title: [Molecular mechanism of the K+ATP channel in pancreatic beta-cells].
abstract: The ATP-sensitive K+ (K+ATP) channel plays a key role in secretion of insulin in response to glucose-stimulation in pancreatic beta-cells. Inhibition of the channel does not require hydrolysis of ATP and results from a direct binding of ATP4- to the channel. MgADP relieves the channel inhibition by ATP by decreasing affinity of the channel to ATP. We suggest two-sites model regarding channel modulations by these nucleotides; one is the ATP-inhibition site which is bound by ATP4-, and the other the modulation site, which is bound by MgADP and thereby decreases the sensitivity of the channel to ATP. Sulphonylureas-binding sites may be different from these nucleotide-binding sites described above.
authors.affiliation: 1st Department of Internal Medicine, Faculty of Medicine, Kagoshima University.
authors.forename: M
authors.initials: M
authors.lastname: Kakei
authors.forename: N
authors.initials: N
authors.lastname: Koriyama
authors.forename: M
authors.initials: M
authors.lastname: Nakazaki
authors.forename: K
authors.initials: K
authors.lastname: Yaekura
authors.forename: H
authors.initials: H
authors.lastname: Tanaka
mesh_terms: D000255:Adenosine Triphosphate / Q000502:physiology; D000818:Animals; D001665:Binding Sites; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D015221:Potassium Channels / Q000378:metabolism / Q000502:physiology*
chemical_list: D007328:Insulin; D015221:Potassium Channels; D000255:Adenosine Triphosphate