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Characterization of a new response to bacterial pore-forming toxin that promotes cell survival in a caspase-1 dependent activation of SREBPs

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Defense Thèse de doctorat : Univ. Genève, 2006 - Sc. 3801 - 2006/10/16
Abstract Many pathogenic organisms produce poreforming toxins as virulence factors. Target cells however mount a response to such membrane damage. Here we show that toxin-induced membrane permeabilization leads to a decrease in cytoplasmic potassium, which promotes the formation of a multiprotein oligomeric innate immune complex, called the inflammasome, and the activation of caspase-1. Further, we find that when rendered proteolytic in this context caspase-1 induces the activation of the central regulators of membrane biogenesis, the Sterol Regulatory Element Binding Proteins (SREBPs), which in turn promote cell survival upon toxin challenge possibly by facilitating membrane repair. This study highlights that, in addition to its well-established role in triggering inflammation via the processing of the precursor forms of interleukins, caspase-1 has a broader role, in particular linking the intracellular ion composition to lipid metabolic pathways, membrane biogenesis, and survival.
Keywords SREBPCell survivalCaspase-1Pore-forming toxinAerolysinLipid metabolismInnate immunityNod-like receptorInflammasomePotassium efflux
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URN: urn:nbn:ch:unige-4355
Note Texte en anglais avec résumé en français
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GURCEL, Laure. Characterization of a new response to bacterial pore-forming toxin that promotes cell survival in a caspase-1 dependent activation of SREBPs. Université de Genève. Thèse, 2006. https://archive-ouverte.unige.ch/unige:435

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Deposited on : 2008-10-29

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