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<title lang=en>The cleaved FAS ligand activates the Na+/H+ exchanger NHE1 through Akt/ROCK1 to stimulate cell motility</title>
<creator>Monet, Michaël</creator>
<creator>Poet, Mallorie</creator>
<creator>Tauzin, Sébastien</creator>
<creator>Fouque, Amelie</creator>
<creator>Cophignon, Auréa</creator>
<creator>Lagadic-Gossmann, Dominique</creator>
<creator>Vacher, Pierre</creator>
<creator>Legembre, Patrick</creator>
<creator>Counillon, Laurent</creator>
<contributor>Laboratoire de PhysioMédecine Moléculaire (LP2M) ; Centre National de la Recherche Scientifique (CNRS) - Université Nice Sophia Antipolis (UNS) ; Université Côte d'Azur (UCA) - Université Côte d'Azur (UCA)</contributor>
<contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Oncogenesis Stress Signaling (OSS) ; Université de Rennes 1 (UR1) - CRLCC Eugène Marquis (CRLCC)</contributor>
<contributor>Centre de recherche Cardio-Thoracique de Bordeaux [Bordeaux] (CRCTB) ; Université Bordeaux Segalen - Bordeaux 2 - CHU Bordeaux [Bordeaux] - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>This work was supported by CNRS and the University of Nice-Sophia Antipolis, the ICST Labex, grants from INCa PLBIOL, Ligue Contre le Cancer (Comités d’Ille-et-Vilaine/du Morbihan/des Côtes d’Armor/du Maine et Loire), ARC, Région Bretagne, Rennes Métropole. </contributor>
<description>International audience</description>
<source>ISSN: 2045-2322</source>
<source>EISSN: 2045-2322</source>
<source>Scientific Reports</source>
<publisher>Nature Publishing Group</publisher>
<identifier>hal-01334067</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01334067</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01334067/document</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01334067/file/Cleaved%20FAS%20ligand%20CC-BY.pdf</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01334067</source>
<source>Scientific Reports, Nature Publishing Group, 2016, 6, pp.28008. 〈10.1038/srep28008〉</source>
<identifier>DOI : 10.1038/srep28008</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1038/srep28008</relation>
<identifier>PUBMED : 27302366</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/27302366</relation>
<identifier>PUBMEDCENTRAL : PMC4908414</identifier>
<language>en</language>
<subject lang=en>Cell migration</subject>
<subject lang=en>Metastasis</subject>
<subject>[SDV.CAN] Life Sciences [q-bio]/Cancer</subject>
<subject>[SDV.BC] Life Sciences [q-bio]/Cellular Biology</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Transmembrane CD95L (Fas ligand) can be cleaved to release a promigratory soluble ligand, cl-CD95L, which can contribute to chronic inflammation and cancer cell dissemination. The motility signaling pathway elicited by cl-CD95L remains poorly defined. Here, we show that in the presence of cl-CD95L, CD95 activates the Akt and RhoA signaling pathways, which together orchestrate an allosteric activation of the Na+/H+ exchanger NHE1. Pharmacologic inhibition of Akt or ROCK1 independently blocks the cl-CD95L-induced migration. Confirming these pharmacologic data, disruption of the Akt and ROCK1 phosphorylation sites on NHE1 decreases cell migration in cells exposed to cl-CD95L. Together, these findings demonstrate that NHE1 is a novel molecular actor in the CD95 signaling pathway that drives the cl-CD95L-induced cell migration through both the Akt and RhoA signaling pathways.</description>
<date>2016-06</date>
</dc>
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