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Titlebook: Bacterial Virulence Factors and Rho GTPases; Patrice Boquet (Professor Dr.),Emmanuel Lemichez ( Book 2005 The Editor(s) (if applicable) an

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Modulation of Rho GTPases and the Actin Cytoskeleton by YopT of , ,minal cysteine. This cleavage results in release of RhoA from the cell membrane and subsequently in blockage of stress fiber formation. Thus YopT impairs cellular functions associated with cytoskeleton rearrangements.
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,Grundbegriffe der Erzählanalyse,g pathways in infected host cells. In contrast, a domain of SptP inactivates RhoGTPases by mimicking the activity of eukaryotic GTPase-activating proteins. The .-host cell interaction provides an excellent example for the use of molecular mimicry by bacterial pathogens.
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Triggered Phagocytosis by ,: Bacterial Molecular Mimicry of RhoGTPase Activation/Deactivation,lls. Here, we focus on the functional mechanism of three of these toxins: SopE, SopE2, and SptP. All three effector proteins change the GTP/GDP loading state of RhoGTPases by transient interactions. SopE and SopE2 mimic eukaryotic G-nucleotide exchange factors and thereby activate RhoGTPase signalin
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Regulation of Phagocytosis by Rho GTPases,de, and eventually present peptides derived from particulate antigens. The phagocytic process comprises several sequential and complex events initiated by the recognition of ligands on the surface of the particles by specific receptors on the surface of the phagocytic cells. Receptor clustering at t
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The Immunological Synapse and Rho GTPases,now recognized as pivotal regulators of antigen-specific T cell activation by APCs and immunological synapse formation. This review summarizes recent advances in our understanding of how Rho GTPase-dependent pathways control T lymphocyte motility, polarization and activation.
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Rho GTPases and the Control of the Oxidative Burst in Polymorphonuclear Leukocytes,en species (ROS) that are used to kill bacteria within the phagosome. This chapter describes this multicomponent NADPH oxidase system, one of the first cellular systems shown to be directly regulated by Rac GTPases. We present current models of NADPH oxidase regulation by Rac2 and describe how Rac2
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The Type III Cytotoxins of , and , That Modulate the Actin Cytoskeleton,tudies have addressed the molecular interactions of these toxins with host cell signaling pathways and how toxins modulate cellular physiology. Although each individual toxin has a unique mode of action, general themes have started to emerge between bacterial pathogens. During the course of an infec
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