{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,6]],"date-time":"2026-05-06T20:50:33Z","timestamp":1778100633079,"version":"3.51.4"},"reference-count":83,"publisher":"Portland Press Ltd.","issue":"03","license":[{"start":{"date-parts":[[2025,6,3]],"date-time":"2025-06-03T00:00:00Z","timestamp":1748908800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,6,30]]},"abstract":"<jats:p>A rise in cytosolic Ca2+ is used as a key signalling messenger in eukaryotic cells. The Ca2+ signal drives life and death and controls myriad responses in between. Inherent in the use of such a multifarious signal is the danger of disease, arising from dysregulated Ca2+ signalling. One ancient, highly conserved and widespread Ca2+ entry pathway is the store-operated Ca2+ release-activated Ca2+ (CRAC) channel. Mutations in STIM1 and ORAI1, the genes that encode the functional channel, are tightly linked to a CRAC channelopathy in humans, which encompasses severe combined immune deficiency, myopathy and anhidrotic ectodermal dysplasia. Moreover, sustained Ca2+ entry through the channels leads to a range of systemic disorders, including acute pancreatitis, asthma and inflammatory bowel disease. In this review, we describe how aberrant CRAC channel activity causes a range of diseases, highlighting commonalities between these diverse pathologies.<\/jats:p>","DOI":"10.1042\/bst20253062","type":"journal-article","created":{"date-parts":[[2025,6,3]],"date-time":"2025-06-03T14:41:39Z","timestamp":1748961699000},"page":"627-642","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["CRAC channels and patho-physiology of peripheral organ systems"],"prefix":"10.1042","volume":"53","author":[{"given":"Rajesh","family":"Bhardwaj","sequence":"first","affiliation":[{"name":"Molecular & Cellular Biology Laboratory, National Institute of Environmental Health Sciences, National Institute of Health, Durham, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4860-1644","authenticated-orcid":false,"given":"Anant B.","family":"Parekh","sequence":"additional","affiliation":[{"name":"Molecular & Cellular Biology Laboratory, National Institute of Environmental Health Sciences, National Institute of Health, Durham, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"288","published-online":{"date-parts":[[2025,6,3]]},"reference":[{"key":"2025070702412384800_BST-2025-3062C1","doi-asserted-by":"crossref","first-page":"1047","DOI":"10.1016\/j.cell.2007.11.028","article-title":"Calcium signaling","volume":"131","author":"Clapham","year":"2007","journal-title":"Cell"},{"key":"2025070702412384800_BST-2025-3062C2","doi-asserted-by":"crossref","first-page":"78","DOI":"10.1016\/j.tibs.2010.07.013","article-title":"Decoding cytosolic Ca2+ oscillations","volume":"36","author":"Parekh","year":"2011","journal-title":"Trends Biochem. 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