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• W2289254 abstract "Event Abstract Back to Event Mechanisms of Axl Signaling in Cerebral Endothelial Cells Imola Wilhelm1, Attila E. Farkas1, Csilla Fazakas1, Peter Nagyoszi1 and Istvan Krizbai1* 1 Institute of Biophysics, Biological Research Centre, Hungary Tyrosine phosphorylation plays a significant role in different intracellular signaling processes. By using a screening method based on antibody arrays we have identified the receptor tyrosine kinase Axl as a signaling molecule activated by osmotic stress in cerebral endothelial cells. Axl is emerging as a regulator of a large number of cellular functions and has been shown to be involved in the regulation of different aspects of endothelial function including apoptosis, cell migration, vascular remodeling and angiogenesis. The aim of the present study was to elucidate the mechanisms of Axl-mediated signal transduction in brain endothelial cells. We have found that osmotic stress induces tyrosine phosphorylation of Axl followed by activation of Akt. Moreover, Axl was also cleaved in response to osmotic stress resulting in a 50-55 kDa double degradation product which remained phosphorylated. This process was mediated by a metalloproteinase-dependent cleavage, followed by a proteasomal cleavage. The upper degradation band was detergent-soluble whereas the lower degradation band was soluble in water as well, suggesting that the cleavage product with higher molecular weight is still membrane bound. No direct relationship between phosphorylation and cleavage of Axl was found. In order to address the functional implications of Axl activation, we have performed knockdown experiments. We observed that Axl silencing inhibited Akt activation and increased the rate of apoptosis in hyperosmotic mannitol-treated cells. Our results identify Axl as an important element of osmotic stress-induced signaling. Conference: 12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009. Presentation Type: Poster Presentation Topic: Research on the cerebral cortex and related structures Citation: Wilhelm I, Farkas AE, Fazakas C, Nagyoszi P and Krizbai I (2009). Mechanisms of Axl Signaling in Cerebral Endothelial Cells. Front. Syst. Neurosci. Conference Abstract: 12th Meeting of the Hungarian Neuroscience Society. doi: 10.3389/conf.neuro.01.2009.04.209 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 06 Mar 2009; Published Online: 06 Mar 2009. * Correspondence: Istvan Krizbai, Institute of Biophysics, Biological Research Centre, Szeged, Hungary, krizbai@brc.hu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Imola Wilhelm Attila E Farkas Csilla Fazakas Peter Nagyoszi Istvan Krizbai Google Imola Wilhelm Attila E Farkas Csilla Fazakas Peter Nagyoszi Istvan Krizbai Google Scholar Imola Wilhelm Attila E Farkas Csilla Fazakas Peter Nagyoszi Istvan Krizbai PubMed Imola Wilhelm Attila E Farkas Csilla Fazakas Peter Nagyoszi Istvan Krizbai Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page." @default.
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• W2289254 title "Mechanisms of Axl Signaling in Cerebral Endothelial Cells" @default.
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