ArticleAntimicrobial agents and chemotherapy2014
Molecular basis for the differential quinolone susceptibility of mycobacterial DNA gyrase.
Article in Antimicrobial agents and chemotherapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- A high-throughput fluorescent DNA cleavage assay for discovering bacterial DNA gyrase poisons.Nucleic acids research · 2026Article
- Gyrase and Topoisomerase IV: Recycling Old Targets for New Antibacterials to Combat Fluoroquinolone Resistance.ACS infectious diseases · 2024Review
- Isolation of quinic acid from droppedFrontiers in chemistry · 2024Article
- Article
- Synthesis, Docking Studies, and In Vitro Evaluation of Some Novel Thienopyridines and Fused Thienopyridine-Quinolines as Antibacterial Agents and DNA Gyrase Inhibitors.Molecules (Basel, Switzerland) · 2019Article
- Synthesis, antimicrobial evaluation and docking studies of some novel quinazolinone Schiff base derivatives.Research in pharmaceutical sciences · 2018Article
- Boldine-Derived Alkaloids Inhibit the Activity of DNA Topoisomerase I and Growth ofFrontiers in microbiology · 2018Article
- Docking study, synthesis and antimicrobial evaluation of some novel 4-anilinoquinazoline derivatives.Research in pharmaceutical sciences · 2017Article
- Interactions between Quinolones and Bacillus anthracis Gyrase and the Basis of Drug Resistance.Biochemistry · 2017Article
- Topoisomerase Inhibitors: Fluoroquinolone Mechanisms of Action and Resistance.Cold Spring Harbor perspectives in medicine · 2016Review
- Fluoroquinolone interactions with Mycobacterium tuberculosis gyrase: Enhancing drug activity against wild-type and resistant gyrase.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Mechanisms of drug resistance: quinolone resistance.Annals of the New York Academy of Sciences · 2015Review
- Targeting Mycobacterium tuberculosis topoisomerase I by small-molecule inhibitors.Antimicrobial agents and chemotherapy · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA gyrase is a type II topoisomerase that catalyzes the introduction of negative supercoils in the genomes of eubacteria. Fluoroquinolones (FQs), successful as drugs clinically, target the enzyme to trap the gyrase-DNA complex, leading to the accumulation of double-strand breaks in the genome. Mycobacteria are less susceptible to commonly used FQs. However, an 8-methoxy-substituted FQ, moxifloxacin (MFX), is a potent antimycobacterial, and a higher susceptibility of mycobacterial gyrase to MFX has been demonstrated. Although several models explain the mechanism of FQ action and gyrase-DNA-FQ interaction, the basis for the differential susceptibility of mycobacterial gyrase to various FQs is not understood. We have addressed the basis of the differential susceptibility of the gyrase and revisited the mode of action of FQs. We demonstrate that FQs bind both Escherichia coli and Mycobacterium tuberculosis gyrases in the absence of DNA and that the addition of DNA enhances the drug binding. The FQs bind primarily to the GyrA subunit of mycobacterial gyrase, while in E. coli holoenzyme is the target. The binding of MFX to GyrA of M. tuberculosis correlates with its effectiveness as a better inhibitor of the enzyme and its efficacy in cell killing.
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