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Repair of AP lesions takes place predominantly by the base excision pathway (BER). However, among chemically heterogeneous AP lesions formed in DNA, some are resistant to the endonuclease APE1 and thus refractory to BER. Here, we employed two types of reporter constructs accommodating synthetic APE1-resistant AP lesions to investigate the auxiliary repair mechanisms in human cells. By combined analyses of recovery of the transcription rate and suppression of transcriptional mutagenesis at specifically positioned AP lesions, we demonstrate that nucleotide excision repair pathway (NER) efficiently removes BER-resistant AP lesions and significantly enhances the repair of APE1-sensitive ones. Our results further indicate that core NER components XPA and XPF are equally required and that both global genome (GG-NER) and transcription coupled (TC-NER) subpathways contribute to the repair.<\/jats:p>","DOI":"10.1093\/nar\/gkz558","type":"journal-article","created":{"date-parts":[[2019,6,18]],"date-time":"2019-06-18T11:10:33Z","timestamp":1560856233000},"page":"8537-8547","source":"Crossref","is-referenced-by-count":51,"title":["Nucleotide excision repair of abasic DNA lesions"],"prefix":"10.1093","volume":"47","author":[{"given":"Nataliya","family":"Kitsera","sequence":"first","affiliation":[{"name":"Unit \u201cResponses to DNA Lesions\u201d, Institute of Toxicology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz\u00a055131, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marta","family":"Rodriguez-Alvarez","sequence":"additional","affiliation":[{"name":"Unit \u201cResponses to DNA Lesions\u201d, Institute of Toxicology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz\u00a055131, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steffen","family":"Emmert","sequence":"additional","affiliation":[{"name":"Clinic and Policlinic for Dermatology and Venereology, University Medical Center Rostock, Rostock\u00a018057, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Carell","sequence":"additional","affiliation":[{"name":"Center for Integrated Protein Science at the Department of Chemistry, Ludwig-Maximilians-Universit\u00e4t M\u00fcnchen, Munich\u00a081377, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9165-3557","authenticated-orcid":false,"given":"Andriy","family":"Khobta","sequence":"additional","affiliation":[{"name":"Unit \u201cResponses to DNA Lesions\u201d, Institute of Toxicology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz\u00a055131, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2019,6,21]]},"reference":[{"key":"2019120523332749600_B1","doi-asserted-by":"crossref","first-page":"709","DOI":"10.1038\/362709a0","article-title":"Instability and decay of the primary structure of DNA","volume":"362","author":"Lindahl","year":"1993","journal-title":"Nature"},{"key":"2019120523332749600_B2","doi-asserted-by":"crossref","first-page":"201","DOI":"10.1146\/annurev.ge.20.120186.001221","article-title":"Mutagenesis by apurinic\/apyrimidinic sites","volume":"20","author":"Loeb","year":"1986","journal-title":"Annu. 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Cell"},{"key":"2019120523332749600_B6","doi-asserted-by":"crossref","first-page":"8919","DOI":"10.1073\/pnas.93.17.8919","article-title":"The redox\/DNA repair protein, Ref-1, is essential for early embryonic development in mice","volume":"93","author":"Xanthoudakis","year":"1996","journal-title":"Proc. Natl. Acad. Sci. U.S.A."},{"key":"2019120523332749600_B7","doi-asserted-by":"crossref","first-page":"17","DOI":"10.1016\/S0921-8777(98)00039-1","article-title":"A murine AP-endonuclease gene-targeted deficiency with post-implantation embryonic progression and ionizing radiation sensitivity","volume":"409","author":"Ludwig","year":"1998","journal-title":"Mutat. 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