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Authordc.contributor.authorMercado, Gabriela 
Authordc.contributor.authorCastillo, Valentina 
Authordc.contributor.authorSoto, Paulina 
Authordc.contributor.authorLópez, Nélida 
Authordc.contributor.authorAxten, Jeffrey M. 
Authordc.contributor.authorSardi, Sergio P. 
Authordc.contributor.authorHoozemans, Jeroen J.M. 
Authordc.contributor.authorHetz Flores, Claudio
Admission datedc.date.accessioned2019-03-18T12:01:11Z
Available datedc.date.available2019-03-18T12:01:11Z
Publication datedc.date.issued2018
Cita de ítemdc.identifier.citationNeurobiology of Disease, Volumen 112,
Identifierdc.identifier.issn1095953X
Identifierdc.identifier.issn09699961
Identifierdc.identifier.other10.1016/j.nbd.2018.01.004
Identifierdc.identifier.urihttp://repositorio.uchile.cl/handle/2250/167345
Abstractdc.description.abstract© 2018 Elsevier Inc. Parkinson's disease (PD) is the second most common neurodegenerative disorder, leading to the progressive decline of motor control due to the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Accumulating evidence suggest that altered proteostasis is a salient feature of PD, highlighting perturbations to the endoplasmic reticulum (ER), the main compartment involved in protein folding and secretion. PERK is a central ER stress sensor that enforces adaptive programs to recover homeostasis through a block of protein translation and the induction of the transcription factor ATF4. In addition, chronic PERK signaling results in apoptosis induction and neuronal dysfunction due to the repression in the translation of synaptic proteins. Here we confirmed the activation of PERK signaling in postmortem brain tissue derived from PD patients and three different rodent models of the disease. Pharmacological targeting of PERK by the oral administration of
Lenguagedc.language.isoen
Publisherdc.publisherAcademic Press Inc.
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
Sourcedc.sourceNeurobiology of Disease
Keywordsdc.subjectER stress
Keywordsdc.subjectGSK2606414
Keywordsdc.subjectISR
Keywordsdc.subjectParkinson's disease
Keywordsdc.subjectPERK
Keywordsdc.subjectProteostasis
Keywordsdc.subjectUPR
Títulodc.titleTargeting PERK signaling with the small molecule GSK2606414 prevents neurodegeneration in a model of Parkinson's disease
Document typedc.typeArtículo de revista
Catalogueruchile.catalogadorSCOPUS
Indexationuchile.indexArtículo de publicación SCOPUS
uchile.cosechauchile.cosechaSI


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile