{"doi":"10.1016/j.molcel.2015.08.012","title":"Tripartite DNA Lesion Recognition and Verification by XPC, TFIIH, and XPA in Nucleotide Excision Repair","abstract":null,"journal":"Molecular Cell","year":2015,"id":632467,"datarank":0.7649799641736299,"base_score":5.099866427824199,"endowment":5.099866427824199,"self_citation_contribution":0.7649799641736299,"citation_network_contribution":0.0,"self_endowment_contribution":0.7649799641736299,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":163,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":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":1639435,"name":"Filip M. Golebiowski","orcid":null,"position":1,"is_corresponding":false},{"id":1639436,"name":"Yuki Onishi","orcid":null,"position":2,"is_corresponding":false},{"id":1639437,"name":"Nadine L. Samara","orcid":null,"position":3,"is_corresponding":false},{"id":1022183,"name":"Kaoru Sugasawa","orcid":"0000-0001-7937-4053","position":4,"is_corresponding":false},{"id":274262,"name":"Wei Yang","orcid":"0000-0003-3065-1843","position":5,"is_corresponding":false},{"id":1639434,"name":"Chia-Lung Li","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Tripartite DNA Lesion Recognition and Verification by XPC, TFIIH, and XPA in Nucleotide Excision Repair","abstract":"Transcription factor IIH (TFIIH) is essential for both transcription and nucleotide excision repair (NER). DNA lesions are initially detected by NER factors XPC and XPE or stalled RNA polymerases, but only bulky lesions are preferentially repaired by NER. To elucidate substrate specificity in NER, we have prepared homogeneous human ten-subunit TFIIH and its seven-subunit core (Core7) without the CAK module and show that bulky lesions in DNA inhibit the ATPase and helicase activities of both XPB and XPD in Core7 to promote NER, whereas non-genuine NER substrates have no such effect. Moreover, the NER factor XPA activates unwinding of normal DNA by Core7, but inhibits the Core7 helicase activity in the presence of bulky lesions. Finally, the CAK module inhibits DNA binding by TFIIH and thereby enhances XPC-dependent specific recruitment of TFIIH. Our results support a tripartite lesion verification mechanism involving XPC, TFIIH, and XPA for efficient NER.","is_dataset_classified":null,"base_score":5.099866427824199,"endowment":5.099866427824199,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"26384665","pmcid":"PMC4617536","openalex_id":"https://openalex.org/W1942110646","authors":[],"funders":[{"funder_name":"NIDDK NIH HHS","grant_id":"DK075037-06","title":null},{"funder_name":"Intramural NIH HHS","grant_id":"ZIA DK075037","title":null}],"total_grants":2,"fwci":5.7883,"citation_percentile":0.96948335,"influential_citations":0,"citation_trend":[{"year":2015,"count":1},{"year":2016,"count":16},{"year":2017,"count":16},{"year":2018,"count":9},{"year":2019,"count":22},{"year":2020,"count":21},{"year":2021,"count":15},{"year":2022,"count":17},{"year":2023,"count":18},{"year":2024,"count":14},{"year":2025,"count":7},{"year":2026,"count":7}],"oa_status":"bronze","license":"https://www.elsevier.com/open-access/userlicense/1.0/","oa_locations":[{"url":"http://www.cell.com/article/S1097276515006589/pdf","host_type":"journal"},{"url":"http://www.cell.com/article/S1097276515006589/pdf","host_type":"publisher"},{"url":"https://api.elsevier.com/content/article/PII:S1097276515006589?httpAccept=text/plain","host_type":"publisher"},{"url":"https://api.elsevier.com/content/article/PII:S1097276515006589?httpAccept=text/xml","host_type":"publisher"},{"url":"https://doi.org/10.1016/j.molcel.2015.08.012","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/26384665","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/4617536","host_type":"repository"}],"fields_of_study":["DNA Repair Mechanisms","RNA modifications and cancer","Advanced biosensing and bioanalysis techniques","Animals","Cisplatin","DNA Adducts","DNA Repair","DNA, Single-Stranded","DNA-Binding Proteins","Electrophoretic Mobility Shift Assay","Humans","Protein Binding","Sf9 Cells","Spodoptera","Transcription Factor TFIIH","Xeroderma Pigmentosum Group A Protein"],"mesh_terms":["Animals","Cisplatin","DNA Repair","DNA-Binding Proteins","DNA, Single-Stranded","Humans","Protein Binding","Spodoptera","DNA Adducts","Electrophoretic Mobility Shift Assay","Transcription Factor TFIIH","Xeroderma Pigmentosum Group A Protein","Sf9 Cells"],"keywords":["Transcription factor II H","Nucleotide excision repair","Helicase","Biology","DNA repair","DNA","Molecular biology","Transcription (linguistics)","Cell biology","Genetics","RNA","Gene","Mutation","Cisplatin","Motor","Cy5","Abasic Site","Walker A Motif"],"sdg_mappings":[],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-06T09:49:49.935117Z","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":[]}