磷脂酰肌醇-4,5-二磷酸（PIP2）和磷脂酰肌醇-4-磷酸（PIP）作为三磷酸腺苷（ATP）抑制钾离子ATP通道的决定因素。

PIP2 and PIP as determinants for ATP inhibition of KATP channels.

作者信息

Baukrowitz T, Schulte U, Oliver D, Herlitze S, Krauter T, Tucker S J, Ruppersberg J P, Fakler B

机构信息

Department of Physiology II, University of Tübingen, Gmelinstrasse 5, 72076 Tübingen, Germany.

出版信息

Science. 1998 Nov 6;282(5391):1141-4. doi: 10.1126/science.282.5391.1141.

DOI:10.1126/science.282.5391.1141

PMID:9804555

Abstract

Adenosine triphosphate (ATP)-sensitive potassium (KATP) channels couple electrical activity to cellular metabolism through their inhibition by intracellular ATP. ATP inhibition of KATP channels varies among tissues and is affected by the metabolic and regulatory state of individual cells, suggesting involvement of endogenous factors. It is reported here that phosphatidylinositol-4, 5-bisphosphate (PIP2) and phosphatidylinositol-4-phosphate (PIP) controlled ATP inhibition of cloned KATP channels (Kir6.2 and SUR1). These phospholipids acted on the Kir6.2 subunit and shifted ATP sensitivity by several orders of magnitude. Receptor-mediated activation of phospholipase C resulted in inhibition of KATP-mediated currents. These results represent a mechanism for control of excitability through phospholipids.

摘要

三磷酸腺苷（ATP）敏感性钾（KATP）通道通过细胞内ATP对其的抑制作用，将电活动与细胞代谢联系起来。KATP通道的ATP抑制作用在不同组织中有所不同，并受单个细胞的代谢和调节状态影响，提示内源性因素的参与。本文报道，磷脂酰肌醇-4,5-二磷酸（PIP2）和磷脂酰肌醇-4-磷酸（PIP）可控制克隆的KATP通道（Kir6.2和SUR1）的ATP抑制作用。这些磷脂作用于Kir6.2亚基，并使ATP敏感性改变几个数量级。受体介导的磷脂酶C激活导致KATP介导的电流受到抑制。这些结果代表了一种通过磷脂控制兴奋性的机制。