ArticleThe Journal of biological chemistry2009
Homologous recombination but not nucleotide excision repair plays a pivotal role in tolerance of DNA-protein cross-links in mammalian cells.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 132 citations in OpenAlex.
- Evaluation of noncytotoxic DNMT1-depleting therapy in patients with myelodysplastic syndromes.The Journal of clinical investigation · 2015Trial
- Living Cells Employ Ubiquitin-Proteasomal System and Nucleotide Excision Repair Pathways to Remove Reactive Oxygen Species-Induced DNA-Protein Crosslinks (ROS-DPCs).bioRxiv : the preprint server for biology · 2026Article
- Genome-wide mapping of formaldehyde-induced DNA-protein crosslinks reveals unique patterns of formation and transcription-coupled removal in mammalian cells.Nucleic acids research · 2025Article
- DNA-protein cross-links emerge as major contributors to chemotherapeutic cytotoxicity at physiological equitoxic doses.Scientific reports · 2025Article
- Article
- From the TOP: Formation, recognition and resolution of topoisomerase DNA protein crosslinks.DNA repair · 2024Review
- Endogenous Cellular Metabolite Methylglyoxal Induces DNA-Protein Cross-Links in Living Cells.ACS chemical biology · 2024Article
- Endogenous aldehyde-induced DNA-protein crosslinks are resolved by transcription-coupled repair.Nature cell biology · 2024Article
- Isolation and detection of DNA-protein crosslinks in mammalian cells.Nucleic acids research · 2024Article
- Enzymatic Processing of DNA-Protein Crosslinks.Genes · 2024Review
- Aldehyde-induced DNA-protein crosslinks- DNA damage, repair and mutagenesis.Frontiers in oncology · 2024Review
- Ubiquitin signaling and the proteasome drive human DNA-protein crosslink repair.Nucleic acids research · 2023Article
- Abasic site-peptide cross-links are blocking lesions repaired by AP endonucleases.Nucleic acids research · 2023Article
- Ubx5-Cdc48 assists the protease Wss1 at DNA-protein crosslink sites in yeast.The EMBO journal · 2023Article
- SPRTN-dependent DPC degradation precedes repair of damaged DNA: a proof of concept revealed by the STAR assay.Nucleic acids research · 2023Article
- Editorial: The repair of DNA-protein crosslinks.Frontiers in molecular biosciences · 2023Article
- Human TDP1, APE1 and TREX1 repair 3'-DNA-peptide/protein cross-links arising from abasic sites in vitro.Nucleic acids research · 2022Article
- Mechanisms and Regulation of DNA-Protein Crosslink Repair During DNA Replication by SPRTN Protease.Frontiers in molecular biosciences · 2022Review
- The protease SPRTN and SUMOylation coordinate DNA-protein crosslink repair to prevent genome instability.Cell reports · 2021Article
- DNA polymerases η and κ bypass NThe Journal of biological chemistry · 2021Article
23 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA-protein cross-links (DPCs) are unique among DNA lesions in their unusually bulky nature. The steric hindrance imposed by cross-linked proteins (CLPs) will hamper DNA transactions, such as replication and transcription, posing an enormous threat to cells. In bacteria, DPCs with small CLPs are eliminated by nucleotide excision repair (NER), whereas oversized DPCs are processed exclusively by RecBCD-dependent homologous recombination (HR). Here we have assessed the roles of NER and HR for DPCs in mammalian cells. We show that the upper size limit of CLPs amenable to mammalian NER is relatively small (8-10 kDa) so that NER cannot participate in the repair of chromosomal DPCs in mammalian cells. Moreover, CLPs are not polyubiquitinated and hence are not subjected to proteasomal degradation prior to NER. In contrast, HR constitutes the major pathway in tolerance of DPCs as judged from cell survival and RAD51 and gamma-H2AX nuclear foci formation. Induction of DPCs results in the accumulation of DNA double strand breaks in HR-deficient but not HR-proficient cells, suggesting that fork breakage at the DPC site initiates HR and reactivates the stalled fork. DPCs activate both ATR and ATM damage response pathways, but there is a time lag between two responses. These results highlight the differential involvement of NER in the repair of DPCs in bacterial and mammalian cells and demonstrate the versatile and conserved role of HR in tolerance of DPCs among species.
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