[Molecular mechanism of the K+ATP channel in pancreatic beta-cells].
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.
Kakei
M
M
1st Department of Internal Medicine, Faculty of Medicine, Kagoshima University.
Koriyama
N
N
Nakazaki
M
M
Yaekura
K
K
Tanaka
H
H
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*
D007328:Insulin; D015221:Potassium Channels; D000255:Adenosine Triphosphate