Like marRAB , acrAB are positively regulated by MarA .
Other regulators of MarA did not contrib-ute to acrAB induction by indole in Salmonella .
8 -- 13 _ shown that MarA , play a role in antimicrobial resistance by activating acrAB
However , acrAB are also induced by stress signals in additional ways , it was suggested that S. enterica to salicylate activates MarA through binding to its repressor , MarR .
However , acrAB are also induced by stress signals in additional ways , it was suggested that exposure of E. coli activates MarA through binding to its repressor , MarR .
These results , together with the results of the induction of acrAB by salicylate in the lack of the induction of acrAB by salicylate in the DmarA mutant strongly support the hypothesis that the salicylate-dependent increase in tolerance to ciprofloxacin in broth at 378C is mediated by the induction of MarA by salicylate .
These results , together with the results of the induction of acrAB by salicylate in the lack of the induction of acrAB by salicylate in the DmarA mutant strongly support the hypothesis that the salicylate-dependent increase in tolerance to ciprofloxacin in broth at 378C is mediated by the induction of MarA by salicylate .
These results , together with the results of the induction of acrAB by salicylate in the lack of the induction of acrAB by salicylate in the DmarA mutant strongly support the hypothesis that the salicylate-dependent increase in tolerance to ciprofloxacin in broth at 378C is mediated by the induction of MarA by salicylate .
These results , together with the results of the induction of acrAB by salicylate in broth at 378C by salicylate in the DmarA mutant strongly support the hypothesis that the salicylate-dependent increase in tolerance to ciprofloxacin in broth at 378C is mediated by the induction of MarA by salicylate .
These results , together with the results of the induction of acrAB by salicylate in broth at 378C by salicylate in the DmarA mutant strongly support the hypothesis that the salicylate-dependent increase in tolerance to ciprofloxacin in broth at 378C is mediated by the induction of MarA by salicylate .
These results , together with the results of the induction of micF by salicylate in the lack of the induction of acrAB by salicylate in the DmarA mutant strongly support the hypothesis that the salicylate-dependent increase in tolerance to ciprofloxacin in broth at 378C is mediated by the induction of MarA by salicylate .
These results , together with the results of the induction of micF by salicylate in the lack of the induction of acrAB by salicylate in the DmarA mutant strongly support the hypothesis that the salicylate-dependent increase in tolerance to ciprofloxacin in broth at 378C is mediated by the induction of MarA by salicylate .
These results , together with the results of the induction of marA by salicylate in the lack of the induction of acrAB by salicylate in the DmarA mutant strongly support the hypothesis that the salicylate-dependent increase in tolerance to ciprofloxacin in broth at 378C is mediated by the induction of MarA by salicylate .
These results , together with the results of the induction of marA by salicylate in the lack of the induction of acrAB by salicylate in the DmarA mutant strongly support the hypothesis that the salicylate-dependent increase in tolerance to ciprofloxacin in broth at 378C is mediated by the induction of MarA by salicylate .
The MarA proteins can activate acrAB expression .
MarA is induced following acrAB
The MarA protein positively regulates transcription of acrAB