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S100A1 and calmodulin regulation of ryanodine receptor in striated muscle

期刊

CELL CALCIUM
卷 50, 期 4, 页码 323-331

出版社

ELSEVIER SCI LTD
DOI: 10.1016/j.ceca.2011.06.001

关键词

Skeletal muscle; Cardiac muscle; Excitation-contraction coupling; Dihydropyridine receptors; Voltage-sensors; Transverse tubule; Ryanodine receptor; Sarcoplasmic reticulum; Calcium release; Ca2+-induced Ca2+ release; S100A1; Calmodulin; RyR modulation; Muscular contraction

资金

  1. NIH [R01AR055099]

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The release of Ca2+ ions from the sarcoplasmic reticulum through ryanodine receptor calcium release channels represents the critical step linking electrical excitation to muscular contraction in the heart and skeletal muscle (excitation-contraction coupling). Two small Ca2+ binding proteins, S100A1 and calmodulin, have been demonstrated to bind and regulate ryanodine receptor in vitro. This review focuses on recent work that has revealed new information about the endogenous roles of S100A1 and calmodulin in regulating skeletal muscle excitation-contraction coupling. S100A1 and calmodulin bind to an overlapping domain on the ryanodine receptor type 1 to tune the Ca2+ release process, and thereby regulate skeletal muscle function. We also discuss past, current and future work surrounding the regulation of ryanodine receptors by calmodulin and S100A1 in both cardiac and skeletal muscle, and the implications for excitation-contraction coupling. (C) 2011 Elsevier Ltd. All rights reserved.

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