Life after the birth of the mitochondrial Na^+/Ca^(2+) exchanger,NCLX

作     者：NITA Lulia I. HERSHFINKEL Michal SEKLER Israel 

作者机构：Department of Physiology and Cell BiologyFaculty of Health SciencesBen-Gurion University of the Negev 

出 版 物：《Science China(Life Sciences)》 (中国科学（生命科学英文版）)

年 卷 期：2015年第58卷第1期

页      面：59-65页

核心收录：

学科分类：0710[理学-生物学] 07[理学] 071009[理学-细胞生物学] 09[农学] 0901[农学-作物学] 090102[农学-作物遗传育种] 

主　　题：NCLX MCU mitochondrial Ca^2+ signaling Na^+/Ca^2+ exchanger Na+ signaling 

摘      要：Powered by the mitochondrial membrane potential,Ca2+ permeates the mitochondria via a Ca2+ channel termed Ca2+ uniporter and is pumped out by a Na+/Ca2+ exchanger,both of which are located on the inner mitochondrial *** Ca2+ transients are critical for metabolic activity and regulating global Ca2+ *** the other hand,failure to control mitochondrial Ca2+ is a hallmark of ischemic and neurodegenerative *** their importance,identifying the uniporter and exchanger remains elusive and their inhibitors are *** review will focus on the mitochondrial exchanger,initially describing how it was molecularly identified and linked to a novel member of the Na+/Ca2+ exchanger superfamily termed *** control of NCLX expression provides a selective tool to determine its physiological role in a variety of cell *** lymphocytes,NCLX is essential for refilling the endoplasmic reticulum Ca2+ stores required for antigen-dependent *** of NCLX with the store-operated channel in astroglia controls Ca2+ influx and thereby neuro-transmitter release and cell *** refilling of the Ca2+ stores in the sarcoplasmic reticulum,which is controlled by NCLX,determines the frequency of action potential and Ca2+ transients in *** is emerging as a hub for integrating glucose-dependent Na+ and Ca2+ signaling in pancreatic β cells,and the specific molecular control of NCLX expression resolved the controversy regarding its role in neurons and β *** studies on an NCLX knockdown mouse model and identification of human NCLX mutations are expected to determine the role of mitochondrial Ca2+ efflux in organ activity and whether NCLX inactivation is linked to ischemic and/or neurodegenerative ***-function analysis and protein analysis will identify the NCLX mode of regulation and its partners in the inner membrane of the mitochondria.