{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T04:18:29Z","timestamp":1791087509016,"version":"4.1.0"},"reference-count":49,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2003,6,1]],"date-time":"2003-06-01T00:00:00Z","timestamp":1054425600000},"content-version":"vor","delay-in-days":1095,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2000,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    A wide range of DNA lesions, both UV and chemically induced, are dealt with by the nucleotide excision repair (NER) pathway. Defects in NER result in human syndromes such as xeroderma pigmen\u2010tosum (XP), where there is a 1000\u2010fold increased incidence of skin cancer. The ERCC1 protein is essential for NER, but ERCC1 knockout mice are not a model for XP. In the absence of exogenous DNA\u2010damaging agents, these mice are runted and die before weaning, with dramatically accelerated liver polyploidy and elevated levels of p53. Here we present a morphological, immunological, and molecular study to understand the mechanism for the unusual liver pathology in ERCC1\u2010deficient mice. We show that the enlarged ERCC1\u2010deficient hepatocytes are arrested in G\n                    <jats:sub>2<\/jats:sub>\n                    and that DNA replication and the normal process of binucleation are both reduced. This is associated with a p53\u2010independent increase in expression of the cyclin\u2010dependent kinase inhibitor p21. The most dramatic feature of the ERCC1\u2010deficient liver phenotype, the accelerated polyploidy, is not rescued by p53 deficiency, but we show that p53 is responsible for the reduced DNA replication and binucleation. We consider that the liver phenotype is a response to unrepaired endogenous DNA damage, which may reflect an additional non\u2010NER\u2010related function for the ERCC1 protein.\u2014N\u00fa\u00f1ez, F., Chipchase, M. D., Clarke, A. R., Melton, D. W. Nucleotide excision repair gene (ERCC1) deficiency causes G\n                    <jats:sub>2<\/jats:sub>\n                    arrest in hepatocytes and a reduction in liver binucleation: the role of p53 and p21.\n                    <jats:italic>FASEB J.<\/jats:italic>\n                    14, 1073\u20131082 (2000)\n                  <\/jats:p>","DOI":"10.1096\/fasebj.14.9.1073","type":"journal-article","created":{"date-parts":[[2018,1,18]],"date-time":"2018-01-18T07:59:22Z","timestamp":1516262362000},"page":"1073-1082","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":51,"title":["Nucleotide excision repair gene (ERCC1) deficiency causes G\n                    <sub>2<\/sub>\n                    arrest in hepatocytes and a reduction in liver binucleation: the role of p53 and p21"],"prefix":"10.1096","volume":"14","author":[{"given":"Fatima","family":"N\u00fa\u00f1ez","sequence":"first","affiliation":[{"name":"Institute of Cell and Molecular Biology Edinburgh University King's Buildings  Edinburgh Scotland UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael D.","family":"Chipchase","sequence":"additional","affiliation":[{"name":"Institute of Cell and Molecular Biology Edinburgh University King's Buildings  Edinburgh Scotland UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alan R.","family":"Clarke","sequence":"additional","affiliation":[{"name":"Department of Pathology Edinburgh University  Teviot Place Edinburgh Scotland UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David W.","family":"Melton","sequence":"additional","affiliation":[{"name":"Institute of Cell and Molecular Biology Edinburgh University King's Buildings  Edinburgh Scotland UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2003,6]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.65.070196.001031"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.38.23465"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/310425a0"},{"key":"e_1_2_5_5_1","first-page":"123","article-title":"Transfection of the cloned human excision repair gene ERCC\u20101 to UV\u2010sensitive CHO mutants only corrects the repair defect in complementation group\u20102 mutants","volume":"193","author":"Duin M.","year":"1988","journal-title":"Mutat. Res."},{"key":"e_1_2_5_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/0921-8777(89)90059-1"},{"key":"e_1_2_5_7_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.39.22657"},{"key":"e_1_2_5_8_1","volume-title":"DNA Repair and Mutagenesis","author":"Friedberg E. C.","year":"1995"},{"key":"e_1_2_5_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(86)90014-0"},{"key":"e_1_2_5_10_1","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/20.23.6347"},{"key":"e_1_2_5_11_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.24.13122"},{"key":"e_1_2_5_12_1","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.111.3.395"},{"key":"e_1_2_5_13_1","first-page":"U7","article-title":"p21 in differentiation. DNA\u2010repair, tumor progression, and senescence","volume":"4","author":"Fisher P. B.","year":"1996","journal-title":"Mol. Cell. 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P.","year":"1994","journal-title":"Oncogene"},{"key":"e_1_2_5_49_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.7863329"},{"key":"e_1_2_5_50_1","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.19.3.2366"}],"container-title":["The FASEB Journal"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1096\/fasebj.14.9.1073","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/full-xml\/10.1096\/fasebj.14.9.1073","content-type":"application\/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/faseb.onlinelibrary.wiley.com\/doi\/pdf\/10.1096\/fasebj.14.9.1073","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T22:32:19Z","timestamp":1761690739000},"score":1,"resource":{"primary":{"URL":"https:\/\/faseb.onlinelibrary.wiley.com\/doi\/10.1096\/fasebj.14.9.1073"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2000,6]]},"references-count":49,"journal-issue":{"issue":"9","published-print":{"date-parts":[[2000,6]]}},"alternative-id":["10.1096\/fasebj.14.9.1073"],"URL":"https:\/\/doi.org\/10.1096\/fasebj.14.9.1073","archive":["Portico"],"relation":{},"ISSN":["0892-6638","1530-6860"],"issn-type":[{"value":"0892-6638","type":"print"},{"value":"1530-6860","type":"electronic"}],"subject":[],"published":{"date-parts":[[2000,6]]},"assertion":[{"value":"2000-01-06","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2000-01-06","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2003-06-01","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}