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dc.contributor.authorde Alvaro, Cristina
dc.contributor.authorMartinez, Natalia 
dc.contributor.authorRojas-Cabañeros, Jose Maria 
dc.contributor.authorLorenzo, Margarita
dc.date.accessioned2019-01-11T12:22:12Z
dc.date.available2019-01-11T12:22:12Z
dc.date.issued2005-09
dc.identifier.citationMol Biol Cell. 2005;16(9):4454-61.es_ES
dc.identifier.issn1059-1524es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/6996
dc.description.abstractMyoblast C2C12 cells cultured in the presence of FGF2 actively proliferate and showed a differentiation-defective phenotype compared with cells cultured in low serum or in the presence of insulin. These FGF2 effects are associated with sustained activation of p44/p42-MAPK and lack of activation of AKT. Here we demonstrate that Sprouty-2, a protein involved in the negative feedback of receptor tyrosine kinase signaling, when stably overexpressed in C2C12 cells and in the presence of FGF2 produces growth arrest (precluding the expression of PCNA and the phosphorylation of retinoblastoma and inducing the expression of p21(CIP)) and myogenesis (multinucleated myotubes formation, induction of creatine kinase and expression of myosin heavy chain protein). These events were accompanied by repression of p44/p42-MAPK and activation of AKT. When C2C12 cells were stably transfected with a Sprouty-2 (Y55F) mutant defective in inhibiting p44/p42-MAPK activation by FGF, myoblasts in the presence of FGF continue to grow and completely fail to form myotubes. This work is the first evidence of the contribution of sprouty genes to myogenic differentiation in the presence of FGF2.es_ES
dc.description.sponsorshipThis work was supported by Grants BMC2002-01322 and SAF2003-02604 from Ministerio de Ciencia y Tecnologia (Spain); 08.6/0002.1/2003 and GR/SAL/0291/2004 from Comunidad de Madrid (Spain). We also thank the support of COST B17 Action from the European Commission, and Red de grupos de Diabetes Mellitus G03/212 from Instituto de Salud Carlos III, Ministerio de Sanidad y Consumo.es_ES
dc.language.isoenges_ES
dc.publisherAmerican Society for Cell Biologyes_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/*
dc.subject.meshAdaptor Proteins, Signal Transducing es_ES
dc.subject.meshAmino Acid Substitution es_ES
dc.subject.meshAnimals es_ES
dc.subject.meshCell Differentiation es_ES
dc.subject.meshCell Line es_ES
dc.subject.meshFibroblast Growth Factor 2 es_ES
dc.subject.meshHumans es_ES
dc.subject.meshIntracellular Signaling Peptides and Proteins es_ES
dc.subject.meshMembrane Proteins es_ES
dc.subject.meshMice es_ES
dc.subject.meshMitogen-Activated Protein Kinase 1 es_ES
dc.subject.meshMitogen-Activated Protein Kinase 3 es_ES
dc.subject.meshMuscle, Skeletal es_ES
dc.subject.meshMutation es_ES
dc.subject.meshMyoblasts es_ES
dc.subject.meshProteins es_ES
dc.subject.meshSpry2 protein, mousees_ES
dc.titleSprouty-2 overexpression in C2C12 cells confers myogenic differentiation properties in the presence of FGF2es_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 3.0*
dc.identifier.pubmedID16000370es_ES
dc.format.volume16es_ES
dc.format.number9es_ES
dc.format.page4454-61es_ES
dc.identifier.doi10.1091/mbc.E05-05-0419es_ES
dc.contributor.funderMinisterio de Educacion y Ciencia (España)es_ES
dc.contributor.funderMinisterio de Ciencia y Tecnologia (España)es_ES
dc.contributor.funderGobierno de la Comunidad Autónoma de Madrides_ES
dc.contributor.funderEuropean Commissiones_ES
dc.contributor.funderInstituto de Salud Carlos III - ISCIIIes_ES
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1091/mbc.E05-05-0419es_ES
dc.identifier.journalMolecular Biology of the Celles_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.institucionISCIIIes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/BMC2002-01322es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2003-02604es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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