| Literature DB >> 25534729 |
Quanxin Long1, Qinglin Du2, Tiwei Fu2, Karl Drlica3, Xilin Zhao4, Jianping Xie5.
Abstract
The absence of the Holliday-junction Ruv resolvase of Mycobacterium smegmatis increased the bacteriostatic and bactericidal activities of the fluoroquinolone moxifloxacin, an important antituberculosis agent. The treatment of ruvAB-deficient cells with thiourea and 2,2'-bipyridyl lowered moxifloxacin lethality to wild-type levels, indicating that the absence of ruvAB stimulates a lethal pathway involving reactive oxygen species. A hexapeptide that traps the Holliday junction substrate of RuvAB potentiated moxifloxacin-mediated lethality, supporting the development of small-molecule enhancers for moxifloxacin activity against mycobacteria.Entities:
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Year: 2014 PMID: 25534729 PMCID: PMC4325773 DOI: 10.1128/AAC.04434-14
Source DB: PubMed Journal: Antimicrob Agents Chemother ISSN: 0066-4804 Impact factor: 5.191