{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T00:48:56Z","timestamp":1792802936653,"version":"4.5.0"},"reference-count":75,"publisher":"Life Science Alliance, LLC","issue":"9","license":[{"start":{"date-parts":[[2020,7,10]],"date-time":"2020-07-10T00:00:00Z","timestamp":1594339200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["DK59599 and DK117654"],"award-info":[{"award-number":["DK59599 and DK117654"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Presbyterian Health Foundation, University of Oklahoma Health Sciences Center","id":[{"id":"https:\/\/ror.org\/0457zbj98","id-type":"ROR","asserted-by":"crossref"}]}],"content-domain":{"domain":["life-science-alliance.org"],"crossmark-restriction":true},"short-container-title":["Life Sci. Alliance"],"published-print":{"date-parts":[[2020,9]]},"abstract":"<jats:p>\n                    The primary cilium is a microtubule-based, antenna-like organelle housing several signaling pathways. It follows a cyclic pattern of assembly and deciliation (disassembly and\/or shedding), as cells exit and re-enter the cell cycle, respectively. In general, primary cilia loss leads to kidney cystogenesis. However, in animal models of autosomal dominant polycystic kidney disease, a major disease caused by mutations in the\n                    <jats:italic>polycystin<\/jats:italic>\n                    genes (\n                    <jats:italic>Pkd1<\/jats:italic>\n                    or\n                    <jats:italic>Pkd2<\/jats:italic>\n                    ), primary cilia ablation or acceleration of deciliation suppresses cystic growth, whereas deceleration of deciliation enhances cystogenesis. Here, we show that deciliation is delayed in the cystic epithelium of a mouse model of postnatal deletion of\n                    <jats:italic>Pkd1<\/jats:italic>\n                    and in\n                    <jats:italic>Pkd1<\/jats:italic>\n                    - or\n                    <jats:italic>Pkd2<\/jats:italic>\n                    -null cells in culture. Mechanistic experiments show that PKD1 depletion activates the centrosomal integrity\/mitotic surveillance pathway involving 53BP1, USP28, and p53 leading to a delay in deciliation. Reduced deciliation rate causes prolonged activation of cilia-based signaling pathways that could promote cystic growth. Our study links polycystins to cilia dynamics, identifies cellular deciliation downstream of the centrosomal integrity pathway, and helps explain pro-cystic effects of primary cilia in autosomal dominant polycystic kidney disease.\n                  <\/jats:p>","DOI":"10.26508\/lsa.202000750","type":"journal-article","created":{"date-parts":[[2020,7,10]],"date-time":"2020-07-10T14:55:17Z","timestamp":1594392917000},"page":"e202000750","update-policy":"https:\/\/doi.org\/10.26508\/lsa.crossmarkpolicy","source":"Crossref","is-referenced-by-count":21,"title":["Loss of polycystins suppresses deciliation via the activation of the centrosomal integrity pathway"],"prefix":"10.26508","volume":"3","author":[{"given":"Vasileios","family":"Gerakopoulos","sequence":"first","affiliation":[{"name":"Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 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