Bridging the myoplasmic gap II: more recent advances in skeletal muscle excitation-contraction coupling

被引：27

作者：

Bannister, Roger A. ^{[1
]}

机构：

[1] Univ Colorado, Dept Med, Div Cardiol, Denver Anschutz Med Campus,12700 East 19th Ave,Ro, Aurora, CO 80045 USA

来源：

JOURNAL OF EXPERIMENTAL BIOLOGY | 2016年 / 219卷 / 02期

关键词：

1,4-dihydropyridine receptor; DHPR; Ca(V)1.1; alpha S-1; L-type; Excitation-contraction coupling; Skeletal muscle; RECEPTOR BETA-1A SUBUNIT; CALCIUM-RELEASE CHANNEL; C-TERMINAL TAIL; DIHYDROPYRIDINE-RECEPTOR; CA2+ CHANNEL; RYANODINE RECEPTORS; BETA(1A) SUBUNIT; CRYSTAL-STRUCTURES; CHARGE MOVEMENT; CARBOXYL-TERMINUS;

D O I：

10.1242/jeb.124123

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

In skeletal muscle, excitation-contraction (EC) coupling relies on the transmission of an intermolecular signal from the voltage-sensing regions of the L-type Ca2+ channel (Ca(V)1.1) in the plasma membrane to the channel pore of the type 1 ryanodine receptor (RyR1) nearly 10 nm away in the membrane of the sarcoplasmic reticulum (SR). Even though the roles of Ca(V)1.1 and RyR1 as voltage sensor and SR Ca2+ release channel, respectively, have been established for nearly 25 years, the mechanism underlying communication between these two channels remains undefined. In the course of this article, I will review current viewpoints on this topic with particular emphasis on recent studies.

引用

页码：175 / 182

页数：8

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