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Review
, 121 (3), 265-72

New Molecular Components Supporting Ryanodine Receptor-Mediated Ca(2+) Release: Roles of Junctophilin and TRIC Channel in Embryonic Cardiomyocytes

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Review

New Molecular Components Supporting Ryanodine Receptor-Mediated Ca(2+) Release: Roles of Junctophilin and TRIC Channel in Embryonic Cardiomyocytes

Daiju Yamazaki et al. Pharmacol Ther.

Abstract

Ca(2+) mobilization from intracellular stores is mediated by Ca(2+) release channels, designated ryanodine and IP(3) receptors, and directly regulates important cellular reactions including muscle contraction, endo/exocrine secretion, and neural excitability. In order to function as an intracellular store, the endo/sarcoplasmic reticulum is equipped with cooperative Ca(2+) uptake, storage and release machineries, comprising synergic collaborations among integral-membrane, cytoplasmic and luminal proteins. Our recent studies have demonstrated that junctophilins form junctional membrane complexes between the plasma membrane and the endo/sarcoplasmic reticulum in excitable cells, and that TRIC (trimeric intracellular cation) channels act as novel monovalent cation-specific channels on intracellular membrane systems. Knockout mice have provided evidence that both junctophilins and TRIC channels support efficient ryanodine receptor-mediated Ca(2+) release in muscle cells. This review focuses on cardiac Ca(2+) release by discussing pathological defects of mutant cardiomyocytes lacking ryanodine receptors, junctophilins, or TRIC channels.

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