2013
DOI: 10.1111/mmi.12410
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Comparative study ofSoxRactivation by redox‐active compounds

Abstract: Summary SoxR from E. coli and related enterobacteria is activated by a broad range of redox-active compounds through oxidation or nitrosylation of its [2Fe-2S] cluster. Activated SoxR then induces SoxS, which subsequently activates more than 100 genes in response. In contrast, non-enteric SoxRs directly activate their target genes in response to redox-active compounds that include endogenously produced metabolites. We compared the responsiveness of SoxRs from Streptomyces coelicolor (ScSoxR), Pseudomonas aerug… Show more

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Cited by 57 publications
(84 citation statements)
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“…It is unclear why high concentrations of PL and PMS treatment were not sufficient to induce sinE gene. This pattern was also reported when S. coelicolor was exposed to high concentrations of RACs (20). High concentrations of these chemicals may impose transcriptional defects, or they may trigger the degradation of the SoxR Fe-S cluster beyond its functional oxidized form.…”
Section: Resultssupporting
confidence: 68%
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“…It is unclear why high concentrations of PL and PMS treatment were not sufficient to induce sinE gene. This pattern was also reported when S. coelicolor was exposed to high concentrations of RACs (20). High concentrations of these chemicals may impose transcriptional defects, or they may trigger the degradation of the SoxR Fe-S cluster beyond its functional oxidized form.…”
Section: Resultssupporting
confidence: 68%
“…The redox potentials of all RACs individually could not explain the differential sensitivity of AoSoxR to various RACs. Unlike ScSoxR, which could not sense PQ (20), AoSoxR was activated by PQ in a wide concentration range, with maximal expression between 1 and 1.5 mM (Fig. 4).…”
Section: Resultsmentioning
confidence: 99%
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“…As this was, to our knowledge, the first demonstration of SoxR homolog activation by an endogenous metabolite, it led to a reevaluation of the physiological activators of SoxR in E. coli, where previous studies had led to a long-standing model of SoxR activation by superoxide (typically generated by xenobiotics) (26)(27)(28)(29). Although still under discussion in the community (30)(31)(32)(33), the current prevailing view is that endogenously produced or exogenously added redox-cycling compounds activate SoxR by direct oxidation of its iron-sulfur cluster and that the SoxR targets, or targets of transcription factors controlled by SoxR, function to protect cells from at least some of these inducing compounds (28,34).…”
mentioning
confidence: 99%