ArticleDNA repair2008
DNA mismatch repair-induced double-strand breaks.
Article in DNA repair, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 167 citations in OpenAlex.
- NUDT5 regulates purine metabolism and thiopurine sensitivity by interacting with PPAT.Science (New York, N.Y.) · 2025Article
- DNA repair and the contribution to chemotherapy resistance.Genome medicine · 2025Review
- Mechanisms and applications of N-Methyl-N'-nitro-N-nitrosoguanidine in animal tumor models: current situation and challenges.Frontiers in oncology · 2025Review
- Loss of OScientific reports · 2024Article
- TDP43 interacts with MLH1 and MSH6 proteins in a DNA damage-inducible manner.Molecular brain · 2024Article
- TDP43 Interacts with MLH1 and MSH6 Proteins in A DNA Damage-Inducible Manner.Research square · 2024Article
- Prophage-like gene transfer agents promote Caulobacter crescentus survival and DNA repair during stationary phase.PLoS biology · 2022Article
- CNOT6: A Novel Regulator of DNA Mismatch Repair.Cells · 2022Article
- Article
- Yeast mismatch repair components are required for stable inheritance of gene silencing.PLoS genetics · 2020Article
- Article
- Radiation resistance in thermophiles: mechanisms and applications.World journal of microbiology & biotechnology · 2017Review
- Article
- Distinct Phenotypes Caused by Mutation of MSH2 in Trypanosome Insect and Mammalian Life Cycle Forms Are Associated with Parasite Adaptation to Oxidative Stress.PLoS neglected tropical diseases · 2015Article
- Oxidative DNA damage is instrumental in hyperreplication stress-induced inviability of Escherichia coli.Nucleic acids research · 2014Article
- Complete genome sequence of the Radiation-Resistant bacterium Rubrobacter radiotolerans RSPS-4.Standards in genomic sciences · 2014Article
- Article
- High efficiency generalized transduction in Escherichia coli O157:H7.F1000Research · 2013Article
- DNA Mismatch Repair.EcoSal Plus · 2012Article
- Article
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
Escherichia coli dam mutants are sensitized to the cytotoxic action of base analogs, cisplatin and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), while their mismatch repair (MMR)-deficient derivatives are tolerant to these agents. We showed previously, using pulse field gel electrophoresis (PFGE), that MMR-mediated double-strand breaks (DSBs) are produced by cisplatin in dam recB(Ts) cells at the non-permissive temperature. We demonstrate here that the majority of these DSBs require DNA replication for their formation, consistent with a model in which replication forks collapse at nicks or gaps formed during MMR. DSBs were also detected in dam recB(Ts) ada ogt cells exposed to MNNG in a dose- and MMR-dependent manner. In contrast to cisplatin, the formation of these DSBs was not affected by DNA replication and it is proposed that two separate mechanisms result in DSB formation. Replication-independent DSBs arise from overlapping base excision and MMR repair tracts on complementary strands and constitute the majority of detectable DSBs in dam recB(Ts) ada ogt cells exposed to MNNG. Replication-dependent DSBs result from replication fork collapse at O(6)-methylguanine (O(6)-meG) base pairs undergoing MMR futile cycling and are more likely to contribute to cytotoxicity. This model is consistent with the observation that fast-growing dam recB(Ts) ada ogt cells, which have more chromosome replication origins, are more sensitive to the cytotoxic effect of MNNG than the same cells growing slowly.
Indexed as
Identifiers
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.