BMB Rep. 2014; 47(2): 69-79  
Store-operated Ca2+ entry in muscle physiology and diseases
Zui Pan1,3,*, Marco Brotto4 & Jianjie Ma2,3,*
1Department of Internal Medicine-Cardiovascular Medicine, 2Department of Surgery, 3Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, 4Muscle Biology Research Group-MUBIG, Schools of Nursing & Medicine, University of Missouri-Kansas City, MO, USA
Correspondence to: Zui Pan, Tel: +1-614-292-2213; Fax: +1-614-247-7799; E-mail: Zui.Pan@osumc.edu, Jianjie Ma, Tel: +1-614-292-2636; Fax: +1-614-247-7799; E-mail: Jianjie.Ma@osumc.edu
Received: January 13, 2014; Published online: February 28, 2014.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

Abstract
Ca2+ release from intracellular stores and influx from extracellular reservoir regulate a wide range of physiological functions including muscle contraction and rhythmic heartbeat. One of the most ubiquitous pathways involved in controlled Ca2+ influx into cells is store-operated Ca2+ entry (SOCE), which is activated by the reduction of Ca2+ concentration in the lumen of endoplasmic or sarcoplasmic reticulum (ER/SR). Although SOCE is pronounced in non-excitable cells, accumulating evidences highlight its presence and important roles in skeletal muscle and heart. Recent discovery of STIM proteins as ER/SR Ca2+ sensors and Orai proteins as Ca2+ channel pore forming unit expedited the mechanistic understanding of this pathway. This review focuses on current advances of SOCE components, regulation and physiologic and pathophysiologic roles in muscles. The specific property and the dysfunction of this pathway in muscle diseases, and new directions for future research in this rapidly growing field are discussed.
Keywords: Aging, Junctophilin, Mitsugumin29, Muscular dystrophy, Muscle fatigue, Orai1, Sarcopenia, STIM1


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