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.

中文翻译：

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使SOCE陷入变化的振荡中

ER / SR-胞质溶胶Ca ²⁺循环缺陷与ER应激，病理性心脏病和肌肉缺陷增加有关。在SR中，激发/收缩偶联需要使用ryanodine受体2（RyR2）。从SR释放的Ca ²⁺被通过三聚体细胞内阳离子（TRIC）通道的K ⁺流入抵消，以维持ER / SR极性。已经发现了TRIC频道的新功能。