{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360004231237339264.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1007/s00424-012-1197-5"}},{"identifier":{"@type":"URI","@value":"http://link.springer.com/content/pdf/10.1007/s00424-012-1197-5.pdf"}},{"identifier":{"@type":"URI","@value":"http://link.springer.com/article/10.1007/s00424-012-1197-5/fulltext.html"}},{"identifier":{"@type":"URI","@value":"http://link.springer.com/content/pdf/10.1007/s00424-012-1197-5"}},{"identifier":{"@type":"PMID","@value":"23242030"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"TRIC channels supporting efficient Ca2+ release from intracellular stores"}],"description":[{"notation":[{"@value":"Trimeric intracellular cation-selective (TRIC) channel subtypes, namely TRIC-A and TRIC-B, are derived from distinct genes and distributed throughout the sarco/endoplasmic reticulum (SR/ER) and nuclear membranes. TRIC-A is preferentially expressed at high levels in excitable tissues, while TRIC-B is ubiquitously detected at relatively low levels in various tissues. TRIC channels are composed of ~300 amino acid residues and contain three putative membrane-spanning segments to form a bullet-shaped homo-trimeric assembly. Both native and purified recombinant TRIC subtypes form functional monovalent cation-selective channels in a lipid bilayer reconstitution system. The electrophysiological data indicate that TRIC channels behave as K(+) channels under intracellular conditions, although the detailed channel characteristics remain to be investigated. The pathophysiological defects detected in knockout mice suggest that TRIC channels support SR/ER Ca(2+) release mediated by ryanodine (RyR) and inositol trisphosphate receptor (IP(3)R) channels. For example, Tric-a-knockout mice develop hypertension resulting from vascular hypertonicity, and the mutant vascular smooth muscle cells exhibit insufficient RyR-mediated Ca(2+) release for inducing hyperpolarization. Tric-b-knockout mice show respiratory failure at birth, and IP(3)R-mediated Ca(2+) release essential for surfactant handling is impaired in the mutant alveolar epithelial cells. Moreover, double-knockout mice lacking both TRIC subtypes show embryonic heart failure, and SR Ca(2+) handling is deranged in the mutant cardiomyocytes. Current evidence strongly suggests that TRIC channels mediate counter-K(+) movements, in part, to facilitate physiological Ca(2+) release from intracellular stores."}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380004231237339532","@type":"Researcher","foaf:name":[{"@value":"Elisa Venturi"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004231237339533","@type":"Researcher","foaf:name":[{"@value":"Rebecca 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