ReviewScience China. Life sciences2017
Formation and repair of DNA-protein crosslink damage.
Review in Science China. Life sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 68 citations in OpenAlex.
- Fanconi Anemia: Interplay Between DNA Repair Defects, Mitochondrial Dysfunction, and Oxidative Stress.Cells · 2026Review
- DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026Review
- Peptide Sequence and Cross-Link Structure Influence Translesion Synthesis Polymerase Bypass of 5-Formylcytosine-Mediated DNA-Peptide Cross-Links.Chemical research in toxicology · 2025Article
- DNA Damage and Repair in Pancreatic Cancer-The Latest Findings.International journal of molecular sciences · 2025Review
- Comprehensive review on Fanconi anemia: insights into DNA interstrand cross-links, repair pathways, and associated tumors.Orphanet journal of rare diseases · 2025Review
- DNA-Protein Cross-Links Derived from Abasic DNA Lesions: Recent Progress and Future Directions.Chemical research in toxicology · 2025Review
- Flap endonuclease 1 repairs DNA-protein cross-links via ADP-ribosylation-dependent mechanisms.Science advances · 2025Article
- RETRACTED: Genotyping strategies for tissues fixed with various embalming fluids for human identification, databasing, and traceability.Journal of forensic sciences · 2025Article
- Nitrogen mustard induces dynamic nuclear protein spectrum change and DNA-protein crosslinking, with p97 mediating repair.Heliyon · 2024Article
- Di- and tri-methylation of histone H3K36 play distinct roles in DNA double-strand break repair.Science China. Life sciences · 2024Article
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
- Enzymatic Processing of DNA-Protein Crosslinks.Genes · 2024Review
- Viral Prevalence and Genomic Xenology in the Coevolution of HzNV-2 (Nudiviridae) with HostInsects · 2023Article
- Quantitative Detection of DNA-Protein Crosslinks and Their Post-Translational Modifications.Journal of visualized experiments : JoVE · 2023Article
- SMC5/6 complex-mediated SUMOylation stimulates DNA-protein cross-link repair in Arabidopsis.The Plant cell · 2023Article
- Editorial: The repair of DNA-protein crosslinks.Frontiers in molecular biosciences · 2023Article
- Fanconi anemia: current insights regarding epidemiology, cancer, and DNA repair.Human genetics · 2022Review
- Comparative transcriptome and metabolome analyses reveal the methanol dissimilation pathway of Pichia pastoris.BMC genomics · 2022Article
- Human TDP1, APE1 and TREX1 repair 3'-DNA-peptide/protein cross-links arising from abasic sites in vitro.Nucleic acids research · 2022Article
- Participation of Histones in DNA Damage and Repair within Nucleosome Core Particles: Mechanism and Applications.Accounts of chemical research · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
DNA is constantly exposed to a wide array of genotoxic agents, generating a variety of forms of DNA damage. DNA-protein crosslinks (DPCs)-the covalent linkage of proteins with a DNA strand-are one of the most deleterious and understudied forms of DNA damage, posing as steric blockades to transcription and replication. If not properly repaired, these lesions can lead to mutations, genomic instability, and cell death. DPCs can be induced endogenously or through environmental carcinogens and chemotherapeutic agents. Endogenously, DPCs are commonly derived through reactions with aldehydes, as well as through trapping of various enzymatic intermediates onto the DNA. Proteolytic cleavage of the protein moiety of a DPC is a general strategy for removing the lesion. This can be accomplished through a DPC-specific protease and and/or proteasome-mediated degradation. Nucleotide excision repair and homologous recombination are each involved in repairing DPCs, with their respective roles likely dependent on the nature and size of the adduct. The Fanconi anemia pathway may also have a role in processing DPC repair intermediates. In this review, we discuss how these lesions are formed, strategies and mechanisms for their removal, and diseases associated with defective DPC repair.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.