ArticleDNA repair2020
Unhooking of an interstrand cross-link at DNA fork structures by the DNA glycosylase NEIL3.
Article in DNA repair, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Generation of Interstrand DNA Cross-Links under Conditions of Acid Stress.Chemical research in toxicology · 2026Article
- DNA binding and lesion recognition by the bacterial interstrand DNA crosslink glycosylase AlkX.EMBO reports · 2026Article
- DNA binding and lesion recognition by the bacterial interstrand DNA crosslink glycosylase AlkX.bioRxiv : the preprint server for biology · 2025Article
- Mechanistic insights into alcohol-induced DNA crosslink repair by Slx4-Xpf-Ercc1 nuclease complex in the Fanconi anaemia pathway.Communications biology · 2025Article
- Research progress on the role of the NEIL family in cancer.Frontiers in cell and developmental biology · 2025Review
- Repair of genomic interstrand crosslinks.DNA repair · 2024Review
- Structure andmBio · 2024Article
- Review
- Repair and tolerance of DNA damage at the replication fork: A structural perspective.Current opinion in structural biology · 2023Review
- Recent Advances in DNA Lesion Mapping and Repair Mechanisms.Chemical research in toxicology · 2023Article
- Mycobacterial helicase Lhr abets resistance to DNA crosslinking agents mitomycin C and cisplatin.Nucleic acids research · 2023Article
- Article
- Establishing Linkages Among DNA Damage, Mutagenesis, and Genetic Diseases.Chemical research in toxicology · 2022Review
- Model of abasic site DNA cross-link repair; from the architecture of NEIL3 DNA binding domains to the X-structure model.Nucleic acids research · 2022Article
- Facile preparation of model DNA interstrand cross-link repair intermediates using ribonucleotide-containing DNA.DNA repair · 2022Article
- CircNEIL3 mediates pyroptosis to influence lung adenocarcinoma radiotherapy by upregulating PIF1 through miR-1184 inhibition.Cell death & disease · 2022Article
- Unexpected Complexity in the Products Arising from NaOH-, Heat-, Amine-, and Glycosylase-Induced Strand Cleavage at an Abasic Site in DNA.Chemical research in toxicology · 2022Article
- Products Generated by Amine-Catalyzed Strand Cleavage at Apurinic/Apyrimidinic Sites in DNA: New Insights from a Biomimetic Nucleoside Model System.Chemical research in toxicology · 2022Article
- Synthesis of DNA Duplexes Containing Site-Specific Interstrand Cross-Links via Sequential Reductive Amination Reactions Involving Diamine Linkers and Abasic Sites on Complementary Oligodeoxynucleotides.Chemical research in toxicology · 2021Article
- Interstrand Cross-Link Formation Involving Reaction of a Mispaired Cytosine Residue with an Abasic Site in Duplex DNA.Chemical research in toxicology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Interstrand DNA-DNA cross-links (ICLs) are generated by endogenous processes, drugs, and environmental toxins. Understanding the cellular pathways by which various ICLs are repaired is critical to understanding their biological effects. Recent studies showed that replication-dependent repair of an ICL derived from the reaction of an abasic (AP) site with an adenine residue (dA) on the opposing strand of duplex DNA proceeds via a novel mechanism in which the DNA glycosylase NEIL3 unhooks the ICL. Here we examined the ability of the glycosylase domain of murine NEIL3 (MmuNEIL3-GD) to unhook dA-AP ICLs. The enzyme selectively unhooks the dA-AP ICL located at the duplex/single-strand junction of splayed duplexes that model the strand-separated DNA at the leading edge of a replication fork. We show that the ability to unhook the dA-AP ICL is a specialized function of NEIL3 as this activity is not observed in other BER enzymes. Importantly, NEIL3 only unhooks the dA-AP ICL when the AP residue is located on what would be the leading template strand of a model replication fork. The same specificity for the leading template strand was observed with a 5,6-dihydrothymine monoadduct, demonstrating that this preference is a general feature of the glycosylase and independent of the type of DNA damage. Overall, the results show that the glycosylase domain of NEIL3, lacking the C-terminal NPL4 and GRF zinc finger motifs, is competent to unhook the dA-AP ICL in splayed substrates and independently enforces important substrate preferences on the repair process.
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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.