{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T00:14:33Z","timestamp":1791159273191,"version":"4.1.0"},"reference-count":62,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,11,16]],"date-time":"2004-11-16T00:00:00Z","timestamp":1100563200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Carcinogenesis"],"published-print":{"date-parts":[[2005,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The ubiquitin\u2010proteasome pathway is fundamental to synchronized continuation of many cellular processes, for example, cell\u2010cycle progression, stress response, and cell differentiation. Recent studies have shown that the ubiquitin\u2010proteasome pathway functions in the regulation of nucleotide excision repair (NER) in yeast. In order to investigate the role of the ubiquitin\u2010proteasome pathway in the NER of mammalian cells, global genomic repair (GGR), and transcription\u2010coupled repair (TCR) were examined in a mouse ts20 cell line that harbors a temperature\u2010sensitive ubiquitin\u2010activating enzyme (E1). We found that E1 inactivation\u2010induced ubiquitination deficiency decreased both GGR and TCR, indicating that the ubiquitination system is involved in the optimization of entire NER machinery in mammalian cells. We specifically inhibited the function of 19S proteasome subunit by overexpressing 19S regulatory complex hSug1 or its mutant protein hSug1mk in repair competent human fibroblast, OSU\u20102, cells and compared their capacity for NER. The results showed that 19S regulatory complex positively modulates NER in cells. In addition, we treated OSU\u20102 cells with the inhibitors of 20S subunit function, MG132 and lactacystin, and demonstrated that the catalytic activity of 20S subunit is also required for efficient NER. Moreover, the UV\u2010induced recruitment of repair factor xeroderma pigmentosum protein C (XPC) to damage sites was negatively affected by treatment of repair competent cells with MG132. Taken together, we conclude that the ubiquitin\u2010proteasome pathway has a positive regulatory role for optimal NER capacity in mammalian cells and appears to act through facilitating the recruitment of repair factors to DNA damage sites. \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/mc.20065","type":"journal-article","created":{"date-parts":[[2004,11,17]],"date-time":"2004-11-17T07:17:15Z","timestamp":1100675835000},"page":"53-64","source":"Crossref","is-referenced-by-count":41,"title":["Cellular ubiquitination and proteasomal functions positively modulate mammalian nucleotide excision repair"],"prefix":"10.1002","volume":"42","author":[{"given":"Qi\u2010En","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manzoor 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