ArticleScientific reports2017
The Human DNA glycosylases NEIL1 and NEIL3 Excise Psoralen-Induced DNA-DNA Cross-Links in a Four-Stranded DNA Structure.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Role of NEIL1 in genome maintenance.DNA repair · 2025Review
- Repair of genomic interstrand crosslinks.DNA repair · 2024Review
- Structure andmBio · 2024Article
- Review
- Base excision repair of the N-(2-deoxy-d-erythro-pentofuranosyl)-urea lesion by the hNEIL1 glycosylase.Nucleic acids research · 2023Article
- NEIL3-mediated proteasomal degradation facilitates the repair of cisplatin-induced DNA damage in human cells.Scientific reports · 2023Article
- Article
- Biological Functions of the DNA Glycosylase NEIL3 and Its Role in Disease Progression Including Cancer.Cancers · 2022Review
- Article
- TRIM26 Maintains Cell Survival in Response to Oxidative Stress through Regulating DNA Glycosylase Stability.International journal of molecular sciences · 2022Article
- Long-term association of pregnancy and maternal brain structure: the Rotterdam Study.European journal of epidemiology · 2022Article
- NEIL1 and NEIL2 Are Recruited as Potential Backup for OGG1 upon OGG1 Depletion or Inhibition by TH5487.International journal of molecular sciences · 2021Article
- DNA Sequence Modulates the Efficiency of NEIL1-Catalyzed Excision of the Aflatoxin BChemical research in toxicology · 2021Article
- Targeting Chromosomal Architectural HMGB Proteins Could Be the Next Frontier in Cancer Therapy.Cancer research · 2020Review
- The FANC/BRCA Pathway Releases Replication Blockades by Eliminating DNA Interstrand Cross-Links.Genes · 2020Review
- Cooperation of the NEIL3 and Fanconi anemia/BRCA pathways in interstrand crosslink repair.Nucleic acids research · 2020Article
- Unhooking of an interstrand cross-link at DNA fork structures by the DNA glycosylase NEIL3.DNA repair · 2020Article
- Role of Base Excision Repair Pathway in the Processing of Complex DNA Damage Generated by Oxidative Stress and Anticancer Drugs.Frontiers in cell and developmental biology · 2020Review
- Cooperation and interplay between base and nucleotide excision repair pathways: From DNA lesions to proteins.Genetics and molecular biology · 2020Article
- DNA-Histone Cross-Links: Formation and Repair.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Interstrand cross-links (ICLs) are highly cytotoxic DNA lesions that block DNA replication and transcription by preventing strand separation. Previously, we demonstrated that the bacterial and human DNA glycosylases Nei and NEIL1 excise unhooked psoralen-derived ICLs in three-stranded DNA via hydrolysis of the glycosidic bond between the crosslinked base and deoxyribose sugar. Furthermore, NEIL3 from Xenopus laevis has been shown to cleave psoralen- and abasic site-induced ICLs in Xenopus egg extracts. Here we report that human NEIL3 cleaves psoralen-induced DNA-DNA cross-links in three-stranded and four-stranded DNA substrates to generate unhooked DNA fragments containing either an abasic site or a psoralen-thymine monoadduct. Furthermore, while Nei and NEIL1 also cleave a psoralen-induced four-stranded DNA substrate to generate two unhooked DNA duplexes with a nick, NEIL3 targets both DNA strands in the ICL without generating single-strand breaks. The DNA substrate specificities of these Nei-like enzymes imply the occurrence of long uninterrupted three- and four-stranded crosslinked DNA-DNA structures that may originate in vivo from DNA replication fork bypass of an ICL. In conclusion, the Nei-like DNA glycosylases unhook psoralen-derived ICLs in various DNA structures via a genuine repair mechanism in which complex DNA lesions can be removed without generation of highly toxic double-strand breaks.
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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.