{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T04:25:13Z","timestamp":1792211113281,"version":"4.4.0"},"reference-count":48,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2022,12,15]],"date-time":"2022-12-15T00:00:00Z","timestamp":1671062400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2022,12,15]],"date-time":"2022-12-15T00:00:00Z","timestamp":1671062400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2023,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    SIGIRR (single immunoglobulin IL\u20101 related receptor), PKP3 (plakophilin 3), and TMEM16J (anoctamin 9), a putative calcium\u2010activated ion channel and phospholipid scramblase, control the immune response and the extent of inflammation. Variants of SIGIRR\/PKP3\/TMEM16J lead to severe inflammatory diseases such as pneumonia, enterocolitis, and kidney graft rejection. Meta\u2010analysis of genome\u2010wide association studies identified TMEM16J\u2010T604A as a promotor for chronic kidney disease (CKD), but the disease mechanism and function of TMEM16J remain unknown. Here, we demonstrate TMEM16J as a calcium\u2010activated calcium\u2010permeable channel, which is expressed in the endoplasmic reticulum (ER). TMEM16J controls the intracellular distribution of calcium, and inhibits intracellular receptor\u2010mediated Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signals and Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010dependent activation of ion channels, but augments transcription and release of pro\u2010inflammatory cytokines. Renal epithelial cells expressing the variant TMEM16J\u2010T604A show enhanced calcium signals when compared to cells expressing wt\u2010TMEM16J, and demonstrate spontaneous transcription and release of cytokines. This study identifies TMEM16J as an important regulator of intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signals, ion channel activity, and cytokine release. TMEM16J may therefore affect immune response in renal tissue and immune cells.\n                  <\/jats:p>","DOI":"10.1096\/fj.202200968r","type":"journal-article","created":{"date-parts":[[2022,12,15]],"date-time":"2022-12-15T09:59:59Z","timestamp":1671098399000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["A\n                    <scp>TMEM16J<\/scp>\n                    variant leads to dysregulated cytosolic calcium which may lead to renal disease"],"prefix":"10.1096","volume":"37","author":[{"given":"Rainer","family":"Schreiber","sequence":"first","affiliation":[{"name":"Institut f\u00fcr Physiologie Universit\u00e4t Regensburg  Regensburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Khaoula","family":"Talbi","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Physiologie Universit\u00e4t Regensburg  Regensburg 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