ArticleNature structural & molecular biology2016
Neil DNA glycosylases promote substrate turnover by Tdg during DNA demethylation.
Article in Nature structural & molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 90 citations in OpenAlex.
- Establishment of neuronal and glial competence of neural stem cells requires distinct enzymatic activities of TET enzymes.Stem cell reports · 2025Article
- DNA glycosylases Ogg1 and Mutyh influence gene expression of PRC2 targets associated with cognition.Cellular and molecular life sciences : CMLS · 2025Article
- Chemical Switching: A Concept Inspired by Strategies from Biocatalysis and Organocatalysis.Chembiochem : a European journal of chemical biology · 2025Review
- Role of NEIL1 in genome maintenance.DNA repair · 2025Review
- DNA repair and disease: insights from the human DNA glycosylase NEIL family.Experimental & molecular medicine · 2025Review
- The role of lncRNAs in the interplay of signaling pathways and epigenetic mechanisms in glioma.Epigenomics · 2025Review
- Research progress on the role of the NEIL family in cancer.Frontiers in cell and developmental biology · 2025Review
- NEIL1 block IFN-β production and enhance vRNP function to facilitate influenza A virus proliferation.Npj viruses · 2024Article
- Functional roles and cancer variants of the bifunctional glycosylase NEIL2.Environmental and molecular mutagenesis · 2024Review
- Inspiring basic and applied research in genome integrity mechanisms: Dedication to Samuel H. Wilson.Environmental and molecular mutagenesis · 2024Review
- Epigenetic marks or not? The discovery of novel DNA modifications in eukaryotes.The Journal of biological chemistry · 2024Review
- DNA methylation restricts coordinated germline and neural fates in embryonic stem cell differentiation.Nature structural & molecular biology · 2024Article
- Enhanced thermal stability enables human mismatch-specific thymine-DNA glycosylase to catalyse futile DNA repair.PloS one · 2024Article
- Back-Up Base Excision DNA Repair in Human Cells Deficient in the Major AP Endonuclease, APE1.International journal of molecular sciences · 2023Article
- Structural and biochemical insights into NEIL2's preference for abasic sites.Nucleic acids research · 2023Article
- Base Excision Repair: Mechanisms and Impact in Biology, Disease, and Medicine.International journal of molecular sciences · 2023Review
- Deficiency in mammalian STN1 promotes colon cancer development via inhibiting DNA repair.Science advances · 2023Article
- Phosphorylation of the Human DNA Glycosylase NEIL2 Is Affected by Oxidative Stress and Modulates Its Activity.Antioxidants (Basel, Switzerland) · 2023Article
- NEIL1 Recoding due to RNA Editing Impacts Lesion-Specific Recognition and Excision.Journal of the American Chemical Society · 2022Article
- Novel interaction interfaces mediate the interaction between the NEIL1 DNA glycosylase and mitochondrial transcription factor A.Frontiers in cell and developmental biology · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
DNA 5-methylcytosine is a dynamic epigenetic mark with important roles in development and disease. In the Tet-Tdg demethylation pathway, methylated cytosine is iteratively oxidized by Tet dioxygenases, and unmodified cytosine is restored via thymine DNA glycosylase (Tdg). Here we show that human NEIL1 and NEIL2 DNA glycosylases coordinate abasic-site processing during TET-TDG DNA demethylation. NEIL1 and NEIL2 cooperate with TDG during base excision: TDG occupies the abasic site and is displaced by NEILs, which further process the baseless sugar, thereby stimulating TDG-substrate turnover. In early Xenopus embryos, Neil2 cooperates with Tdg in removing oxidized methylcytosines and specifying neural-crest development together with Tet3. Thus, Neils function as AP lyases in the coordinated AP-site handover during oxidative DNA demethylation.
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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.