{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T19:43:53Z","timestamp":1792266233948,"version":"4.4.0"},"reference-count":79,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"43","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Adv."],"published-print":{"date-parts":[[2024,10,25]]},"abstract":"<jats:p>\n            Cells that lack p53 signaling frequently occur in ulcerative colitis (UC) and are considered early drivers in UC-associated colorectal cancer (CRC). Epithelial injury during colitis is associated with transient stem cell reprogramming from the adult, homeostatic to a \u201cfetal-like\u201d regenerative state. Here, we use murine and organoid-based models to study the role of\n            <jats:italic>Trp53<\/jats:italic>\n            during epithelial reprogramming. We find that p53 signaling is silent and dispensable during homeostasis but strongly up-regulated in the epithelium upon DSS-induced colitis. While in WT cells this causes termination of the regenerative state, crypts that lack\n            <jats:italic>Trp53<\/jats:italic>\n            remain locked in the highly proliferative, regenerative state long-term. The regenerative state in WT cells requires high Wnt signaling to maintain elevated levels of glycolysis. Instead,\n            <jats:italic>Trp53<\/jats:italic>\n            deficiency enables Wnt-independent glycolysis due to overexpression of rate-limiting enzyme PKM2. Our study reveals the context-dependent relevance of p53 signaling specifically in the injury-induced regenerative state, explaining the high abundance of clones lacking p53 signaling in UC and UC-associated CRC.\n          <\/jats:p>","DOI":"10.1126\/sciadv.adp8783","type":"journal-article","created":{"date-parts":[[2024,10,25]],"date-time":"2024-10-25T17:58:39Z","timestamp":1729879119000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":18,"title":["p53 terminates the regenerative fetal-like state after colitis-associated injury"],"prefix":"10.1126","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2965-0512","authenticated-orcid":true,"given":"Kimberly","family":"Hartl","sequence":"first","affiliation":[{"name":"Medical Department, Division of Gastroenterology and Hepatology, Campus Virchow-Klinikum, Charit\u00e9-Universit\u00e4tsmedizin Berlin, Corporate Member of Freie Universit\u00e4t Berlin and Humboldt-Universit\u00e4t zu Berlin, Berlin, Germany."},{"name":"Berlin Institute for Medical Systems Biology (BIMSB), Max Delbr\u00fcck Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-5245-5473","authenticated-orcid":true,"given":"\u015eafak","family":"Bayram","sequence":"additional","affiliation":[{"name":"Medical Department, Division of Gastroenterology and Hepatology, Campus Virchow-Klinikum, Charit\u00e9-Universit\u00e4tsmedizin Berlin, Corporate Member of Freie Universit\u00e4t Berlin and Humboldt-Universit\u00e4t zu Berlin, Berlin, Germany."},{"name":"Berlin Institute for Medical Systems Biology (BIMSB), Max Delbr\u00fcck Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexandra","family":"Wetzel","sequence":"additional","affiliation":[{"name":"Medical 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