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Jonathan A. Winkler

Researcher at Boston University

Publications -  13
Citations -  2057

Jonathan A. Winkler is an academic researcher from Boston University. The author has contributed to research in topics: Apoptosis & Membrane permeability. The author has an hindex of 8, co-authored 12 publications receiving 1682 citations. Previous affiliations of Jonathan A. Winkler include Howard Hughes Medical Institute.

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Silver Enhances Antibiotic Activity Against Gram-Negative Bacteria

TL;DR: This work shows that silver can be used to enhance the action of existing antibiotics against Gram-negative bacteria, thus strengthening the antibiotic arsenal for fighting bacterial infections.
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Oxidation of the Guanine Nucleotide Pool Underlies Cell Death by Bactericidal Antibiotics

TL;DR: In this paper, the authors proposed a model in which the cytotoxicity of beta-lactams and quinolones predominantly results from lethal double-strand DNA breaks caused by incomplete repair of closely spaced 8-oxo-deoxyguanosine lesions.
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Potentiating antibacterial activity by predictably enhancing endogenous microbial ROS production

TL;DR: It is shown that ROS production can be predictably enhanced in Escherichia coli, increasing the bacteria's susceptibility to oxidative attack and establishing a systems-based method to tune ROS production in bacteria.

Oxidation of the Guanine Nucleotide Pool Underlies Cell Death by Bactericidal Antibiotics

TL;DR: The efforts to understand why DinB (DNA polymerase IV) overproduction is cytotoxic to Escherichia coli led to the unexpected insight that oxidation of guanine to 8-oxo-guanine in the nucleotide pool underlies much of the cell death caused by both DinB overproduction and bactericidal antibiotics.
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Hydroxyurea Induces Hydroxyl Radical-Mediated Cell Death in Escherichia coli

TL;DR: This work uses a systems-level approach to determine the genomic and physiological responses of E. coli to HU treatment and suggests a model by which H U treatment rapidly induces a set of protective responses to manage genomic instability.