{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T21:43:41Z","timestamp":1791236621806,"version":"4.1.0"},"reference-count":30,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2012,1,16]],"date-time":"2012-01-16T00:00:00Z","timestamp":1326672000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes to Cells"],"published-print":{"date-parts":[[2012,2]]},"abstract":"<jats:p>DNA polymerase \u03b7 (Pol\u03b7), whose gene mutation is responsible for the inherited disorder xeroderma pigmentosum variant (XP\u2010V), carries out accurate and efficient translesion synthesis (TLS) across cyclobutane pyrimidine dimer (CPD). As Pol\u03b7 interacts with REV1, and REV1 interacts with other TLS polymerases including Pol\u03b9, Pol\u03ba and Pol\u03b6, Pol\u03b7 may play a role in recruitment of these TLS polymerases at lesion site. But it is unclear whether UV sensitivity of XP\u2010V patients is caused not only by defect of Pol\u03b7 activity but also by dysfunction of network between Pol\u03b7 and other TLS polymerases. Here, we examined whether the TLS polymerase network via Pol\u03b7 is important for replicative bypass of CPDs and DNA damage tolerance induced by UV in mouse cells. We observed that UV sensitivity of Pol\u03b7\u2010deficient mouse cells was moderately rescued by the expression of a catalytically inactive Pol\u03b7. Moreover, this recovery of cellular UV sensitivity was mediated by the interaction between Pol\u03b7 and REV1. However, expression of the inactive mutant Pol\u03b7 was not able to suppress the incidence of UV\u2010induced mutation observed in Pol\u03b7\u2010deficient cells. We propose the model that REV1 and Pol\u03ba are involved in DNA damage tolerance via Pol\u03b7\u2013REV1 interaction when Pol\u03b7 fails to bypass its cognate substrates.<\/jats:p>","DOI":"10.1111\/j.1365-2443.2011.01576.x","type":"journal-article","created":{"date-parts":[[2012,1,16]],"date-time":"2012-01-16T07:25:22Z","timestamp":1326698722000},"page":"98-108","source":"Crossref","is-referenced-by-count":18,"title":["Stalled Pol\u03b7 at its cognate substrate initiates an alternative translesion synthesis pathway via interaction with REV1"],"prefix":"10.1111","volume":"17","author":[{"given":"Wakana","family":"Ito","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masayuki","family":"Yokoi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nobutaka","family":"Sakayoshi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasutaka","family":"Sakurai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun\u2010ichi","family":"Akagi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroshi","family":"Mitani","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fumio","family":"Hanaoka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,1,16]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.dnarep.2008.12.006"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature09196"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.022473899"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/cdg626"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.21.21.7199-7206.2001"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.252524999"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1038\/jid.2008.48"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.285.5425.263"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.23.15975"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1101\/gad.187501"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.dnarep.2007.11.016"},{"key":"e_1_2_6_13_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M211765200"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/18.12.3491"},{"key":"e_1_2_6_15_1","doi-asserted-by":"publisher","DOI":"10.1038\/21447"},{"key":"e_1_2_6_16_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M102051200"},{"key":"e_1_2_6_17_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.222377899"},{"key":"e_1_2_6_18_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2443.2008.01255.x"},{"key":"e_1_2_6_19_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1356-9597.2004.00747.x"},{"key":"e_1_2_6_20_1","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.01076-06"},{"key":"e_1_2_6_21_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0027-5107(01)00131-2"},{"key":"e_1_2_6_22_1","first-page":"4375","article-title":"Inhibition 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