ArticleProceedings of the National Academy of Sciences of the United States of America2009
An 8-oxo-guanine repair pathway coordinated by MUTYH glycosylase and DNA polymerase lambda.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 118 citations in OpenAlex.
- OGG1 and MUTYH DNA Glycosylases, the Dynamic Duo Against 8-Oxoguanine DNA Lesion: Structure, Regulation, and Novel Emerging Roles.Biomolecules · 2026Review
- 8-Oxoguanine: A Lesion, an Epigenetic Mark, or a Molecular Signal?International journal of molecular sciences · 2025Review
- Mono-allelic MUTYH mutation as the likely inherited etiology of hereditary breast cancer in a patient from a multi-cancer family- report of a family and literature review.BMC medical genomics · 2025Review
- Oxidative Stress and DNA Damage at Telomeres.Cold Spring Harbor perspectives in biology · 2025Review
- OGG1 and MUTYH repair activities promote telomeric 8-oxoguanine induced senescence in human fibroblasts.Nature communications · 2025Article
- Analysis of Nucleotide Variations in Human G-Quadruplex Forming Regions Associated with Disease States.Genes · 2023Article
- Base Excision DNA Repair in Plants:International journal of molecular sciences · 2023Review
- UV-DDB as a General Sensor of DNA Damage in Chromatin: Multifaceted Approaches to Assess Its Direct Role in Base Excision Repair.International journal of molecular sciences · 2023Review
- 8-Oxo-2'-deoxyguanosine Replication in Mutational Hot Spot Sequences of theChemical research in toxicology · 2023Article
- Polymerases and DNA Repair in Neurons: Implications in Neuronal Survival and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2022Review
- Review
- Sequence context effects of replication of Fapy•dG in three mutational hot spot sequences of the p53 gene in human cells.DNA repair · 2021Article
- Human MettL3-MettL14 RNA adenine methyltransferase complex is active on double-stranded DNA containing lesions.Nucleic acids research · 2021Article
- Genome-Wide Analysis of Cadmium-Induced, Germline Mutations in a Long-TermEnvironmental health perspectives · 2021Article
- Single molecule analysis indicates stimulation of MUTYH by UV-DDB through enzyme turnover.Nucleic acids research · 2021Article
- Structure of the mammalian adenine DNA glycosylase MUTYH: insights into the base excision repair pathway and cancer.Nucleic acids research · 2021Article
- A Role for N6-Methyladenine in DNA Damage Repair.Trends in biochemical sciences · 2021Review
- Roles for the 8-Oxoguanine DNA Repair System in Protecting Telomeres From Oxidative Stress.Frontiers in cell and developmental biology · 2021Review
- The DNA repair enzyme MUTYH potentiates cytotoxicity of the alkylating agent MNNG by interacting with abasic sites.The Journal of biological chemistry · 2020Article
- Estimation of the Mutagenic Potential of 8-Oxog in Nuclear Extracts of Mouse Cells Using the "Framed Mirror" Method.Methods and protocols · 2020Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) interact with DNA, frequently generating highly mutagenic 7,8-dihydro-8-oxoguanine (8-oxo-G) lesions. Replicative DNA polymerases (pols) often misincorporate adenine opposite 8-oxo-G. The subsequent repair mechanism allowing the removal of adenine and formation of C:8-oxo-G base pair is essential to prevent C:G to A:T transversion mutations. Here, we show by immunofluorescence experiments, in cells exposed to ROS, the involvement of MutY glycosylase homologue (MUTYH) and DNA pol lambda in the repair of A:8-oxo-G mispairs. We observe specific recruitment of MUTYH, DNA pol lambda, proliferating cell nuclear antigen (PCNA), flap endonuclease 1 (FEN1) and DNA ligases I and III from human cell extracts to A:8-oxo-G DNA, but not to undamaged DNA. Using purified human proteins and a DNA template, we reconstitute the full pathway for the faithful repair of A:8-oxo-G mispairs involving MUTYH, DNA pol lambda, FEN1, and DNA ligase I. These results reveal a cellular response pathway to ROS, important to sustain genomic stability and modulate carcinogenesis.
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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.