The SoxRS response of Escherichia coli is directly activated by redox-cycling drugs rather than by superoxide

The soxRS response of Escherichia coli can be induced in the absence of oxidative stress and oxygen by modulation of NADPH content

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Hydrogen peroxide inactivates the Escherichia coli Isc iron-sulphur assembly system, and OxyR induces the Suf system to compensate

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SoxRS-Mediated Lipopolysaccharide Modification Enhances Resistance against Multiple Drugs in Escherichia coli

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Endogenous Phenazine Antibiotics Promote Anaerobic Survival of Pseudomonas aeruginosa via Extracellular Electron Transfer

(2009) Y. Wang et al.   JOURNAL OF BACTERIOLOGY

Manganese import is a key element of the OxyR response to hydrogen peroxide inEscherichia coli

(2009) Adil Anjem et al.   MOLECULAR MICROBIOLOGY

Cellular Defenses against Superoxide and Hydrogen Peroxide

(2008) James A. Imlay   Annual Review of Biochemistry

Redox Reactions of Phenazine Antibiotics with Ferric (Hydr)oxides and Molecular Oxygen

(2008) Yun Wang et al.   ENVIRONMENTAL SCIENCE & TECHNOLOGY

Crystal structure of the [2Fe-2S] oxidative-stress sensor SoxR bound to DNA

(2008) S. Watanabe et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Redox-Active Antibiotics Control Gene Expression and Community Behavior in Divergent Bacteria

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