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This article reviews current viewpoints and recent advances regarding the mechanism underlying communication between Ca(V)1.1 and RyR1 in skeletal muscle excitation-contraction coupling.
This review summarizes current viewpoints on the mechanism underlying communication between Ca(V)1.1 and RyR1 in skeletal muscle excitation-contraction coupling.
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Synthesizes current Ca(V)1.1-RyR1 views in skeletal ECC; leaves open precise mechanisms for targeted experiments.
In skeletal muscle, excitation-contraction (EC) coupling relies on the transmission of an intermolecular signal from the voltage-sensing regions of the L-type Ca(2+) 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 Ca(2+) 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.
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Roger A. Bannister (2016) conducted a review in Skeletal muscle excitation-contraction coupling. This article reviews current viewpoints and recent advances regarding the mechanism underlying communication between Ca(V)1.1 and RyR1 in skeletal muscle excitation-contraction coupling.
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