ReviewChemical research in toxicology2006
Methylating agents and DNA repair responses: Methylated bases and sources of strand breaks.
Review in Chemical research in toxicology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 216 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.
The trial behind it
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
216 citing papers in PubMed, 454 citations in OpenAlex.
- The B. subtilis translesion polymerase Pol Y1 is not strongly recruited to sites of replication upon different types of DNA damage.PLoS genetics · 2026Article
- Article
- Long-Term PET-Nanoplastic Exposure Alters DNA Damage Response Capacity in BEAS-2B Human Bronchial Epithelial Cells.International journal of molecular sciences · 2026Article
- Hsp70 is phosphorylated in a conserved response to DNA damage and contributes to cell cycle control.eLife · 2026Article
- Ethyl methanesulfonate mutagenesis in fungi: genetic mechanisms, applications, and implications for agricultural biotechnology.Archives of microbiology · 2026Review
- "ThebioRxiv : the preprint server for biology · 2026Article
- Exploring the intersection between necromass reutilization and genome protection reveals novel proteins that contribute to both processes in Ustilago maydis.Biology direct · 2026Article
- Agent-specific DNA repair kinetic in 3T3 cells: a comparative study using the in vitro comet assay.Toxicology research · 2025Article
- Review
- Glutathionylated DNA adducts accumulate in mitochondrial DNA and are regulated by AP endonuclease 1 and tyrosyl-DNA phosphodiesterase 1.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A conserved Hsp70 phosphorylation regulates cell cycle progression after DNA damage.bioRxiv : the preprint server for biology · 2025Article
- Prominent fibroblast growth factor 21 with less abundant tumor-associated macrophages in hepatic mass of the conditional mgmt-deleted mice using LysM-Cre system.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Preparation of molecularly imprinted ratiometric fluorescent probe and test strip for visual detection of methyl methanesulfonate.Mikrochimica acta · 2025Article
- Can pristine/modified graphene repair N7-methylated guanine lesions? A DFT study.Journal of molecular modeling · 2025Article
- DNA content, repeatome composition and origin of the Zea mays micronuclei.Scientific reports · 2025Article
- Advantages of Mutant Generation by Genome Rearrangements of Non-Conventional Yeast via Direct Nuclease Transfection.Genes to cells : devoted to molecular & cellular mechanisms · 2025Article
- Genome-wide conditional degron libraries for functional genomics.The Journal of cell biology · 2025Article
- Spontaneous and environment induced genomic alterations in yeast model.Cell insight · 2025Review
- Patterns of spontaneous and induced genomic alterations inApplied and environmental microbiology · 2025Article
- Mechanisms and applications of N-Methyl-N'-nitro-N-nitrosoguanidine in animal tumor models: current situation and challenges.Frontiers in oncology · 2025Review
156 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The chemical methylating agents methylmethane sulfonate (MMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) have been used for decades as classical DNA damaging agents. These agents have been utilized to uncover and explore pathways of DNA repair, DNA damage response, and mutagenesis. MMS and MNNG modify DNA by adding methyl groups to a number of nucleophilic sites on the DNA bases, although MNNG produces a greater percentage of O-methyl adducts. There has been substantial progress elucidating direct reversal proteins that remove methyl groups and base excision repair (BER), which removes and replaces methylated bases. Direct reversal proteins and BER, thus, counteract the toxic, mutagenic, and clastogenic effects of methylating agents. Despite recent progress, the complexity of DNA damage responses to methylating agents is still being discovered. In particular, there is growing understanding of pathways such as homologous recombination, lesion bypass, and mismatch repair that react when the response of direct reversal proteins and BER is insufficient. Furthermore, the importance of proper balance within the steps in BER has been uncovered with the knowledge that DNA structural intermediates during BER are deleterious. A number of issues complicate the elucidation of the downstream responses when direct reversal is insufficient or BER is imbalanced. These include inter-species differences, cell-type-specific differences within mammals and between cancer cell lines, and the type of methyl damage or BER intermediate encountered. MMS also carries a misleading reputation of being a radiomimetic, that is, capable of directly producing strand breaks. This review focuses on the DNA methyl damage caused by MMS and MNNG for each site of potential methylation to summarize what is known about the repair of such damage and the downstream responses and consequences if the damage is not repaired.
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What OpenQuestion holds
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.