ArticleJournal of molecular cell biology2016
Mismatch repair proteins recruit DNA methyltransferase 1 to sites of oxidative DNA damage.
Article in Journal of molecular cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
53 citing papers in PubMed, 85 citations in OpenAlex.
- Dnmt1 associatedEpigenetics · 2026Article
- Association Between Biochemical, Inflammatory, Oxidative Stress and DNA Methylation Biomarkers with Perceived Stress in Mexican Individuals.Biomolecules · 2026Article
- NOX4-derived oxidative DNA damage impairs thyroid differentiation through an epigenetic mechanism in BRAF-mutated radioactive iodine refractory papillary thyroid cancer cells.International journal of biological sciences · 2026Article
- Normal bronchial field basal cells show persistent methylome-wide impact of tobacco smoking, including in known cancer genes.Epigenetics · 2025Article
- Reproductive Dysfunction and Testicular Epigenetic Alterations in Male Rats with Experimental Amebiasis: Evaluation of SPATA6 Methylation and Therapeutic Outcomes.Acta parasitologica · 2025Article
- The OGG1 Ser326Cys polymorphism: molecular mechanisms of disease susceptibility and precision medicine applications.Clinical epigenetics · 2025Review
- SIRT1 as a potential target for age-related eye diseases: mechanisms and therapeutic strategies.Human cell · 2025Review
- SIRT1 as a masterful reciprocal regulator of molecular mechanisms and signaling pathways involved in tumor growth and expansion.Clinical and experimental medicine · 2025Review
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- MSH2 is not required for either maintenance of DNA methylation or repeat contraction at the FMR1 locus in fragile X syndrome or the FXN locus in Friedreich's ataxia.Epigenetics & chromatin · 2025Article
- From genetic variants to therapeutic targets: insights into understanding rheumatoid arthritis.Frontiers in immunology · 2025Review
- The Role of SIRT1 in Leukemia.Current treatment options in oncology · 2024Review
- Rhabdomyosarcoma: Current Therapy, Challenges, and Future Approaches to Treatment Strategies.Cancers · 2023Review
- Recent advances in understanding DNA methylation of prostate cancer.Frontiers in oncology · 2023Review
- Making sense of the ageing methylome.Nature reviews. Genetics · 2022Review
- The mismatch-repair proteins MSH2 and MSH6 interact with the imprinting control regions through the ZFP57-KAP1 complex.Epigenetics & chromatin · 2022Article
- Colon Tumors in Enterotoxigenic Bacteroides fragilis (ETBF)-Colonized Mice Do Not Display a Unique Mutational Signature but Instead Possess Host-Dependent Alterations in the APC Gene.Microbiology spectrum · 2022Article
- Review
- DissectingCancers · 2022Review
- Decitabine improves MMS-induced retinal photoreceptor cell damage by targeting DNMT3A and DNMT3B.Frontiers in molecular neuroscience · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
At sites of chronic inflammation, epithelial cells are exposed to high levels of reactive oxygen species and undergo cancer-associated DNA methylation changes, suggesting that inflammation may initiate epigenetic alterations. Previously, we demonstrated that oxidative damage causes epigenetic silencing proteins to become part of a large complex that is localized to GC-rich regions of the genome, including promoter CpG islands that are epigenetically silenced in cancer. However, whether these proteins were recruited directly to damaged DNA or during the DNA repair process was unknown. Here we demonstrate that the mismatch repair protein heterodimer MSH2-MSH6 participates in the oxidative damage-induced recruitment of DNA methyltransferase 1 (DNMT1) to chromatin. Hydrogen peroxide treatment induces the interaction of MSH2-MSH6 with DNMT1, suggesting that the recruitment is through a protein-protein interaction. Importantly, the reduction in transcription for genes with CpG island-containing promoters caused by oxidative damage is abrogated by knockdown of MSH6 and/or DNMT1. Our findings provide evidence that the role of DNMT1 at sites of oxidative damage is to reduce transcription, potentially preventing transcription from interfering with the repair process. This study uniquely brings together several factors that are known to contribute to colon cancer, namely inflammation, mismatch repair proteins, and epigenetic changes.
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Registered trials
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.