First Author | Yamazaki D | Year | 2009 |
Journal | Pharmacol Ther | Volume | 121 |
Issue | 3 | Pages | 265-72 |
PubMed ID | 19095005 | Mgi Jnum | J:146924 |
Mgi Id | MGI:3838924 | Doi | 10.1016/j.pharmthera.2008.11.004 |
Citation | Yamazaki D, et al. (2009) New molecular components supporting ryanodine receptor-mediated Ca(2+) release: Roles of junctophilin and TRIC channel in embryonic cardiomyocytes. Pharmacol Ther 121(3):265-72 |
abstractText | 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. |