Kakei M, Koriyama N, Nakazaki M, Yaekura K, Tanaka H
1st Department of Internal Medicine, Faculty of Medicine, Kagoshima University.
Nihon Rinsho. 1994 Oct;52(10):2587-92.
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.
ATP敏感性钾通道（K⁺ATP通道）在胰腺β细胞中响应葡萄糖刺激分泌胰岛素的过程中起关键作用。该通道的抑制并不需要ATP水解，而是由ATP⁴⁻直接与通道结合所致。MgADP通过降低通道对ATP的亲和力来解除ATP对通道的抑制作用。我们提出了关于这些核苷酸对通道调节的双位点模型；一个是被ATP⁴⁻结合的ATP抑制位点，另一个是被MgADP结合从而降低通道对ATP敏感性的调节位点。磺脲类药物结合位点可能与上述核苷酸结合位点不同。
