{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T10:55:02Z","timestamp":1790852102047,"version":"4.1.0"},"reference-count":33,"publisher":"National Academy of Sciences","issue":"29","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2013,7,16]]},"abstract":"<jats:p>\n                    Excitation\u2013contraction (EC) coupling comprises events in muscle that convert electrical signals to Ca\n                    <jats:sup>2+<\/jats:sup>\n                    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\n                    <jats:sup>2+<\/jats:sup>\n                    release from the sarcoplasmic reticulum (SR). Consequently, homozygous deletion of src homology 3 and cysteine rich domain 3 (\n                    <jats:italic>Stac3<\/jats:italic>\n                    ) 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\n                    <jats:sup>2+<\/jats:sup>\n                    release from the SR of cultured myotubes from\n                    <jats:italic>Stac3<\/jats:italic>\n                    mutant mice could be restored by application of 4-chloro-\n                    <jats:italic>m<\/jats:italic>\n                    -cresol, a ryanodine receptor agonist, indicating that the sarcomeres, SR Ca\n                    <jats:sup>2+<\/jats:sup>\n                    store, and ryanodine receptors are functional in\n                    <jats:italic>Stac3<\/jats:italic>\n                    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.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1310571110","type":"journal-article","created":{"date-parts":[[2013,7,2]],"date-time":"2013-07-02T00:42:22Z","timestamp":1372725742000},"page":"11881-11886","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":142,"title":["Skeletal muscle-specific T-tubule protein STAC3 mediates voltage-induced Ca\n                    <sup>2+<\/sup>\n                    release and contractility"],"prefix":"10.1073","volume":"110","author":[{"given":"Benjamin R.","family":"Nelson","sequence":"first","affiliation":[{"name":"Departments of aMolecular Biology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fenfen","family":"Wu","sequence":"additional","affiliation":[{"name":"Neurology and 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