{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T15:00:57Z","timestamp":1791644457000,"version":"4.3.4"},"reference-count":38,"publisher":"National Academy of Sciences","issue":"26","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2009,6,30]]},"abstract":"<jats:p>\n                    The xeroderma pigmentosum complementation group E (XP-E) gene product damaged-DNA binding protein 2 (DDB2) plays important roles in nucleotide excision repair (NER). Previously, we showed that DDB2 participates in NER by regulating the level of p21\n                    <jats:sup>Waf1\/Cip1<\/jats:sup>\n                    . Here we show that the p21\n                    <jats:sup>Waf1\/Cip1<\/jats:sup>\n                    -regulatory function of DDB2 plays a central role in defining the response (apoptosis or arrest) to DNA damage. The DDB2-deficient cells are resistant to apoptosis in response to a variety of DNA-damaging agents, despite activation of p53 and the pro-apoptotic genes. Instead, these cells undergo cell cycle arrest. Also, the DDB2-deficient cells are resistant to E2F1-induced apoptosis. The resistance to apoptosis of the DDB2-deficient cells is caused by an increased accumulation of p21\n                    <jats:sup>Waf1\/Cip1<\/jats:sup>\n                    after DNA damage. We provide evidence that DDB2 targets p21\n                    <jats:sup>Waf1\/Cip1<\/jats:sup>\n                    for proteolysis. The resistance to apoptosis in DDB2-deficient cells also involves Mdm2 in a manner that is distinct from the p53-regulatory activity of Mdm2. Our results provide evidence for a new regulatory loop involving the NER protein DDB2, Mdm2, and p21\n                    <jats:sup>Waf1\/Cip1<\/jats:sup>\n                    that is critical in deciding cell fate (apoptosis or arrest) upon DNA damage.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0812254106","type":"journal-article","created":{"date-parts":[[2009,6,16]],"date-time":"2009-06-16T21:50:13Z","timestamp":1245189013000},"page":"10690-10695","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":87,"title":["DDB2 decides cell fate following DNA damage"],"prefix":"10.1073","volume":"106","author":[{"given":"Tanya","family":"Stoyanova","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Genetics (M\/C 669), Cancer Center, University of Illinois at Chicago, 900 South Ashland Avenue, Chicago, IL 60607; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nilotpal","family":"Roy","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Genetics (M\/C 669), Cancer Center, University of Illinois at Chicago, 900 South Ashland Avenue, Chicago, IL 60607; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dragana","family":"Kopanja","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Genetics (M\/C 669), Cancer Center, University of Illinois at Chicago, 900 South Ashland Avenue, Chicago, IL 60607; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Srilata","family":"Bagchi","sequence":"additional","affiliation":[{"name":"Center of Molecular Biology of Oral Diseases (M\/C 860), College of Dentistry, Cancer Center, University of Illinois at Chicago, 801 South Paulina Avenue, Chicago, IL 60612"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pradip","family":"Raychaudhuri","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Genetics (M\/C 669), Cancer Center, University of Illinois at Chicago, 900 South Ashland Avenue, Chicago, IL 60607; and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2009,6,30]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M000960200"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.40.24317"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0306551101"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1208211"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-05-2295"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0511160103"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2006.03.035"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2005.02.035"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M511834200"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/30.11.2588"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.00880-07"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.10.7.2119"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.270.37.22008"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(93)90500-P"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.22.10.3247-3254.2002"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkg152"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(03)00180-1"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.00086-06"},{"key":"e_1_3_3_19_2","first-page":"679","article-title":"p21WAF1\/CIP1 antisense therapy radiosensitizes human colon cancer by converting growth arrest to apoptosis","volume":"60","author":"Tian H","year":"2000","unstructured":"H Tian, EK Wittmack, TJ Jorgensen, p21WAF1\/CIP1 antisense therapy radiosensitizes human colon cancer by converting growth arrest to apoptosis. 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