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Dysfunction of the unfolded protein response increases neurodegeneration in aged rat hippocampus following proteasome inhibition

Opened Access Dysfunction of the unfolded protein response increases neurodegeneration in aged rat hippocampus following proteasome inhibition

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Autor: Gavilán, María Paz
Pintado, Cristina
Gavilán Dorronzoro, Elena
Jiménez, Sebastián
Ríos, Rosa M.
Vitorica Ferrández, Francisco Javier
Castaño Navarro, Angélica
Ruano Caballero, Diego
Departamento: Universidad de Sevilla. Departamento de Bioquímica y Biología Molecular
Fecha: 2009
Publicado en: Aging Cell, 8 (6), 654-665.
Tipo de documento: Artículo
Resumen: Dysfunctions of the ubiquitin proteasome system (UPS) have been proposed to be involved in the aetiology and/or progression of several age-related neurodegenerative disorders. However, the mechanisms linking proteasome dysfunction to cell degeneration are poorly understood. We examined in young and aged rat hippocampus the activation of the unfolded protein response (UPR) under cellular stress induced by proteasome inhibition. Lactacystin injection blocked proteasome activity in young and aged animals in a similar extent and increased the amount of ubiquitinated proteins. Young animals activated the three UPR arms, IRE1α, ATF6α and PERK, whereas aged rats failed to induce the IRE1α and ATF6α pathways. In consequence, aged animals did not induce the expression of pro-survival factors (chaperones, Bcl-XL and Bcl-2), displayed a more sustained expression of proapoptotic markers (CHOP, Bax, Bak and JKN), an increased caspase-3 processing. At the cellular level, proteasome inhibition induc...
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Cita: Gavilán, M.P., Pintado, C., Gavilán Dorronzoro, E., Jiménez, S., Ríos, R.M., Vitorica Ferrández, F.J.,...,Ruano Caballero, D. (2009). Dysfunction of the unfolded protein response increases neurodegeneration in aged rat hippocampus following proteasome inhibition. Aging Cell, 8 (6), 654-665.
Tamaño: 647.1Kb
Formato: PDF

URI: http://hdl.handle.net/11441/41544

DOI: http://dx.doi.org/ 10.1111/j.1474-9726.2009.00519.x

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