ArticleNucleic acids research2010
Repair of mitomycin C mono- and interstrand cross-linked DNA adducts by UvrABC: a new model.
Article in Nucleic acids research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 76 citations in OpenAlex.
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- Mitomycin C as an Anti-Persister Strategy againstAntibiotics (Basel, Switzerland) · 2024Article
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- Insight Into Factors Governing Formation, Synthesis and Stereochemical Configuration of DNA Adducts Formed by Mitomycins.Chemical record (New York, N.Y.) · 2023Review
- The SMC-like RecN protein is at the crossroads of several genotoxic stress responses inFrontiers in microbiology · 2023Article
- RecA and RecB: probing complexes of DNA repair proteins with mitomycin C in liveJournal of the Royal Society, Interface · 2022Article
- Structure and kinase activity of bacterial cell cycle regulator CcrZ.PLoS genetics · 2022Article
- Synthesis of Oligonucleotides Containing Trans Mitomycin C DNA Adducts at NChemistry (Weinheim an der Bergstrasse, Germany) · 2021Article
- Genotoxic Agents Produce Stressor-Specific Spectra of Spectinomycin Resistance Mutations Based on Mechanism of Action and Selection in Bacillus subtilis.Antimicrobial agents and chemotherapy · 2021Article
- Assessment of mitotically inactivated mosquito cell feeder layers produced with mitomycin C.In vitro cellular & developmental biology. Animal · 2021Article
- Antitumor Activity of a Novel Double-Targeted System for Folate Receptor-Mediated Delivery of Mitomycin C.ACS omega · 2020Article
- An Epistasis Analysis ofGenetics · 2020Article
- Enhancing the sensitivity of the thymidine kinase assay by using DNA repair-deficient human TK6 cells.Environmental and molecular mutagenesis · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Mitomycin C induces both MC-mono-dG and cross-linked dG-adducts in vivo. Interstrand cross-linked (ICL) dG-MC-dG-DNA adducts can prevent strand separation. In Escherichia coli cells, UvrABC repairs ICL lesions that cause DNA bending. The mechanisms and consequences of NER of ICL dG-MC-dG lesions that do not induce DNA bending remain unclear. Using DNA fragments containing a MC-mono-dG or an ICL dG-MC-dG adduct, we found (i) UvrABC incises only at the strand containing MC-mono-dG adducts; (ii) UvrABC makes three types of incisions on an ICL dG-MC-dG adduct: type 1, a single 5' incision on 1 strand and a 3' incision on the other; type 2, dual incisions on 1 strand and a single incision on the other; and type 3, dual incisions on both strands; and (iii) the cutting kinetics of type 3 is significantly faster than type 1 and type 2, and all of 3 types of cutting result in producing DSB. We found that UvrA, UvrA+UvrB and UvrA+UvrB+UvrC bind to MC-modified DNA specifically, and we did not detect any UvrB- and UvrB+UvrC-DNA complexes. Our findings challenge the current UvrABC incision model. We propose that DSBs resulted from NER of ICL dG-MC-dG adducts contribute to MC antitumor activity and mutations.
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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.