Bridging the myoplasmic gap II: more recent advances in skeletal muscle excitation–contraction coupling | Zendy

Roger A. Bannister | Zendy

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

Author(s) -

Roger A. Bannister

Publication year - 2016

Publication title -

journal of experimental biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.367

H-Index - 185

eISSN - 1477-9145

pISSN - 0022-0949

DOI - 10.1242/jeb.124123

Subject(s) - ryr1 , excitation–contraction coupling , ryanodine receptor , endoplasmic reticulum , skeletal muscle , biophysics , coupling (piping) , chemistry , muscle contraction , bridging (networking) , materials science , biology , anatomy , computer science , biochemistry , metallurgy , computer network

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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