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oai:repisalud.isciii.es:20.500.12105/78992025-05-05T12:13:19Zcom_20.500.12105_2052com_20.500.12105_2051col_20.500.12105_19617

00925njm 22002777a 4500 dc Leon-Espinosa, Gonzalo author Sanchez-Ruiloba, Lucia author Perez-Rodriguez, Andrea author Gragera, Teresa author Martinez, Natalia author Hernandez, Silvia author Anta-Felez, Berta author Calero, Olga author Garcia-Dominguez, Carlota A author Dura, Lara M author Peña-Jimenez, Daniel author Castro, Judith author Zarich-Dimitrievich, Natasha author Sánchez-Gómez, Pilar author Calero, Miguel author Iglesias, Teresa author Oliva-Martinez, Jose Luis author Rojas-Cabañeros, Jose Maria author 2014 The 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. PLoS One. 2014 Dec 16;9(12):e114837 10.1371/journal.pone.0114837 1932-6203 1932-6203 PLoS ONE 25514808 http://hdl.handle.net/20.500.12105/7899 Shoc2/Sur8 Protein Regulates Neurite Outgrowth