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Minor sarcoplasmic reticulum membrane components that modulate excitation–contraction coupling in striated muscles

机译:小肌浆网膜组件,调节横纹肌中的激发 - 收缩耦合

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摘要

In striated muscle, activation of contraction is initiated by membrane depolarisation caused by an action potential, which triggers the release of Ca2+ stored in the sarcoplasmic reticulum by a process called excitation–contraction coupling. Excitation–contraction coupling occurs via a highly sophisticated supramolecular signalling complex at the junction between the sarcoplasmic reticulum and the transverse tubules. It is generally accepted that the core components of the excitation–contraction coupling machinery are the dihydropyridine receptors, ryanodine receptors and calsequestrin, which serve as voltage sensor, Ca2+ release channel, and Ca2+ storage protein, respectively. Nevertheless, a number of additional proteins have been shown to be essential both for the structural formation of the machinery involved in excitation–contraction coupling and for its fine tuning. In this review we discuss the functional role of minor sarcoplasmic reticulum protein components. The definition of their roles in excitation–contraction coupling is important in order to understand how mutations in genes involved in Ca2+ signalling cause neuromuscular disorders.
机译:在横纹肌中,收缩的激活是由动作电位引起的膜去极化引起的,该动作通过一种称为激发-收缩耦合的过程触发了储存在肌质网中的Ca2 +的释放。兴奋与收缩的耦合是通过高度复杂的超分子信号复合物在肌质网与横管之间的连接处发生的。人们普遍认为,激发-收缩耦合机制的核心成分是二氢吡啶受体,ryanodine受体和calsequestrin,它们分别用作电压传感器,Ca 2+释放通道和Ca 2+储存蛋白。然而,已经显示出许多其他蛋白质对于参与激发-收缩耦合的机械结构及其微调都是必不可少的。在这篇综述中,我们讨论了次要肌浆网蛋白成分的功能作用。为了了解Ca2 +信号传导基因中的突变如何引起神经肌肉疾病,定义它们在兴奋-收缩偶联中的作用非常重要。

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