{"doi":"10.1016/j.mrfmmm.2013.03.010","title":"Ku80-deleted cells are defective at base excision repair","abstract":null,"journal":"Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis","year":2013,"id":606291,"datarank":0.4636563680037475,"base_score":3.091042453358316,"endowment":3.091042453358316,"self_citation_contribution":0.4636563680037475,"citation_network_contribution":0.0,"self_endowment_contribution":0.4636563680037475,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":21,"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":1299881,"name":"Teresa Marple","orcid":null,"position":1,"is_corresponding":false},{"id":338000,"name":"Paul Hasty","orcid":"0000-0003-3046-0131","position":2,"is_corresponding":false},{"id":275481,"name":"Han Li","orcid":"0000-0003-4978-6502","position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Ku80-deleted cells are defective at base excision repair","abstract":"Ku80 forms a heterodimer with Ku70, called Ku, that repairs DNA double-strand breaks (DSBs) via the nonhomologous end joining (NHEJ) pathway. As a consequence of deleting NHEJ, Ku80-mutant cells are hypersensitive to agents that cause DNA DSBs like ionizing radiation. Here we show that Ku80 deletion also decreased resistance to ROS and alkylating agents that typically cause base lesions and single-strand breaks (SSBs). This is unusual since base excision repair (BER), not NHEJ, typically repairs these types of lesions. However, we show that deletion of another NHEJ protein, DNA ligase IV (Lig4), did not cause hypersensitivity to these agents. In addition, the ROS and alkylating agents did not induce γ-H2AX foci that are diagnostic of DSBs. Furthermore, deletion of Ku80, but not Lig4 or Ku70, reduced BER capacity. Ku80 deletion also impaired BER at the initial lesion recognition/strand scission step; thus, involvement of a DSB is unlikely. Therefore, our data suggests that Ku80 deletion impairs BER via a mechanism that does not repair DSBs.","is_dataset_classified":null,"base_score":3.091042453358316,"endowment":3.091042453358316,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"23567907","pmcid":"PMC3721509","openalex_id":"https://openalex.org/W2011783467","authors":[],"funders":[{"funder_name":"NIA NIH HHS","grant_id":"P01 AG017242","title":null},{"funder_name":"NCI NIH HHS","grant_id":"R01 CA076317","title":null},{"funder_name":"NIEHS NIH HHS","grant_id":"U01 ES011044","title":null},{"funder_name":"NCI NIH HHS","grant_id":"R01 CA76317-05A1","title":null},{"funder_name":"NIA NIH HHS","grant_id":"P01 AG17242","title":null},{"funder_name":"NIEHS NIH HHS","grant_id":"U01 ES11044","title":null}],"total_grants":6,"fwci":1.5134,"citation_percentile":0.8157721,"influential_citations":0,"citation_trend":[{"year":2014,"count":4},{"year":2015,"count":4},{"year":2016,"count":3},{"year":2017,"count":2},{"year":2018,"count":1},{"year":2019,"count":2},{"year":2021,"count":1},{"year":2022,"count":1},{"year":2023,"count":2},{"year":2025,"count":1}],"oa_status":"closed","license":"https://doi.org/10.15223/policy-004","oa_locations":[{"url":"https://api.elsevier.com/content/article/PII:S0027510713000390?httpAccept=text/xml","host_type":"publisher"},{"url":"https://api.elsevier.com/content/article/PII:S0027510713000390?httpAccept=text/plain","host_type":"publisher"},{"url":"https://doi.org/10.1016/j.mrfmmm.2013.03.010","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/23567907","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/3721509","host_type":"repository"}],"fields_of_study":["DNA Repair Mechanisms","Cancer-related Molecular Pathways","Genomics and Chromatin Dynamics","Alkylating Agents","Animals","Antigens, Nuclear","Base Sequence","DNA Breaks, Double-Stranded","DNA End-Joining Repair","DNA Glycosylases","DNA Ligase ATP","DNA Ligases","DNA Repair","DNA, Single-Stranded","DNA-Binding Proteins","Dose-Response Relationship, Drug","Fibroblasts","HeLa Cells","Humans","Hydrogen Peroxide","Ku Autoantigen","Mice","Molecular Sequence Data","Mutagens","Mutation","Paraquat","Reactive Oxygen Species"],"mesh_terms":["Ku Autoantigen","DNA Ligase ATP","Alkylating Agents","Animals","Base Sequence","DNA Repair","DNA-Binding Proteins","DNA, Single-Stranded","Dose-Response Relationship, Drug","Fibroblasts","HeLa Cells","Humans","Hydrogen Peroxide","Molecular Sequence Data","Mutagens","Mutation","Paraquat","DNA Ligases","Reactive Oxygen Species","Antigens, Nuclear","DNA Glycosylases","Mice","DNA Breaks, Double-Stranded","DNA End-Joining Repair","Hela Cells"],"keywords":["Ku80","Ku70","Non-homologous end joining","DNA damage","DNA repair","DNA ligase","Biology","DNA","DNA repair protein XRCC4","Molecular biology","Cancer research","Genetics","Nucleotide excision repair","DNA-binding protein","Gene"],"sdg_mappings":[],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-07-30T04:14:33.881284Z","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":[]}