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dc.contributor.authorManterola, L.
dc.contributor.authorHernando Rodríguez, M.
dc.contributor.authorRuiz Núñez, Asier ORCID
dc.contributor.authorApraiz, A.
dc.contributor.authorArrizabalaga Uriarte, Oskar ORCID
dc.contributor.authorVellon, L.
dc.contributor.authorAlberdi Alfonso, Elena María ORCID
dc.contributor.authorCavaliere, Fabio
dc.contributor.authorLacerda, Hadriano M.
dc.contributor.authorJimenez, S.
dc.contributor.authorParada, L. A.
dc.contributor.authorMatute Almau, Carlos José
dc.contributor.authorZugaza Gurruchaga, José Luis ORCID
dc.date.accessioned2014-02-04T17:53:06Z
dc.date.available2014-02-04T17:53:06Z
dc.date.issued2013-01
dc.identifier.citationTranslational Psychiatry 3 : (2013) // e219es
dc.identifier.issn2158-3188
dc.identifier.urihttp://hdl.handle.net/10810/11340
dc.description.abstract1-42 beta-Amyloid (A beta(1-42)) peptide is a key molecule involved in the development of Alzheimer's disease. Some of its effects are manifested at the neuronal morphological level. These morphological changes involve loss of neurites due to cytoskeleton alterations. However, the mechanism of A beta(1-42) peptide activation of the neurodegenerative program is still poorly understood. Here, A beta(1-42) peptide-induced transduction of cellular death signals through the phosphatidylinositol 3-kinase (PI3K)/phosphoinositol- dependent kinase (PDK)/novel protein kinase C (nPKC)/Rac 1 axis is described. Furthermore, pharmacological inhibition of PDK1 and nPKC activities blocks Rac 1 activation and neuronal cell death. Our results provide insights into an unsuspected connection between PDK1, nPKCs and Rac 1 in the same signal-transduction pathway and points out nPKCs and Rac 1 as potential therapeutic targets to block the toxic effects of A beta(1-42) peptide in neurons.es
dc.description.sponsorshipLM was supported by the Sara Borrell program from the Carlos III Health Institute (Spanish Ministry of Science and Innovation, CD06/00275). MHR was supported by the Programa IKERTU, Department of Industry of the Basque Country Government, and JLZ was supported by grants from the Spanish Ministry of Science and Innovation (CIT-300000-2008-8), Department of Industry of the Basque Country Government (S-PE11UN018) and University of the Basque Country (EHU11/08 and UFI 11/20). We are grateful to SGIKer (UPV/EHU) for the technical and human support provided.es
dc.language.isoenges
dc.publisherNature Publishing Groupes
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectA beta(1-42)es
dc.subjectneuronal death programes
dc.subjectRac 1 GTPasees
dc.title1-42 beta-Amyloid peptide requires PDK1/nPKC/Rac 1 pathway to induce neuronal deathes
dc.typeinfo:eu-repo/semantics/articlees
dc.rights.holder(c)2013 Manterola et al., licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/es
dc.relation.publisherversionhttp://www.nature.com/tp/journal/v3/n1/full/tp2012147a.htmles
dc.departamentoesGenética, antropología física y fisiología animales_ES
dc.departamentoesNeurocienciases_ES
dc.departamentoeuGenetika,antropologia fisikoa eta animalien fisiologiaes_ES
dc.departamentoeuNeurozientziakes_ES
dc.subject.categoriaBIOLOGICAL PSYCHIATRY
dc.subject.categoriaPSYCHIATRY AND MENTAL HEALTH
dc.subject.categoriaCELLULAR AND MOLECULAR NEUROSCIENCE


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