
Research Interests: Bacterial Pathogen-Host Cell Interactions Summary: My laboratory is interested understanding and exploiting the complex interplay of microbial pathogens with eukaryotic cells. To that end, we have investigated the key processes of microbial attachment and entry, intracellular survival, and host cell injury in the context of two important human pathogens, Pseudomonas aeruginosa (PA) and Chlamydia trachomatis (CT). Each of these microorganisms has developed a unique strategy for successful survival that involves subverting and exploiting host cell pathways. Dissecting these processes will allow the development of new diagnostics, therapeutics, and vaccines and will provide a unique window into eukaryotic cell biology.
Publications
The Chlamydia effector Dre1 binds dynactin to reposition host organelles during infection.
The Chlamydia effector IncE employs two short linear motifs to reprogram host vesicle trafficking.
Global mapping of the Chlamydia trachomatis conventional secreted effector - host interactome reveals CebN interacts with nucleoporins and Rae1 to impede STAT1 nuclear translocation.
The Chlamydia effector IncE employs two short linear motifs to reprogram host vesicle trafficking.
Spatial control of sensory adaptation modulates mechanosensing in Pseudomonas aeruginosa.
Peptidoglycan-Targeted [18F]3,3,3-Trifluoro-d-alanine Tracer for Imaging Bacterial Infection.
Two antagonistic response regulators control Pseudomonas aeruginosa polarization during mechanotaxis.
Imaging joint infections using D-methyl-11C-methionine PET/MRI: initial experience in humans.
Mechanotaxis directs Pseudomonas aeruginosa twitching motility.
Enabling genetic analysis of diverse bacteria with Mobile-CRISPRi.
Both the N- and C- terminal regions of the Chlamydial inclusion protein D (IncD) are required for interaction with the pleckstrin homology domain of the ceramide transport protein CERT.
Emerging Role of Retromer in Modulating Pathogen Growth.
Targeting the Mucosal Barrier: How Pathogens Modulate the Cellular Polarity Network.
Par3 integrates Tiam1 and phosphatidylinositol 3-kinase signaling to change apical membrane identity.
A scaffold protein connects type IV pili with the Chp chemosensory system to mediate activation of virulence signaling in Pseudomonas aeruginosa.
Chlamydia cell biology and pathogenesis.
Global Mapping of the Inc-Human Interactome Reveals that Retromer Restricts Chlamydia Infection.
Type IV pili mechanochemically regulate virulence factors in Pseudomonas aeruginosa.
The Pseudomonas aeruginosa type III translocon is required for biofilm formation at the epithelial barrier.
Host cell polarity proteins participate in innate immunity to Pseudomonas aeruginosa infection.
Cystic fibrosis epithelial cell and bacterial binding.
Sugar administration is an effective adjunctive therapy in the treatment of Pseudomonas aeruginosa pneumonia.
Chlamydial intracellular survival strategies.
Endosulfatases SULF1 and SULF2 limit Chlamydia muridarum infection.
Lipid acquisition by intracellular Chlamydiae.
Chlamydia trachomatis co-opts GBF1 and CERT to acquire host sphingomyelin for distinct roles during intracellular development.
Subversion of mucosal barrier polarity by pseudomonas aeruginosa.
Cell migration regulates the kinetics of cytokinesis.
Pseudomonas aeruginosa-mediated damage requires distinct receptors at the apical and basolateral surfaces of the polarized epithelium.
Genetic analysis of the regulation of type IV pilus function by the Chp chemosensory system of Pseudomonas aeruginosa.
CbpA: a polarly localized novel cyclic AMP-binding protein in Pseudomonas aeruginosa.
Role of Pseudomonas aeruginosa type III effectors in disease.
Focal adhesion components are essential for mammalian cell cytokinesis.
Roles of type IV pili, flagellum-mediated motility and extracellular DNA in the formation of mature multicellular structures in Pseudomonas aeruginosa biofilms.
RNAi screen reveals an Abl kinase-dependent host cell pathway involved in Pseudomonas aeruginosa internalization.
RNA interference screen identifies Abl kinase and PDGFR signaling in Chlamydia trachomatis entry.
The Pseudomonas aeruginosa type III secreted toxin ExoT is necessary and sufficient to induce apoptosis in epithelial cells.
Use of a novel coinfection system reveals a role for Rac1, H-Ras, and CrkII phosphorylation in Helicobacter pylori-induced host cell actin cytoskeletal rearrangements.
Pseudomonas aeruginosa exploits a PIP3-dependent pathway to transform apical into basolateral membrane.
Copper and nitric oxide meet in the plasma.
Drosophila melanogaster S2 cells: a model system to study Chlamydia interaction with host cells.
An essential, putative MEK kinase of Leishmania major.
The phosphoinositol-3-kinase-protein kinase B/Akt pathway is critical for Pseudomonas aeruginosa strain PAK internalization.
Pseudomonas aeruginosa fimL regulates multiple virulence functions by intersecting with Vfr-modulated pathways.
Lipid raft-mediated entry is not required for Chlamydia trachomatis infection of cultured epithelial cells.
A mycobacterial virulence gene cluster extending RD1 is required for cytolysis, bacterial spreading and ESAT-6 secretion.
Tarp and Arp: How Chlamydia induces its own entry.
Characterization of a complex chemosensory signal transduction system which controls twitching motility in Pseudomonas aeruginosa.
The ADP ribosyltransferase domain of Pseudomonas aeruginosa ExoT contributes to its biological activities.
Effector ExoU from the Type III Secretion System Is An Important Modulator of Gene Expression in Lung Epithelial Cells in Response to Pseudomonas aeruginosa Infection.
Epithelial cell polarity alters Rho-GTPase responses to Pseudomonas aeruginosa.
Effector ExoU from the type III secretion system is an important modulator of gene expression in lung epithelial cells in response to Pseudomonas aeruginosa infection.
Molecular Pathogenesis of Acute Pseudomonas Aeruginosa Infections.
Modulation of cytosolic Ca(2+) concentration in airway epithelial cells by Pseudomonas aeruginosa.
Pseudomonas aeruginosa ExoT acts in vivo as a GTPase-activating protein for RhoA, Rac1, and Cdc42.
Type III protein secretion is associated with poor clinical outcomes in patients with ventilator-associated pneumonia caused by Pseudomonas aeruginosa.
Pseudomonas aeruginosa ExoT inhibits in vitro lung epithelial wound repair.
Rho GTPase activity modulates Pseudomonas aeruginosa internalization by epithelial cells.
Interaction of bacterial pathogens with polarized epithelium.
Host cell-derived sphingolipids are required for the intracellular growth of Chlamydia trachomatis.
The arginine finger domain of ExoT contributes to actin cytoskeleton disruption and inhibition of internalization of Pseudomonas aeruginosa by epithelial cells and macrophages.
Eukaryotic cell uptake of heparin-coated microspheres: a model of host cell invasion by Chlamydia trachomatis.
Pseudomonas aeruginosa induces type-III-secretion-mediated apoptosis of macrophages and epithelial cells.
Pili binding to asialo-GM1 on epithelial cells can mediate cytotoxicity or bacterial internalization by Pseudomonas aeruginosa.
Pseudomonas aeruginosa gene products PilT and PilU are required for cytotoxicity in vitro and virulence in a mouse model of acute pneumonia.
Fusion of Chlamydia trachomatis-containing inclusions is inhibited at low temperatures and requires bacterial protein synthesis.
Mutational analysis of the Chlamydia trachomatis rRNA P1 promoter defines four regions important for transcription in vitro.
Defects in type III secretion correlate with internalization of Pseudomonas aeruginosa by epithelial cells.
PepA, a secreted protein of Pseudomonas aeruginosa, is necessary for cytotoxicity and virulence.
Infection with Chlamydia trachomatis alters the tyrosine phosphorylation and/or localization of several host cell proteins including cortactin.
Identification of Pseudomonas aeruginosa genes required for epithelial cell injury.
Characterization of the Chlamydia trachomatis vacuole and its interaction with the host endocytic pathway in HeLa cells.
Identification of sequences necessary for transcription in vitro from the Chlamydia trachomatis rRNA P1 promoter.
Transcriptional organization and regulation of the dnaK and groE operons of Chlamydia trachomatis.
Characterization of Pseudomonas aeruginosa-induced MDCK cell injury: glycosylation-defective host cells are resistant to bacterial killing.
Stage-specific regulation of protein phosphorylation in Leishmania major.
Cloning and characterization of the RNA polymerase alpha-subunit operon of Chlamydia trachomatis.
Azithromycin-induced block of elementary body formation in Chlamydia trachomatis.
A developmentally regulated chlamydial gene with apparent homology to eukaryotic histone H1.
Heat shock response of murine Chlamydia trachomatis.
Cloning and characterization of RNA polymerase core subunits of Chlamydia trachomatis by using the polymerase chain reaction.
A polymerase chain reaction-based approach to cloning sigma factors from eubacteria and its application to the isolation of a sigma-70 homolog from Chlamydia trachomatis.
21 Identification and Comparison of Putative Chlamydial Promoter Elements.
Chlamydial gene encoding a 70-kilodalton antigen in Escherichia coli: analysis of expression signals and identification of the gene product.
Chlamydial rRNA operons: gene organization and identification of putative tandem promoters.
Phenytoin hypersensitivity: a case of severe acute rhabdomyolysis.
Phenytoin hypersensitivity: a case of severe acute rhabdomyolysis
Evolutionary conservation in the untranslated regions of actin mRNA's
Isolation and characterization of full-length cDNA clones for human a-, b-, and c- actin mRNA's: skeletal but not cytoplasmic actins have an amino terminal cysteine that is subsequently removed
Isolation and characterization of human actin genes. Ph.D. Dissertation, Stanford University
Molecular genetics of human myogenesis
Human cytoplasmic actin proteins are encoded by a multigene family
Isolation and characterization of human actin genes.
Isolation and characterization of human actin genes
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