Abstract
In skeletal muscle excitation-contraction coupling, depolarization of transverse tubule membrane causes conformational change in dihydropyridine receptor (DHPR), which in turn opens type 1 ryanodine receptor (RyR1) to release Ca2+ from sarcoplasmic reticulum. This 'depolarization-induced Ca2+ release' (DICR) occurs through physical interaction between DHPR and RyR1 and requires additional components (β1a, Stac3, junctophilin-2). However, it remains so far unclear about molecular mechanism of DICR, especially conformational change in RyR1.
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