The distinct roles of Ras and Rac in PI 3-kinase-dependent protrusion during EGF-stimulated cell migration

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dc.contributor.author Yip, Shu-Chin
dc.contributor.author El-Sibai, Mirvat
dc.contributor.author Coniglio, Salvatore J.
dc.contributor.author Mouneimne, Ghassan
dc.contributor.author Eddy, Robert J.
dc.contributor.author Drees, Beth E.
dc.contributor.author Neilsen, Paul O.
dc.contributor.author Goswami, Sumanta
dc.contributor.author Symons, Marc
dc.contributor.author Condeelis, John S.
dc.contributor.author Backer, Jonathan M.
dc.date.accessioned 2015-11-09T10:22:24Z
dc.date.available 2015-11-09T10:22:24Z
dc.date.copyright 2007-06-18
dc.date.issued 2015-11-09
dc.identifier.issn 0021-9533 en_US
dc.identifier.uri http://hdl.handle.net/10725/2493
dc.description.abstract Cell migration involves the localized extension of actinrich protrusions, a process that requires Class I phosphoinositide 3-kinases (PI 3-kinases). Both Rac and Ras have been shown to regulate actin polymerization and activate PI 3-kinase. However, the coordination of Rac, Ras and PI 3-kinase activation during epidermal growth factor (EGF)-stimulated protrusion has not been analyzed. We examined PI 3-kinase-dependent protrusion in MTLn3 rat adenocarcinoma cells. EGF-stimulated phosphatidy l - inositol (3,4,5)-trisphosphate [PtdIns(3,4,5)P3] levels showed a rapid and persistent response, as PI 3-kinase activity remained elevated up to 3 minutes. The activation kinetics of Ras, but not Rac, coincided with those of leading-edge PtdIns(3,4,5)P3 production. Small interfering RNA (siRNA) knockdown of K-Ras but not Rac1 abolished PtdIns(3,4,5)P3 production at the leading edge and inhibited EGF-stimulated protrusion. However, Rac1 knockdown did inhibit cell migration, because of the inhibition of focal adhesion formation in Rac1 siRNAtreated cells. Our data show that in EGF-stimulated MTLn3 carcinoma cells, Ras is required for both PtdIns(3,4,5)P3 production and lamellipod extension, whereas Rac1 is required for formation of adhesive structures. These data suggest an unappreciated role for Ras during protrusion, and a crucial role for Rac in the stabilization of protrusions required for cell motility. en_US
dc.language.iso en en_US
dc.title The distinct roles of Ras and Rac in PI 3-kinase-dependent protrusion during EGF-stimulated cell migration en_US
dc.type Article en_US
dc.description.version Published en_US
dc.author.school SAS en_US
dc.author.idnumber 200703859 en_US
dc.author.woa N/A en_US
dc.author.department Natural Sciences en_US
dc.description.embargo N/A en_US
dc.relation.journal Journal of Cell Science en_US
dc.journal.volume 120 en_US
dc.journal.issue 17 en_US
dc.article.pages 3138-3146 en_US
dc.keywords Ras en_US
dc.keywords Rac en_US
dc.keywords Cdc42 en_US
dc.keywords Rho en_US
dc.keywords Lamellipodia en_US
dc.identifier.doi http://dx.doi.org/10.1242/jcs.005298 en_US
dc.identifier.ctation Yip, S. C., El-Sibai, M., Coniglio, S. J., Mouneimne, G., Eddy, R. J., Drees, B. E., ... & Backer, J. M. (2007). The distinct roles of Ras and Rac in PI 3-kinase-dependent protrusion during EGF-stimulated cell migration. Journal of cell science, 120(17), 3138-3146. en_US
dc.author.email mirvat.elsibai@lau.edu.lb
dc.identifier.url http://jcs.biologists.org/content/120/17/3138.short
dc.orcid.id https://orcid.org/0000-0003-4084-6759 en_US

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