A
Angelyca A. Jackson
Researcher at Dartmouth College
Publications - 4
Citations - 182
Angelyca A. Jackson is an academic researcher from Dartmouth College. The author has contributed to research in topics: Virulence & Phosphorylation. The author has an hindex of 4, co-authored 4 publications receiving 161 citations.
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Journal ArticleDOI
Farnesol Induces Hydrogen Peroxide Resistance in Candida albicans Yeast by Inhibiting the Ras-Cyclic AMP Signaling Pathway
TL;DR: Although farnesol induces the accumulation of intracellular reactive oxygen species (ROS), ROS generation is not necessary for the induction of catalase (Cat1)-mediated oxidative-stress resistance.
Journal ArticleDOI
Anr and Its Activation by PlcH Activity in Pseudomonas aeruginosa Host Colonization and Virulence
Angelyca A. Jackson,Maegan J. Gross,Emily F. Daniels,Thomas H. Hampton,John H. Hammond,Isabelle Vallet-Gely,Simon L. Dove,Bruce A. Stanton,Deborah A. Hogan +8 more
TL;DR: Several lines of evidence indicate that Anr is important for the colonization of biotic and abiotic surfaces in both P. aeruginosa PAO1 and PA14 and that increases in Anr activity resulted in enhanced biofilm formation.
Journal ArticleDOI
Tobramycin reduces key virulence determinants in the proteome of Pseudomonas aeruginosa outer membrane vesicles.
Katja Koeppen,Roxanna Barnaby,Angelyca A. Jackson,Scott A. Gerber,Deborah A. Hogan,Bruce A Stanton +5 more
TL;DR: Proteomic analysis of OMVs and biological validation suggest that Tobramycin may improve lung function in CF patients infected with P. aeruginosa by reducing several key virulence factors in OMVs that reduce CFTR Cl- secretion, which is essential for bacterial clearance from the lungs.
Journal ArticleDOI
Global regulator Anr represses PlcH phospholipase activity in Pseudomonas aeruginosa when oxygen is limiting.
TL;DR: The presence of a negative feedback loop in which Anr repressed plcH transcription was demonstrated and it was proposed that this regulation allowed for PlcH levels to be maintained in a way that promotes productive host-pathogen interactions.