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- W2287941708 abstract "Significance Moxifloxacin and other fluoroquinolone antibacterial agents are important antituberculosis therapeutic agents. Fluoroquinolones kill Mycobacterium tuberculosis , the causative agent of tuberculosis, by increasing levels of DNA breaks generated by gyrase, an essential type II topoisomerase that regulates DNA topology. As fluoroquinolone use in antituberculosis regimens is becoming more pronounced, understanding the basis of drug–gyrase interactions and resistance is becoming more important. By using a mechanism-based chemical biology approach, our work identified critical drug features that mediate fluoroquinolone interactions with M. tuberculosis gyrase and determined the biochemical basis for fluoroquinolone resistance caused by the most common clinical mutations in gyrase. These findings allowed us to identify a moxifloxacin derivative that displays enhanced activity against WT gyrase and maintains high activity against clinically relevant resistant enzymes." @default.
- W2287941708 created "2016-06-24" @default.
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- W2287941708 date "2016-01-20" @default.
- W2287941708 modified "2023-10-17" @default.
- W2287941708 title "Fluoroquinolone interactions with <i>Mycobacterium tuberculosis</i> gyrase: Enhancing drug activity against wild-type and resistant gyrase" @default.
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- W2287941708 doi "https://doi.org/10.1073/pnas.1525055113" @default.
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- W2287941708 hasPublicationYear "2016" @default.
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