ArticlePloS one2011
New insights in the removal of the hydantoins, oxidation product of pyrimidines, via the base excision and nucleotide incision repair pathways.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 39 citations in OpenAlex.
- DNA Damage Recognition by Bacterial and Human Adenine-DNA Glycosylases: Insights from Non-Canonical Substrates.Biomolecules · 2026Article
- Novel mechanisms for the removal of strong replication-blocking HMCES- and thiazolidine-DNA adducts in humans.Nucleic acids research · 2023Article
- Uracil-DNA Glycosylase Assay by Matrix-assisted Laser Desorption/Ionization Time-of-flight Mass Spectrometry Analysis.Journal of visualized experiments : JoVE · 2022Article
- A Low-Activity Polymorphic Variant of Human NEIL2 DNA Glycosylase.International journal of molecular sciences · 2022Article
- Analysis of nucleotide insertion opposite urea and translesion synthesis across urea by DNA polymerases.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2022Article
- In vitro reconstitution of an efficient nucleotide excision repair system using mesophilic enzymes from Deinococcus radiodurans.Communications biology · 2022Article
- Understanding APE1 cellular functions by the structural preference of exonuclease activities.Computational and structural biotechnology journal · 2021Review
- Removal of oxidatively generated DNA damage by overlapping repair pathways.Free radical biology & medicine · 2017Review
- Poly(ADP-ribose) polymerases covalently modify strand break termini in DNA fragments in vitro.Nucleic acids research · 2016Article
- The current state of eukaryotic DNA base damage and repair.Nucleic acids research · 2015Review
- Uracil in duplex DNA is a substrate for the nucleotide incision repair pathway in human cells.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Induction of base excision repair enzymes NTH1 and APE1 in rat spleen following aniline exposure.Toxicology and applied pharmacology · 2013Article
- Biochemical and structural characterization of the glycosylase domain of MBD4 bound to thymine and 5-hydroxymethyuracil-containing DNA.Nucleic acids research · 2012Article
- Highly mutagenic exocyclic DNA adducts are substrates for the human nucleotide incision repair pathway.PloS one · 2012Article
- Mitochondrial DNA damage and its consequences for mitochondrial gene expression.Biochimica et biophysica actaReview
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOxidative damage to DNA, if not repaired, can be both miscoding and blocking. These genetic alterations can lead to mutations and/or cell death, which in turn cause cancer and aging. Oxidized DNA bases are substrates for two overlapping repair pathways: base excision (BER) and nucleotide incision repair (NIR). Hydantoin derivatives such as 5-hydroxyhydantoin (5OH-Hyd) and 5-methyl-5-hydroxyhydantoin (5OH-5Me-Hyd), major products of cytosine and thymine oxidative degradation pathways, respectively, have been detected in cancer cells and ancient DNA. Hydantoins are blocking lesions for DNA polymerases and excised by bacterial and yeast DNA glycosylases in the BER pathway. However little is known about repair of pyrimidine-derived hydantoins in human cells. METHODOLOGY/PRINCIPAL
findingsHere, using both denaturing PAGE and MALDI-TOF MS analyses we report that the bacterial, yeast and human AP endonucleases can incise duplex DNA 5' next to 5OH-Hyd and 5OH-5Me-Hyd thus initiating the NIR pathway. We have fully reconstituted the NIR pathway for these lesions in vitro using purified human proteins. Depletion of Nfo in E. coli and APE1 in HeLa cells abolishes the NIR activity in cell-free extracts. Importantly, a number of redundant DNA glycosylase activities can excise hydantoin residues, including human NTH1, NEIL1 and NEIL2 and the former protein being a major DNA glycosylase activity in HeLa cells extracts. CONCLUSIONS/SIGNIFICANCE: This study demonstrates that both BER and NIR pathways can compete and/or back-up each other to remove hydantoin DNA lesions in vivo.
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