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Microbiology and Molecular Biology Reviews, December 2007, p. 636-652, Vol. 71, No. 4
1092-2172/07/$08.00+0     doi:10.1128/MMBR.00023-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Manipulation of Rab GTPase Function by Intracellular Bacterial Pathogens

John H. Brumell1,2 and Marci A. Scidmore3*

Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada,1 Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5S 1A8, Canada,2 Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, New York 148533

Summary: Intracellular bacterial pathogens have evolved highly specialized mechanisms to enter and survive within their eukaryotic hosts. In order to do this, bacterial pathogens need to avoid host cell degradation and obtain nutrients and biosynthetic precursors, as well as evade detection by the host immune system. To create an intracellular niche that is favorable for replication, some intracellular pathogens inhibit the maturation of the phagosome or exit the endocytic pathway by modifying the identity of their phagosome through the exploitation of host cell trafficking pathways. In eukaryotic cells, organelle identity is determined, in part, by the composition of active Rab GTPases on the membranes of each organelle. This review describes our current understanding of how selected bacterial pathogens regulate host trafficking pathways by the selective inclusion or retention of Rab GTPases on membranes of the vacuoles that they occupy in host cells during infection.


* Corresponding author. Mailing address: Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853. Phone: (607) 253-4059. Fax: (607) 253-3384. E-mail: ms299{at}cornell.edu


Microbiology and Molecular Biology Reviews, December 2007, p. 636-652, Vol. 71, No. 4
1092-2172/07/$08.00+0     doi:10.1128/MMBR.00023-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.







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Appl. Environ. Microbiol. Infect. Immun. Eukaryot. Cell
Mol. Cell. Biol. J. Virol. J. Bacteriol.
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Copyright © 2007 by the American Society for Microbiology. All rights reserved.