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http://purl.uniprot.org/citations/23818578http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23818578http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23818578http://www.w3.org/2000/01/rdf-schema#comment"Excitation-contraction (EC) coupling comprises events in muscle that convert electrical signals to Ca(2+) transients, which then trigger contraction of the sarcomere. Defects in these processes cause a spectrum of muscle diseases. We report that STAC3, a skeletal muscle-specific protein that localizes to T tubules, is essential for coupling membrane depolarization to Ca(2+) release from the sarcoplasmic reticulum (SR). Consequently, homozygous deletion of src homology 3 and cysteine rich domain 3 (Stac3) in mice results in complete paralysis and perinatal lethality with a range of musculoskeletal defects that reflect a blockade of EC coupling. Muscle contractility and Ca(2+) release from the SR of cultured myotubes from Stac3 mutant mice could be restored by application of 4-chloro-m-cresol, a ryanodine receptor agonist, indicating that the sarcomeres, SR Ca(2+) store, and ryanodine receptors are functional in Stac3 mutant skeletal muscle. These findings reveal a previously uncharacterized, but required, component of the EC coupling machinery of skeletal muscle and introduce a candidate for consideration in myopathic disorders."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.org/dc/terms/identifier"doi:10.1073/pnas.1310571110"xsd:string
http://purl.uniprot.org/citations/23818578http://purl.org/dc/terms/identifier"doi:10.1073/pnas.1310571110"xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Liu Y."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Liu Y."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Lin W."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Lin W."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Wu F."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Wu F."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Bassel-Duby R."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Bassel-Duby R."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Olson E.N."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Olson E.N."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Anderson D.M."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Anderson D.M."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Cannon S.C."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Cannon S.C."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Nelson B.R."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"Nelson B.R."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"McAnally J."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/author"McAnally J."xsd:string
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23818578http://purl.uniprot.org/core/date"2013"xsd:gYear