<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Sarmini, Leen</style></author><author><style face="normal" font="default" size="100%">Meabed, Mohammed</style></author><author><style face="normal" font="default" size="100%">Emmanouil, Eirini</style></author><author><style face="normal" font="default" size="100%">Atsaves, George</style></author><author><style face="normal" font="default" size="100%">Robeska, Elena</style></author><author><style face="normal" font="default" size="100%">Karwowski, Bolesław T</style></author><author><style face="normal" font="default" size="100%">Campalans, Anna</style></author><author><style face="normal" font="default" size="100%">Gimisis, Thanasis</style></author><author><style face="normal" font="default" size="100%">Khobta, Andriy</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Requirement of transcription-coupled nucleotide excision repair for the removal of a specific type of oxidatively induced DNA damage</style></title><secondary-title><style face="normal" font="default" size="100%">Nucleic Acids Research</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2023</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2023/04//</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">https://academic.oup.com/nar/advance-article/doi/10.1093/nar/gkad256/7110754</style></url></web-urls></urls><pages><style face="normal" font="default" size="100%">1 - 13</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Accumulation of DNA damage resulting from reactive oxygen species was proposed to cause neurological and degenerative disease in patients, deficient in nucleotide excision repair (NER) or its transcription-coupled subpathway (TC-NER). Here, we assessed the requirement of TC-NER for the repair of specific types of oxidatively generated DNA modifications. We incorporated synthetic 5′,8-cyclo-2′-deoxypurine nucleotides (cyclo-dA, cyclo-dG) and thymine glycol (Tg) into an EGFP reporter gene to measure transcription-blocking potentials of these modifications in human cells. Using null mutants, we further identified the relevant DNA repair components by a host cell reactivation approach. The results indicated that NTHL1-initiated base excision repair is by far the most efficient pathway for Tg. Moreover, Tg was efficiently bypassed during transcription, which effectively rules out TC-NER as an alternative repair mechanism. In a sharp contrast, both cyclopurine lesions robustly blocked transcription and were repaired by NER, wherein the specific TC-NER components CSB/ERCC6 and CSA/ERCC8 were as essential as XPA. Instead, repair of classical NER substrates, cyclobutane pyrimidine dimer and N-(deoxyguanosin-8-yl)-2-acetylaminofluorene, occurred even when TC-NER was disrupted. The strict requirement of TC-NER highlights cyclo-dA and cyclo-dG as candidate damage types, accountable for cytotoxic and degenerative responses in individuals affected by genetic defects in this pathway.</style></abstract></record></records></xml>