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dc.contributor.authorDubreuil, Ron
dc.contributor.authorSegev, Nava
dc.date.accessioned2012-08-16T19:11:24Z
dc.date.available2012-08-16T19:11:24Z
dc.date.issued2011
dc.identifier.bibliographicCitationDubreuil, R. & Segev, N. 2011. Bringing host-cell takeover by pathogenic bacteria to center stage. Cellular Logistics, 1(4): 120-124. doi: 10.4161/cl.1.4.18984en
dc.identifier.issn2159-2780
dc.identifier.otherdoi: 10.4161/cl.1.4.18984
dc.identifier.urihttp://hdl.handle.net/10027/8501
dc.description© 2011 by Landes Bioscience, Cellular Logistics doi: 10.4161/cl.1.4.18984en
dc.description.abstractIntra-cellular pathogenic bacteria contrive processes in their host cell to create a niche for their own reproduction. One way that has emerged by which bacteria do that is delivery of secreted virulence factors, SVFs, to the cytoplasm of the host cells using the bacterial type IV secretion system, T4SS. These SVFs modulate the activity of their target host proteins, which in turn control key cellular processes. A major mechanism for the evolution of SVFs that modulate targets that do not exist in the bacterial kingdom is horizontal gene transfer. Recently, a number of bacterial SVFs were shown to act on two types of targets in host cells. First, a group of several SVFs modulate the activity and localization of one protein: Rab1 GTPase, a key regulator of intra-cellular trafficking. Second, ankyrin repeats-containing SVFs, referred to by microbiologists as Anks, interact with various binding proteins, which in turn regulate a myriad of cellular processes, including apoptosis. Modulation of trafficking and apoptosis are two examples of how invading bacteria takeover their host phagocyte, which instead of destroying the bacteria becomes a factory for its reproduction.en
dc.description.sponsorshipWe thank Nancy Freitag, from the Department of Microbiology at UIC, for helpful suggestions.en
dc.language.isoen_USen
dc.publisherLandes Bioscienceen
dc.titleBringing host-cell takeover by pathogenic bacteria to center stage: Editorialen
dc.typeArticleen


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