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dc.contributor.authorLeon-Espinosa, Gonzalo 
dc.contributor.authorSanchez-Ruiloba, Lucia
dc.contributor.authorPerez-Rodriguez, Andrea 
dc.contributor.authorGragera, Teresa 
dc.contributor.authorMartinez, Natalia 
dc.contributor.authorHernandez, Silvia 
dc.contributor.authorAnta-Felez, Berta 
dc.contributor.authorCalero, Olga 
dc.contributor.authorGarcia-Dominguez, Carlota A 
dc.contributor.authorDura, Lara M 
dc.contributor.authorPeña-Jiménez, Daniel 
dc.contributor.authorCastro, Judith 
dc.contributor.authorZarich-Dimitrievich, Natasha 
dc.contributor.authorSánchez-Gómez, Pilar 
dc.contributor.authorCalero, Miguel 
dc.contributor.authorIglesias, Teresa
dc.contributor.authorOliva-Martinez, Jose Luis 
dc.contributor.authorRojas-Cabañeros, Jose Maria 
dc.date.accessioned2019-07-12T08:31:12Z
dc.date.available2019-07-12T08:31:12Z
dc.date.issued2014
dc.identifier.citationPLoS One. 2014 Dec 16;9(12):e114837es_ES
dc.identifier.issn1932-6203es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7899
dc.description.abstractThe Shoc2 protein has been implicated in the positive regulation of the Ras-ERK pathway by increasing the functional binding interaction between Ras and Raf, leading to increased ERK activity. Here we found that Shoc2 overexpression induced sustained ERK phosphorylation, notably in the case of EGF stimulation, and Shoc2 knockdown inhibited ERK activation. We demonstrate that ectopic overexpression of human Shoc2 in PC12 cells significantly promotes neurite extension in the presence of EGF, a stimulus that induces proliferation rather than differentiation in these cells. Finally, Shoc2 depletion reduces both NGF-induced neurite outgrowth and ERK activation in PC12 cells. Our data indicate that Shoc2 is essential to modulate the Ras-ERK signaling outcome in cell differentiation processes involved in neurite outgrowth.es_ES
dc.description.sponsorshipThis work was supported by FIS grant (PI10/00815) to JLO; CIBERNED to MC; SAF2008-01951, Comunidad Autónoma de Madrid (CAM) S-SAL-0202-2006-01 and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) to TI; FIS grant PI12/00775 and ISCIII-RETIC (Red Temática de Investigación Cooperativa en Cáncer) RD12/0036/0027 from the Instituto de Salud Carlos III to PSG; and FIS grants (PI09/0562 and PI13/00703), ISCIII-RETIC (RD06/0020/0003 and RD12/0036/0021), and the Spanish Association Against Cancer (AECC) to JMR. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.es_ES
dc.language.isoenges_ES
dc.publisherPublic Library of Science (PLOS) es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subject.meshAnimals es_ES
dc.subject.meshCell Line, Tumor es_ES
dc.subject.meshEnzyme Activation es_ES
dc.subject.meshEpidermal Growth Factor es_ES
dc.subject.meshExtracellular Signal-Regulated MAP Kinases es_ES
dc.subject.meshHEK293 Cells es_ES
dc.subject.meshHumans es_ES
dc.subject.meshIntracellular Signaling Peptides and Proteins es_ES
dc.subject.meshMAP Kinase Signaling System es_ES
dc.subject.meshNeurites es_ES
dc.subject.meshPC12 Cells es_ES
dc.subject.meshPhosphorylation es_ES
dc.subject.meshRNA Interference es_ES
dc.subject.meshRNA, Small Interfering es_ES
dc.subject.meshRats es_ES
dc.subject.meshras Proteins es_ES
dc.titleShoc2/Sur8 Protein Regulates Neurite Outgrowthes_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID25514808es_ES
dc.format.volume9es_ES
dc.format.number12es_ES
dc.format.pagee114837es_ES
dc.identifier.doi10.1371/journal.pone.0114837es_ES
dc.contributor.funderMinisterio de Educación y Ciencia (España) 
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderCentro de Investigación Biomédica en Red - CIBERNED (Enfermedades Neurodegenerativas) 
dc.contributor.funderComunidad de Madrid (España) 
dc.contributor.funderRed Temática de Investigación Cooperativa en Cáncer (RTICC) (España) 
dc.contributor.funderAsociación Española Contra el Cáncer 
dc.description.peerreviewedes_ES
dc.identifier.e-issn1932-6203es_ES
dc.relation.publisherversionhttps://doi.org/10.1371/journal.pone.0114837es_ES
dc.identifier.journalPLoS ONEes_ES
dc.repisalud.centroISCIII::Unidad Funcional de Investigación de Enfermedades Crónicas (UFIEC)es_ES
dc.repisalud.institucionISCIIIes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI10/00815es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2008-01951es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/S-SAL-0202-2006-01es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI12/00775es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RD12/0036/0027es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI09/0562es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI13/00703es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RD06/0020/0003es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RD12/0036/0021es_ES
dc.rights.accessRightsopen accesses_ES


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