Regulation of cardiac inwardly rectifying potassium channels by membrane lipid metabolism

被引：28
|
作者：
Takano, M [1 ]
Kuratomi, S [1 ]
机构：
[1] Kyoto Univ, Grad Sch Med, Dept Physiol & Biophys, Kyoto, Japan
来源：
PROGRESS IN BIOPHYSICS & MOLECULAR BIOLOGY | 2003年 / 81卷 / 01期
关键词：
cardiac myocyte; inward rectifier potassium channel; PIP2;
D O I：
10.1016/S0079-6107(02)00048-2
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Types and distributions of inwardly rectifying potassium (Kir) channels are one of the major determinants of the electrophysiological properties of cardiac myocytes. Kir2.1 (classical inward rectifier K+ channel), Kir6.2/SUR2A (ATP-sensitive K+ channel) and Kir3.1/3.4 (muscarinic K+ channels) in cardiac myocytes are commonly upregulated by a membrane lipid, phosphatidylinositol 4,5-bisphosphates (PIP2). PIP2 interaction sites appear to be conserved by positively charged amino acid residues and the putative alpha-helix in the C-terminals of Kir channels. PIP2 level in the plasma membrane is regulated by the agonist stimulation. Kir channels in the cardiac myocytes seem to be actively regulated by means of the change in PIP2 level rather than by downstream signal transduction pathways. (C) 2003 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码：67 / 79
页数：13
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