期刊
CARDIOVASCULAR RESEARCH
卷 73, 期 4, 页码 641-647出版社
OXFORD UNIV PRESS
DOI: 10.1016/j.cardiores.2006.10.019
关键词
ion channel; calcium; calmodulin; CaMKII; calcium channel; sodium channel; potassium channel; KCNQ1; subunit assembly
资金
- NHLBI NIH HHS [R01 HL071165] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL071165] Funding Source: NIH RePORTER
Because changes in intracellular Ca2+ concentration are the final signals of electrical activity in excitable cells, many mechanisms have evolved to regulate Ca2+ influx. Among the most important are those pathways that directly regulate the ion channels responsible for regulating and generating the Ca2+ influx signal. Recent work has demonstrated that the Ca2+ binding protein calmodulin (CaM) and the Ca2+/CaM-sensitive kinase CaMKII are important modulators of cardiac ion channels. Thus, Ca2+ participates in feedback modulation to control electrical activity. This review highlights various mechanisms by which CaM and CaMKII regulate cardiovascular ion channel activity and presents a novel model for CaMKII regulation of Ca(V)1.2 Ca2+ channel function. (c) 2006 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.
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