ArticleNucleic acids research2016
An interplay of the base excision repair and mismatch repair pathways in active DNA demethylation.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- Changes in active DNA demethylation pathway components during neoadjuvant chemotherapy and their prognostic significance in breast cancer.Breast cancer research : BCR · 2026Article
- 5mC and 5hmC methylation sequencing: the power of 6-base sequencing in a multiomic era.Epigenomics · 2026Review
- 8-Oxoguanine: A Lesion, an Epigenetic Mark, or a Molecular Signal?International journal of molecular sciences · 2025Review
- Mismatch Repair Deficiency and the Role of Non-Canonical Functions in Cancer: Diagnosis and Therapeutic Implications.International journal of molecular sciences · 2025Review
- Damage and Misrepair Signatures: Compact Representations of Pan-cancer Mutational Processes.bioRxiv : the preprint server for biology · 2025Article
- Integrated longitudinal analysis of adult grade 4 diffuse gliomas with long-term relapse interval revealed upregulation of TGF-β signaling in recurrent tumors.Neuro-oncology · 2023Article
- Urinary Measurement of Epigenetic DNA Modifications and 8-oxodG as Possible Noninvasive Markers of Colon Cancer Evolution.International journal of molecular sciences · 2022Article
- Dynamic changes in genomic 5-hydroxymethyluracil and N6-methyladenine levels in the Drosophila melanogaster life cycle and in response to different temperature conditions.Scientific reports · 2022Article
- The mismatch-repair proteins MSH2 and MSH6 interact with the imprinting control regions through the ZFP57-KAP1 complex.Epigenetics & chromatin · 2022Article
- A combinatorial system to examine the enzymatic repair of multiply damaged DNA substrates.Nucleic acids research · 2022Article
- Article
- The threat of programmed DNA damage to neuronal genome integrity and plasticity.Nature genetics · 2022Review
- Gadd45 in DNA Demethylation and DNA Repair.Advances in experimental medicine and biology · 2022Article
- Article
- Deficiency of replication-independent DNA mismatch repair drives a 5-methylcytosine deamination mutational signature in cancer.Science advances · 2021Article
- The urinary excretion of epigenetically modified DNA as a marker of pediatric ALL status and chemotherapy response.Scientific reports · 2021Article
- Genomic Uracil and Aberrant Profile of Demethylation Intermediates in Epigenetics and Hematologic Malignancies.International journal of molecular sciences · 2021Review
- Epigenetic Regulation of Genomic Stability by Vitamin C.Frontiers in genetics · 2021Review
- The role of RNA mInternational journal of biological sciences · 2021Review
- Active turnover of genomic methylcytosine in pluripotent cells.Nature chemical biology · 2020Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Active DNA demethylation (ADDM) in mammals occurs via hydroxylation of 5-methylcytosine (5mC) by TET and/or deamination by AID/APOBEC family enzymes. The resulting 5mC derivatives are removed through the base excision repair (BER) pathway. At present, it is unclear how the cell manages to eliminate closely spaced 5mC residues whilst avoiding generation of toxic BER intermediates and whether alternative DNA repair pathways participate in ADDM. It has been shown that non-canonical DNA mismatch repair (ncMMR) can remove both alkylated and oxidized nucleotides from DNA. Here, a phagemid DNA containing oxidative base lesions and methylated sites are used to examine the involvement of various DNA repair pathways in ADDM in murine and human cell-free extracts. We demonstrate that, in addition to short-patch BER, 5-hydroxymethyluracil and uracil mispaired with guanine can be processed by ncMMR and long-patch BER with concomitant removal of distant 5mC residues. Furthermore, the presence of multiple mispairs in the same MMR nick/mismatch recognition region together with BER-mediated nick formation promotes proficient ncMMR resulting in the reactivation of an epigenetically silenced reporter gene in murine cells. These findings suggest cooperation between BER and ncMMR in the removal of multiple mismatches that might occur in mammalian cells during ADDM.
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