{"doi":"10.1093/nar/gkz558","title":"Nucleotide excision repair of abasic DNA lesions","abstract":"<jats:title>Abstract</jats:title><jats:p>Apurinic/apyrimidinic (AP) sites are a class of highly mutagenic and toxic DNA lesions arising in the genome from a number of exogenous and endogenous sources. 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>","journal":"Nucleic Acids Research","year":2019,"id":35851,"datarank":1.5321629047447565,"base_score":3.9318256327243257,"endowment":3.9318256327243257,"self_citation_contribution":0.5897738449086489,"citation_network_contribution":0.9423890598361077,"self_endowment_contribution":0.5897738449086489,"citer_contribution":0.9423890598361077,"corpus_percentile":null,"corpus_rank":null,"citation_count":50,"citer_count":45,"citers_with_citation_signal":34,"citers_with_endowment":34,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":182799,"name":"Marta Rodriguez-Alvarez","orcid":null,"position":1,"is_corresponding":false},{"id":182800,"name":"Steffen Emmert","orcid":null,"position":2,"is_corresponding":false},{"id":182801,"name":"Thomas Carell","orcid":null,"position":3,"is_corresponding":false},{"id":182802,"name":"Andriy Khobta","orcid":"0000-0001-9165-3557","position":4,"is_corresponding":false},{"id":182798,"name":"Nataliya Kitsera","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"base_score":3.9318256327243257,"endowment":3.9318256327243257,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"31226203","pmcid":"PMC6895268","openalex_id":"https://openalex.org/W2950609079","authors":[],"funders":[{"funder_name":"Deutsche Forschungsgemeinschaft","grant_id":"KH 263/1","title":null},{"funder_name":"Deutsche Forschungsgemeinschaft","grant_id":"KH263/2","title":null},{"funder_name":"Deutsche Forschungsgemeinschaft","grant_id":"KH263/5","title":null},{"funder_name":"Deutsche Forschungsgemeinschaft","grant_id":"SFB1631","title":null},{"funder_name":"European Union","grant_id":"ESF/14-BM-A55","title":null},{"funder_name":"Damp Foundation","grant_id":"2017-05","title":null},{"funder_name":"Deutsche Forschungsgemeinschaft","grant_id":"unidentified","title":"unidentified"}],"total_grants":7,"fwci":2.137,"citation_percentile":0.88082206,"influential_citations":3,"citation_trend":[{"year":2019,"count":1},{"year":2020,"count":9},{"year":2021,"count":6},{"year":2022,"count":9},{"year":2023,"count":10},{"year":2024,"count":5},{"year":2025,"count":6},{"year":2026,"count":4}],"oa_status":"gold","license":"cc-by","oa_locations":[{"url":"https://academic.oup.com/nar/article-pdf/47/16/8537/31234846/gkz558.pdf","host_type":"journal"},{"url":"https://academic.oup.com/nar/article-pdf/47/16/8537/31234846/gkz558.pdf","host_type":"GOLD"},{"url":"https://academic.oup.com/nar/article-pdf/47/16/8537/31234846/gkz558.pdf","host_type":"publisher"},{"url":"http://academic.oup.com/nar/article-pdf/47/16/8537/31234846/gkz558.pdf","host_type":"publisher"},{"url":"https://doi.org/10.1093/nar/gkz558","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/31226203","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/6895268","host_type":"repository"},{"url":"https://europepmc.org/articles/PMC6895268","host_type":"Europe_PMC"},{"url":"https://europepmc.org/articles/PMC6895268?pdf=render","host_type":"Europe_PMC"},{"url":"http://dx.doi.org/10.1093/nar/gkz558","host_type":""},{"url":"https://dx.doi.org/10.1093/nar/gkz558","host_type":""}],"fields_of_study":["DNA Repair Mechanisms","CRISPR and Genetic Engineering","Genomics and Chromatin Dynamics","Biology","Medicine","0301 basic medicine","0303 health sciences","03 medical and health sciences","Base Sequence","CRISPR-Associated Protein 9","CRISPR-Cas Systems","Cell Line, Transformed","DNA","DNA Damage","DNA Repair","DNA-(Apurinic or Apyrimidinic Site) Lyase","DNA-Binding Proteins","Fibroblasts","Gene Editing","Gene Knockout Techniques","Genome, Human","Humans","Mutation","Protein Binding","Skin","Transcription, Genetic","Xeroderma Pigmentosum Group A Protein"],"mesh_terms":["Gene Editing","CRISPR-Associated Protein 9","Base Sequence","Cell Line, Transformed","DNA","DNA Damage","DNA Repair","DNA-Binding Proteins","Fibroblasts","Humans","Mutation","Protein Binding","Skin","Transcription, Genetic","Genome, Human","DNA-(Apurinic or Apyrimidinic Site) Lyase","Xeroderma Pigmentosum Group A Protein","Gene Knockout Techniques","CRISPR-Cas Systems"],"keywords":["AP site","Biology","Base excision repair","Nucleotide excision repair","AP endonuclease","DNA repair","DNA-(apurinic or apyrimidinic site) lyase","Endonuclease","Molecular biology","DNA","DNA glycosylase","DNA damage","Transcription (linguistics)","Mutagenesis","Genetics","Cell biology","Gene","Mutation","Gene Editing","Base Sequence","Transcription, Genetic","Genome, Human","Genome Integrity, Repair and Replication","Fibroblasts","Xeroderma Pigmentosum Group A Protein","DNA-Binding Proteins","Gene Knockout Techniques","CRISPR-Associated Protein 9","Humans","CRISPR-Cas Systems","Cell Line, Transformed","Protein Binding","Skin"],"sdg_mappings":[],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[{"name":"igsr"}],"source":"live","citation_network_status":"fetched"},"created_at":"2026-06-10T10:18:40.602966Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}