ArticleAntimicrobial agents and chemotherapy2013
SatR is a repressor of fluoroquinolone efflux pump SatAB.
Article in Antimicrobial agents and chemotherapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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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.
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Who cites it
7 citing papers in PubMed.
- Regulatory Roles of a Novel MarR-like Protein Lmo0840 in Tetracycline-Associated Growth Phenotype and Virulence ofMicroorganisms · 2026Article
- Review
- Assessment of microbiota in the gut and upper respiratory tract associated with SARS-CoV-2 infection.Microbiome · 2023Article
- How Streptococcus suis escapes antibiotic treatments.Veterinary research · 2022Review
- Role of the Two-Component System CiaRH in the Regulation of Efflux Pump SatAB and Its Correlation with Fluoroquinolone Susceptibility.Microbiology spectrum · 2022Article
- Upregulation of the PatAB Transporter Confers Fluoroquinolone Resistance toFrontiers in microbiology · 2017Article
- The Bacillus subtilis tyrZ gene encodes a highly selective tyrosyl-tRNA synthetase and is regulated by a MarR regulator and T box riboswitch.Journal of bacteriology · 2015Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Streptococcus suis is an emerging zoonotic agent responsible for high-mortality outbreaks among the human population in China. In this species, the ABC transporter SatAB mediates fluoroquinolone resistance when overexpressed. Here, we describe and characterize satR, an open reading frame (ORF) encoding a MarR superfamily regulator that acts as a repressor of satAB. satR is cotranscribed with satAB, and its interruption entails the overexpression of the pump, leading to a clinically relevant increase in resistance to fluoroquinolones.
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