Abstract
Defective ER/SR-cytosol Ca2+ cycling is associated with increased ER stress, pathological heart conditions and muscular defects. Within the SR, ryanodine receptor 2 (RyR2) is required for excitation/contraction coupling. Ca2+ release from the SR is counterbalanced by K+ influx through trimeric intracellular cation (TRIC) channels to maintain ER/SR polarity. New functions of TRIC channels have been discovered.
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