{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kim N"],"funding":["Institute for Basic Science","National Research Foundation of Korea (NRF)","National Research Foundation of Korea","Institute for Basic Science (IBS)"],"pagination":["547"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12644609"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(1)"],"pubmed_abstract":["Ultraviolet (UV)-induced DNA lesions threaten genomic stability and are associated with skin carcinogenesis. These lesions are primarily repaired by the nucleotide excision repair (NER) pathway. However, alternative repair mechanisms and regulators are emerging as critical contributors to managing UV lesions. Here, we used a click chemistry-based proteomic approach to identify DEK and NUMA1 as novel regulators of UV-induced DNA lesion repair. Depletion of DEK or NUMA1 resulted in delayed UV lesion repair and increased cellular UV sensitivity. This was accompanied by delayed recruitment of XPF to UV-damaged sites. Notably, abnormal accumulation of proliferating cell nuclear antigen (PCNA) at UV lesions was observed in DEK- or NUMA1-depleted cells. This PCNA accumulation was not entirely dep"],"journal":["Cell death discovery"],"pubmed_title":["Proteomic discovery of DEK and NUMA1 as new players in UV-induced DNA damage repair mechanisms."],"pmcid":["PMC12644609"],"funding_grant_id":["RS-2024-00349478","IBS-R022-D1","IBS-R022-A1","2022R1A6A3A1307241","RS-2023-00274772"],"pubmed_authors":["Kim BG","Myung K","Jeong E","Scharer OD","Yeo JE","Lee KY","Kim M","Kim N"],"additional_accession":[]},"is_claimable":false,"name":"Proteomic discovery of DEK and NUMA1 as new players in UV-induced DNA damage repair mechanisms.","description":"Ultraviolet (UV)-induced DNA lesions threaten genomic stability and are associated with skin carcinogenesis. These lesions are primarily repaired by the nucleotide excision repair (NER) pathway. However, alternative repair mechanisms and regulators are emerging as critical contributors to managing UV lesions. Here, we used a click chemistry-based proteomic approach to identify DEK and NUMA1 as novel regulators of UV-induced DNA lesion repair. Depletion of DEK or NUMA1 resulted in delayed UV lesion repair and increased cellular UV sensitivity. This was accompanied by delayed recruitment of XPF to UV-damaged sites. Notably, abnormal accumulation of proliferating cell nuclear antigen (PCNA) at UV lesions was observed in DEK- or NUMA1-depleted cells. This PCNA accumulation was not entirely dep","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-06-05T18:59:44.998Z","creation":"2026-05-20T03:14:41.523Z"},"accession":"S-EPMC12644609","cross_references":{"pubmed":["41285742"],"doi":["10.1038/s41420-025-02823-z"]}}