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The charge translocation associated with sarcoplasmic reticulum (SR) Ca2+ efflux is compensated for by a simultaneous SR K+ influx. This influx is essential because, with no countercurrent, the SR membrane potential (Vm) would quickly (<1 ms) reach the Ca2+ equilibrium potential and SR Ca2+ release would cease. The SR K+ trimeric intracellular cation (TRIC) channel has been proposed to carry the...
Sarcoplasmic reticulum (SR) Ca2+ release in striated muscle is mediated by a multiprotein complex that includes the ryanodine receptor (RyR) Ca2+ channel and the intra-SR Ca2+ buffering protein calsequestrin (CSQ). Besides its buffering role, CSQ is thought to regulate RyR channel function. Here, CSQ-dependent luminal Ca2+ regulation of skeletal (RyR1) and cardiac (RyR2) channels is explored. Skeletal...
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