期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 587, 期 13, 页码 3071-3079出版社
WILEY
DOI: 10.1113/jphysiol.2009.171876
关键词
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资金
- Swiss National Science Foundation (SNF) [3200BO-114597]
- Fondation Suisse de Recherche sur les maladies musculaires
- Association Francaise contre les Myopathies
- Telethon Italy
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.
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