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Pathogenic Microbiology Commons

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Full-Text Articles in Pathogenic Microbiology

Regulation Of Rab5 Gtpase Activity During Pseudomonas Aeruginosa-Macrophage Interaction, Sushmita Mustafi Oct 2013

Regulation Of Rab5 Gtpase Activity During Pseudomonas Aeruginosa-Macrophage Interaction, Sushmita Mustafi

FIU Electronic Theses and Dissertations

Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen. Several antibiotic resistant strains of P. aeruginosa are commonly found as secondary infection in immune-compromised patients leaving significant mortality and healthcare cost. Pseudomonas aeruginosa successfully avoids the process of phagocytosis, the first line of host defense, by secreting several toxic effectors. Effectors produced from P. aeruginosa Type III secretion system are critical molecules required to disrupt mammalian cell signaling and holds particular interest to the scientists studying host-pathogen interaction. Exoenzyme S (ExoS) is a bi-functional Type III effector that ADP-ribosylates several intracellular Ras (Rat sarcoma) and Rab (Response to abscisic acid) small GTPases …


Pseudomonas Aeruginosa Ampr Transcriptional Regulatory Network, Deepak Balasubramanian Mar 2013

Pseudomonas Aeruginosa Ampr Transcriptional Regulatory Network, Deepak Balasubramanian

FIU Electronic Theses and Dissertations

In Enterobacteriaceae, the transcriptional regulator AmpR, a member of the LysR family, regulates the expression of a chromosomal β-lactamase AmpC. The regulatory repertoire of AmpR is broader in Pseudomonas aeruginosa, an opportunistic pathogen responsible for numerous acute and chronic infections including cystic fibrosis. Previous studies showed that in addition to regulating ampC, P. aeruginosa AmpR regulates the sigma factor AlgT/U and production of some quorum sensing (QS)-regulated virulence factors. In order to better understand the ampR regulon, the transcriptional profiles generated using DNA microarrays and RNA-Seq of the prototypic P. aeruginosa PAO1 strain with its isogenic ampR deletion …