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dc.contributor.authorPodlesniy, Petar
dc.contributor.authorKichev, Anton Vladimirov
dc.contributor.authorPedraza, Carlos
dc.contributor.authorSaurat, Jordi
dc.contributor.authorEncinas Martín, Mario
dc.contributor.authorPérez, Begoña
dc.contributor.authorFerrer, Isidre
dc.contributor.authorEspinet Mestre, Carme
dc.date.accessioned2015-02-02T09:07:28Z
dc.date.available2015-02-02T09:07:28Z
dc.date.issued2006
dc.identifier.urihttp://hdl.handle.net/10459.1/47781
dc.description.abstractThe pro form of neurotrophic growth factor (pro-NGF), purified by chromatography from human Alzheimer’s disease (AD)-affected brains (ADhbi-pro-NGF), has been shown to induce apoptotic cell death in neuronal cell cultures through its interaction with the p75 neurotrophin receptor (p75NTR). In the present work,we report that ADhbi-pro-NGF stimulates processing of p75NTR with - and -secretases, yielding a 20-kd intracellular domain (p75ICD) that translocates to the nucleus. This process was accompanied by delayed apoptosis. In AD, p75ICD was significantly increased in human entorhinal cortex. Although human frontal cortex has been described as showing a higher pro-NGF increase in AD, the increase in the entorhinal cortex paralleled p75NTR processing in its intracellular domain. In addition, pro- NGF isolated from AD-affected brains differed functionally from pro-NGF isolated from comparably aged control brains, with pro-NGF isolated from control brains being unstable and undergoing degradation to NGF when added to cell culture. As p75ICD and pro-NGF are both mediators of apoptosis and are both found in increased levels in the cerebral cortex in AD, the present data have implications for understanding neuronal degeneration in AD.ca_ES
dc.language.isoengca_ES
dc.publisherElsevier Incca_ES
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.2353/ajpath.2006.050787ca_ES
dc.relation.ispartofAmerican Journal of Pathology, 2006, vol. 169, núm. 1, p. 119-131ca_ES
dc.rights(c) American Society for Investigative Pathology, 2006
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es/*
dc.subject.otherAlzheimer, Malaltia d'ca_ES
dc.subject.otherSistema nerviós--Malaltiesca_ES
dc.titlePro-NGF from Alzheimer's disease and normal human brain displays distinctive abilities to induce processing and nuclear translocation of intracellular domain of p75NTR and apoptosis.ca_ES
dc.typearticleca_ES
dc.identifier.idgrec009247
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_ES
dc.identifier.doihttps://doi.org/10.2353/ajpath.2006.050787


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(c) American Society for Investigative Pathology, 2006
Except where otherwise noted, this item's license is described as (c) American Society for Investigative Pathology, 2006