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CRAC channels are composed of ORAI1 proteins located in the plasma membrane, which form its ion\u2010conducting pore. ORAI1 channels are activated by stromal interaction molecule (STIM) 1 and STIM2 located in the endoplasmic reticulum. Loss\u2010 and gain\u2010of\u2010function gene mutations in\n                    <jats:italic>ORAI1<\/jats:italic>\n                    and\n                    <jats:italic>STIM1<\/jats:italic>\n                    in human patients cause distinct disease syndromes. CRAC channelopathy is caused by loss\u2010of\u2010function mutations in\n                    <jats:italic>ORAI1<\/jats:italic>\n                    and\n                    <jats:italic>STIM1<\/jats:italic>\n                    that abolish CRAC channel function and SOCE; it is characterized by severe combined immunodeficiency (SCID)\u2010like disease, autoimmunity, muscular hypotonia, and ectodermal dysplasia, with defects in sweat gland function and dental enamel formation. The latter defect emphasizes an important role of CRAC channels in tooth development. By contrast, autosomal dominant gain\u2010of\u2010function mutations in\n                    <jats:italic>ORAI1<\/jats:italic>\n                    and\n                    <jats:italic>STIM1<\/jats:italic>\n                    result in constitutive CRAC channel activation, SOCE, and increased intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    levels that are associated with an overlapping spectrum of diseases, including nonsyndromic tubular aggregate myopathy (TAM) and York platelet and Stormorken syndromes. The latter two syndromes are defined, besides myopathy, by thrombocytopenia, thrombopathy, and bleeding diathesis. The fact that myopathy results from both loss\u2010 and gain\u2010of\u2010function mutations in\n                    <jats:italic>ORAI1<\/jats:italic>\n                    and\n                    <jats:italic>STIM1<\/jats:italic>\n                    highlights the importance of CRAC channels for Ca\n                    <jats:sup>2+<\/jats:sup>\n                    homeostasis in skeletal muscle function. The cellular dysfunction and clinical disease spectrum observed in mutant patients provide important information about the molecular regulation of ORAI1 and STIM1 proteins and the role of CRAC channels in human physiology.\n                  <\/jats:p>","DOI":"10.1111\/nyas.12938","type":"journal-article","created":{"date-parts":[[2015,10,15]],"date-time":"2015-10-15T14:41:07Z","timestamp":1444920067000},"page":"45-79","source":"Crossref","is-referenced-by-count":461,"title":["Diseases caused by mutations in\n                    <i>ORAI1<\/i>\n                    and\n                    <i>STIM1<\/i>"],"prefix":"10.1111","volume":"1356","author":[{"given":"Rodrigo S.","family":"Lacruz","sequence":"first","affiliation":[{"name":"Department of Basic Science and Craniofacial Biology New York University College of Dentistry  New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan","family":"Feske","sequence":"additional","affiliation":[{"name":"Department 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