Effect of Phosphatase Activity of the Control of Virulence Sensor (CovS) on Clindamycin-Mediated Streptolysin O Production in Group A Streptococcus
Chuan Chiang-Ni, H. J. Tseng, Yong‐An Shi, Cheng‐Hsun Chiu
Abstract
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Chuan Chiang-Ni, H. J. Tseng, Yong‐An Shi, Cheng‐Hsun Chiu
Abstract
Open-access reader
, which is a CovS phosphatase inhibitor, inhibits the CLI-mediated SLO upregulation in a dose-dependent manner in CLI-susceptible and CLI-resistant strains. These results not only reveal that the phosphorylation of response regulator CovR is essential for responding to CLI stimuli, but also suggest that inhibiting the phosphatase activity of CovS could be a potential strategy for the treatment of invasive GAS infection with CLI.
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, which is a CovS phosphatase inhibitor, inhibits the CLI-mediated SLO upregulation in a dose-dependent manner in CLI-susceptible and CLI-resistant strains. These results not only reveal that the phosphorylation of response regulator CovR is essential for responding to CLI stimuli, but also suggest that inhibiting the phosphatase activity of CovS could be a potential strategy for the treatment of invasive GAS infection with CLI.
Key concepts: Streptolysin, Virulence, Microbiology, Streptococcus pyogenes, Clindamycin, Streptococcus, Biology, Group A