PMID:19095005

Citation	Yamazaki, D, Yamazaki, T and Takeshima, H (2009) New molecular components supporting ryanodine receptor-mediated Ca(2+) release: roles of junctophilin and TRIC channel in embryonic cardiomyocytes. Pharmacol. Ther. 121:265-72
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.
Links	PubMed Online version:10.1016/j.pharmthera.2008.11.004
Keywords	Animals; Calcium/metabolism; Cell Membrane/metabolism; Embryo, Mammalian/cytology; Endoplasmic Reticulum/metabolism; Ion Channels/metabolism; Membrane Proteins/metabolism; Mice; Mice, Knockout; Myocytes, Cardiac/metabolism; Ryanodine Receptor Calcium Release Channel/genetics; Ryanodine Receptor Calcium Release Channel/physiology; Sarcoplasmic Reticulum/metabolism
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