K-ATP channel), intracellular Ca2+ concentration and insulin secretion were studied in a hamster pancreatic beta-cell line, HIT T15. ADP dose-dependently inhibited [3H]glibenclamide binding to membranes and to whole cells in a competitive manner. ADP-agarose also inhibited the binding to whole cells. The activity of the K-ATP channel was assayed by measuring 86Rb efflux from whole cells. ADP inhibited the 86Rb efflux elicited either by diazoxide or by ATP depletion. In the presence, but not in the absence, of extracellular Ca2+, ADP evoked a rapid and sustained increase in intracellular Ca2+ concentration as estimated with the fluorescent dye quin 2. Insulin release from HIT cells was also increased by 0.5-2 mM-ADP in the presence of 0.5 mM-glucose. These effects of ADP on glibenclamide binding, K-ATP channel activity and insulin release were specific for ADP, and were not reproduced by any other nucleotide so far tested. The present findings strongly suggest that ADP and sulphonylureas have common binding sites on the extracellular side of beta-cell plasma membranes, where they inhibit the activity of the K-ATP channel, resulting in an increase in intracellular Ca2+ concentration and insulin release.
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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.