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W. James Gooderham

Researcher at University of British Columbia

Publications -  7
Citations -  1029

W. James Gooderham is an academic researcher from University of British Columbia. The author has contributed to research in topics: Pseudomonas aeruginosa & Polymyxin B. The author has an hindex of 6, co-authored 7 publications receiving 945 citations.

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Adaptive Resistance to the “Last Hope” Antibiotics Polymyxin B and Colistin in Pseudomonas aeruginosa Is Mediated by the Novel Two-Component Regulatory System ParR-ParS

TL;DR: The identification and characterization of a novel P. aeruginosa two-component regulator affecting polymyxin-adaptive resistance, ParR-ParS (PA1799-PA1798), which was required for activation of the arnBCADTEF LPS modification operon in the presence of subinhibitory concentrations of polymyXin, colistin, or the bovine peptide indolicidin, leading to increased resistance to various polycationic
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Regulation of virulence and antibiotic resistance by two‐component regulatory systems in Pseudomonas aeruginosa

TL;DR: In this paper, the authors summarize the current body of knowledge of these and other two-component systems that provides insight into the complex regulation of virulence and resistance in Pseudomonas aeruginosa.
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Construction of a mini-Tn5-luxCDABE mutant library in Pseudomonas aeruginosa PAO1: A tool for identifying differentially regulated genes

TL;DR: This report describes the construction of a mini-Tn5-luxCDABE mutant library and a high-throughput inverse PCR method to amplify DNA flanking the site of insertion for sequencing and insertion site mapping and demonstrates the utility of chromosomal lux fusions.
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The Two-Component System CprRS Senses Cationic Peptides and Triggers Adaptive Resistance in Pseudomonas aeruginosa Independently of ParRS

TL;DR: It was demonstrated that, following exposure to inducing antimicrobial peptides, cprRS mutants did not become adaptively resistant to polymyxins as was observed for wild-type cells, and these findings provide greater insight into the complex regulation of LPS modification in Pseudomonas aeruginosa.
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The sensor kinase PhoQ mediates virulence in Pseudomonas aeruginosa.

TL;DR: This study demonstrated that mutation of phoQ caused reduced twitching motility, biofilm formation and rapid attachment to surfaces, 2.2-fold reduced cytotoxicity to human lung epithelial cells, substantially reduced lettuce leaf virulence, and a major, 10 000-fold reduction in competitiveness in chronic rat lung infections.