dc.creator | Chacón Fernández, Pedro José | es |
dc.creator | García Mejías, Rosa | es |
dc.creator | Rodríguez Tebar, Alfredo | es |
dc.date.accessioned | 2017-09-14T11:14:33Z | |
dc.date.available | 2017-09-14T11:14:33Z | |
dc.date.issued | 2011 | |
dc.identifier.citation | 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. | |
dc.identifier.issn | 1750-1326 | es |
dc.identifier.uri | http://hdl.handle.net/11441/64437 | |
dc.description.abstract | 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. In addition, over-expression of PTP1B also prevents the deleterious effects of Ab on cultured
hippocampal neurons.
Conclusion: Our findings indicate that potentiating the activity of NGF at the level of RhoA inactivation and PTP1B
activation may represent a new means to combat the noxious effects of Ab in Alzheimer’s disease. | es |
dc.description.sponsorship | España, Ministerio de educación y ciencia BFU2005-05629 | es |
dc.format | application/pdf | es |
dc.language.iso | eng | es |
dc.publisher | BioMed Central | es |
dc.relation.ispartof | Molecular Neurodegeneration, 6 (14), 1-11. | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.title | Inhibition of RhoA GTPase and the subsequent activation of PTP1B protects cultured hippocampal neurons against amyloid b toxicity | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.relation.projectID | BFU2005-05629 | es |
dc.relation.publisherversion | http://dx.doi.org/10.1186/1750-1326-6-14 | es |
dc.identifier.doi | 10.1186/1750-1326-6-14 | es |
idus.format.extent | 12 p. | es |
dc.journaltitle | Molecular Neurodegeneration | es |
dc.publication.volumen | 6 | es |
dc.publication.issue | 14 | es |
dc.publication.initialPage | 1 | es |
dc.publication.endPage | 11 | es |
dc.contributor.funder | Ministerio de Educación y Ciencia (MEC). España | |