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Inhibition of RhoA GTPase and the subsequent activation of PTP1B protects cultured hippocampal neurons against amyloid b toxicity

Opened Access Inhibition of RhoA GTPase and the subsequent activation of PTP1B protects cultured hippocampal neurons against amyloid b toxicity

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Autor: Chacón Fernández, Pedro José
García Mejías, Rosa
Rodríguez Tebar, Alfredo
Fecha: 2011
Publicado en: Molecular Neurodegeneration, 6 (14), 1-11.
Tipo de documento: Artículo
Resumen: Background: Amyloid beta (Ab) is the main agent responsible for the advent and progression of Alzheimer’s disease. This peptide can at least partially antagonize nerve growth factor (NGF) signalling in neurons, which may be responsible for some of the effects produced by Ab. Accordingly, better understanding the NGF signalling pathway may provide clues as to how to protect neurons from the toxic effects of Ab. Results: We show here that Ab activates the RhoA GTPase by binding to p75NTR, thereby preventing the NGFinduced activation of protein tyrosine phosphatase 1B (PTP1B) that is required for neuron survival. We also show that the inactivation of RhoA GTPase and the activation of PTP1B protect cultured hippocampal neurons against the noxious effects of Ab. Indeed, either pharmacological inhibition of RhoA with C3 ADP ribosyl transferase or the transfection of cultured neurons with a dominant negative form of RhoA protects cultured hippocampal neurons from the effects of Ab. ...
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Cita: Chacón Fernández, P.J., García Mejías, R. y Rodríguez Tebar, A. (2011). Inhibition of RhoA GTPase and the subsequent activation of PTP1B protects cultured hippocampal neurons against amyloid b toxicity. Molecular Neurodegeneration, 6 (14), 1-11.
Tamaño: 1.509Mb
Formato: PDF

URI: http://hdl.handle.net/11441/64437

DOI: 10.1186/1750-1326-6-14

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