Leon-Espinosa, GonzaloSanchez-Ruiloba, LuciaPerez-Rodriguez, AndreaGragera, TeresaMartinez, NataliaHernandez, SilviaAnta-Felez, BertaCalero, OlgaGarcia-Dominguez, Carlota ADura, Lara MPeña-Jimenez, DanielCastro, JudithZarich-Dimitrievich, NatashaSánchez-Gómez, PilarCalero, MiguelIglesias, TeresaOliva-Martinez, Jose LuisRojas-Cabañeros, Jose Maria2019-07-122019-07-122014PLoS One. 2014 Dec 16;9(12):e1148371932-6203http://hdl.handle.net/20.500.12105/7899The 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.engVoRhttp://creativecommons.org/licenses/by/4.0/AnimalsCell Line, TumorEnzyme ActivationEpidermal Growth FactorExtracellular Signal-Regulated MAP KinasesHEK293 CellsHumansAtribución 4.0 Internacional25514808912e11483710.1371/journal.pone.01148371932-6203PLoS ONEopen access