Truncation of Kir6.2 produces ATP-sensitive K+ channels in the absence of the sulphonylurea receptor

被引：662

作者：

Tucker, SJ ^{[1
]}

Gribble, FM ^{[1
]}

Zhao, C ^{[1
]}

Trapp, S ^{[1
]}

Ashcroft, FM ^{[1
]}

机构：

[1] UNIV OXFORD,PHYSIOL LAB,OXFORD OX1 3PT,ENGLAND

来源：

NATURE | 1997年 / 387卷 / 6629期

基金：

英国惠康基金;

关键词：

D O I：

10.1038/387179a0

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

ATP-sensitive potassium channels (K-ATP channels) couple cell metabolism to electrical activity and are important in the physiology and pathophysiology of many tissues(1). In pancreatic beta-cells, K-ATP channels Link changes in blood glucose concentration to insulin secretion(2). They are also the target for clinically important drugs such as sulphonylureas, which stimulate secretion, and the K+ channel opener diazoxide, which inhibits insulin release(3,4). Metabolic regulation of K-ATP channels is mediated by changes in intracellular ATP and Mg-ADP levels, which inhibit and activate the channel, respectively(2). The beta-cell K-ATP channel is a complex of two proteins(5,6): an inward-rectifier K+ channel subunit, Kir6.2, and the sulphonylurea receptor, SUR1. We show here that the primary site at which ATP acts to mediate K-ATP channel inhibition is located on Kir6.2, and that SUR1 is required for sensitivity to sulphonylureas and diazoxide and for activation by Mg-ADP.

引用

页码：179 / 183

页数：5