Joanne Engel

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi Tarp and Arp: How Chlamydia induces its own entry
    Joanne Engel
    University of California, P.O. Box 0654, Room C443, 521 Parnassus Avenue, San Francisco, CA 94143-0654, USA
    Proc Natl Acad Sci U S A 101:9947-8. 2004
  2. ncbi Role of Pseudomonas aeruginosa type III effectors in disease
    Joanne Engel
    Departments of Microbiology Immunology and Medicine, Microbial Pathogenesis and Host Defense Program, Box 0654 UCSF, 513 Parnassus Ave, San Francisco, CA 94143, USA
    Curr Opin Microbiol 12:61-6. 2009
  3. ncbi The Pseudomonas aeruginosa type III secreted toxin ExoT is necessary and sufficient to induce apoptosis in epithelial cells
    Sasha H Shafikhani
    Department of Medicine, University of California, San Francisco, CA 94143, USA
    Cell Microbiol 10:994-1007. 2008
  4. ncbi Focal adhesion components are essential for mammalian cell cytokinesis
    Sasha H Shafikhani
    Department of Medicine, University of California, San Francisco, California, USA
    Cell Cycle 7:2868-76. 2008
  5. ncbi The ubiquitin ligase Cbl-b limits Pseudomonas aeruginosa exotoxin T-mediated virulence
    Priya Balachandran
    Program in Microbial Pathogenesis and Host Defense, University of California, San Francisco, San Francisco, California 94143, USA
    J Clin Invest 117:419-27. 2007
  6. ncbi Pseudomonas aeruginosa type III-secreted toxin ExoT inhibits host-cell division by targeting cytokinesis at multiple steps
    Sasha H Shafikhani
    Division of Infectious Diseases, Department of Medicine, University of California, San Francisco, CA 94143, USA
    Proc Natl Acad Sci U S A 103:15605-10. 2006
  7. ncbi Pseudomonas aeruginosa exploits a PIP3-dependent pathway to transform apical into basolateral membrane
    Arlinet Kierbel
    Department of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA
    J Cell Biol 177:21-7. 2007
  8. ncbi Genetic analysis of the regulation of type IV pilus function by the Chp chemosensory system of Pseudomonas aeruginosa
    Jacob J Bertrand
    Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94143, USA
    J Bacteriol 192:994-1010. 2010
  9. ncbi 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
    Sabine Brandt
    Department of Medical Microbiology, Otto von Guericke University, Magdeburg, Germany
    FEMS Immunol Med Microbiol 50:190-205. 2007

Research Grants

  1. Mechanism of Pseudomonas-mediated epithelial cell damage
    Joanne Engel; Fiscal Year: 2007
  2. Novel approaches to identify host genes required for Chlamydia pathogenesis
    Joanne Engel; Fiscal Year: 2007
  3. Micorbial Pathogenesis and Host Defense
    Joanne Engel; Fiscal Year: 2007
  4. Mechanism of Pseudomonas-mediated epithelial cell damage
    Joanne Engel; Fiscal Year: 2007
  5. New approaches to Study Pseudomonas-host interactions
    Joanne Engel; Fiscal Year: 2009
  6. Novel approaches to identify host genes required for Chlamydia pathogenesis
    Joanne N Engel; Fiscal Year: 2010
  7. Mechanism of Pseudomonas-mediated epithelial cell damage
    Joanne N Engel; Fiscal Year: 2010
  8. GENERAL CLINICAL RESEARCH CENTER
    David Kessler; Fiscal Year: 2006
  9. New approaches to studying host-chlamydia interactions
    Joanne Engel; Fiscal Year: 2006
  10. MECHANISM OF PSEUDOMONAS MEDIATED EPITHELIAL CELL DAMAGE
    Joanne Engel; Fiscal Year: 2002

Collaborators

Detail Information

Publications9

  1. ncbi Tarp and Arp: How Chlamydia induces its own entry
    Joanne Engel
    University of California, P.O. Box 0654, Room C443, 521 Parnassus Avenue, San Francisco, CA 94143-0654, USA
    Proc Natl Acad Sci U S A 101:9947-8. 2004
  2. ncbi Role of Pseudomonas aeruginosa type III effectors in disease
    Joanne Engel
    Departments of Microbiology Immunology and Medicine, Microbial Pathogenesis and Host Defense Program, Box 0654 UCSF, 513 Parnassus Ave, San Francisco, CA 94143, USA
    Curr Opin Microbiol 12:61-6. 2009
    ....
  3. ncbi The Pseudomonas aeruginosa type III secreted toxin ExoT is necessary and sufficient to induce apoptosis in epithelial cells
    Sasha H Shafikhani
    Department of Medicine, University of California, San Francisco, CA 94143, USA
    Cell Microbiol 10:994-1007. 2008
    ..Our data also indicate that the T3SS apparatus can cause necrotic cell death, which is effectively blocked by ExoT, suggesting that P. aeruginosa may have evolved strategies to prevent T3SS-induced necrosis...
  4. ncbi Focal adhesion components are essential for mammalian cell cytokinesis
    Sasha H Shafikhani
    Department of Medicine, University of California, San Francisco, California, USA
    Cell Cycle 7:2868-76. 2008
    ..These studies reveal a novel role for Crk and paxillin in cytokinesis and suggest that focal adhesion complex, as a unit, may partake in this fundamental cellular process...
  5. ncbi The ubiquitin ligase Cbl-b limits Pseudomonas aeruginosa exotoxin T-mediated virulence
    Priya Balachandran
    Program in Microbial Pathogenesis and Host Defense, University of California, San Francisco, San Francisco, California 94143, USA
    J Clin Invest 117:419-27. 2007
    ..To the best of our knowledge, this represents the first identification of a mammalian gene product that is specifically required for in vivo resistance to disease mediated by a type III-secreted effector...
  6. ncbi Pseudomonas aeruginosa type III-secreted toxin ExoT inhibits host-cell division by targeting cytokinesis at multiple steps
    Sasha H Shafikhani
    Division of Infectious Diseases, Department of Medicine, University of California, San Francisco, CA 94143, USA
    Proc Natl Acad Sci U S A 103:15605-10. 2006
    ..These findings provide an example of a bacterial pathogen targeting cytokinesis...
  7. ncbi Pseudomonas aeruginosa exploits a PIP3-dependent pathway to transform apical into basolateral membrane
    Arlinet Kierbel
    Department of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA
    J Cell Biol 177:21-7. 2007
    ..The end result is that this bacterium transforms AP into BL membrane, creating a local microenvironment that facilitates its colonization and entry into the mucosal barrier...
  8. ncbi Genetic analysis of the regulation of type IV pilus function by the Chp chemosensory system of Pseudomonas aeruginosa
    Jacob J Bertrand
    Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94143, USA
    J Bacteriol 192:994-1010. 2010
    ..We show that PilA is a negative regulator of pilA transcription in P. aeruginosa and that the Chp system functionally regulates pilA transcription by controlling PilA import and export...
  9. ncbi 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
    Sabine Brandt
    Department of Medical Microbiology, Otto von Guericke University, Magdeburg, Germany
    FEMS Immunol Med Microbiol 50:190-205. 2007
    ..In addition, we show that ADP-ribosylation of CrkII by ExoT blocks phosphorylation of CrkII at Y-221, which is also important for the CagA-induced signalling...

Research Grants35

  1. Mechanism of Pseudomonas-mediated epithelial cell damage
    Joanne Engel; Fiscal Year: 2007
    ..We will test the hypothesis that specific components of type IV pill are required for discrete steps in type Ill-mediated secretion and translocation. ..
  2. Novel approaches to identify host genes required for Chlamydia pathogenesis
    Joanne Engel; Fiscal Year: 2007
    ..Chlamydia species are an important cause of human diseases world-wide. This grant will discover what host genes are required for infection. This may allow the development of new drug and vaccine targets. ..
  3. Micorbial Pathogenesis and Host Defense
    Joanne Engel; Fiscal Year: 2007
    ..This new T32 grant application describes the new program at UCSF in Microbial Pathogenesis and Host Defense that will train the next generation of scientists who can combat disease through advances in basic and translational research. ..
  4. Mechanism of Pseudomonas-mediated epithelial cell damage
    Joanne Engel; Fiscal Year: 2007
    ..We will test the hypothesis that specific components of type IV pill are required for discrete steps in type Ill-mediated secretion and translocation. ..
  5. New approaches to Study Pseudomonas-host interactions
    Joanne Engel; Fiscal Year: 2009
    ..abstract_text> ..
  6. Novel approaches to identify host genes required for Chlamydia pathogenesis
    Joanne N Engel; Fiscal Year: 2010
    ..Chlamydia species are an important cause of human diseases world-wide. This grant will discover what host genes are required for infection. This may allow the development of new drug and vaccine targets. ..
  7. Mechanism of Pseudomonas-mediated epithelial cell damage
    Joanne N Engel; Fiscal Year: 2010
    ..It opens up the possibility of targeting host cell processes to treat infectious diseases. ..
  8. GENERAL CLINICAL RESEARCH CENTER
    David Kessler; Fiscal Year: 2006
    ..As we do so, we will continue to perform this research with the highest standards of patient care, ethics, safety and regulatory compliance. ..
  9. New approaches to studying host-chlamydia interactions
    Joanne Engel; Fiscal Year: 2006
    ..trachomatis infection. Together, these studies will significantly advance our knowledge of infectious disease pathogenesis and pave the way for new therapies and vaccines. ..
  10. MECHANISM OF PSEUDOMONAS MEDIATED EPITHELIAL CELL DAMAGE
    Joanne Engel; Fiscal Year: 2002
    ..In addition, the study of the complex interplay between P. aeruginosa and the host epithelium may reveal new insights into epithelial cell biology. ..
  11. BIOGENESIS OF THE CHLAMYDIA TRACHOMATIS VACUOLE
    Joanne Engel; Fiscal Year: 2004
    ..trachomatis vacuole. This will help to further define the pathway involved. These studies may lead to the development of new anti-chlamydial drug therapies and further our understanding of lipid trafficking in eukaryotic cells. ..
  12. New approaches to Study Pseudomonas-host interactions
    Joanne N Engel; Fiscal Year: 2010
    ..Pseudomonas is able to directly enter into cells and this is important in its ability to cause disease. We are investigating the mechanisms by which it enters into cells. This may lead to novel therapeutic approaches. ..