Calmodulin and CaMKII as molecular switches for cardiac ion channels.

Published

Journal Article (Review)

Because changes in intracellular Ca(2+) concentration are the final signals of electrical activity in excitable cells, many mechanisms have evolved to regulate Ca(2+) influx. Among the most important are those pathways that directly regulate the ion channels responsible for regulating and generating the Ca(2+) influx signal. Recent work has demonstrated that the Ca(2+) binding protein calmodulin (CaM) and the Ca(2+)/CaM-sensitive kinase CaMKII are important modulators of cardiac ion channels. Thus, Ca(2+) 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 Ca(2+) channel function.

Full Text

Duke Authors

Cited Authors

  • Pitt, GS

Published Date

  • March 1, 2007

Published In

Volume / Issue

  • 73 / 4

Start / End Page

  • 641 - 647

PubMed ID

  • 17137569

Pubmed Central ID

  • 17137569

International Standard Serial Number (ISSN)

  • 0008-6363

Digital Object Identifier (DOI)

  • 10.1016/j.cardiores.2006.10.019

Language

  • eng

Conference Location

  • England