Proteasome stress leads to APP axonal transport defects by promoting its amyloidogenic processing in lysosomes

Alzheimer disease (AD) pathology includes the accumulation of poly-ubiquitylated (also known as poly-ubiquitinated) proteins and failures in proteasome-dependent degradation. Whereas the distribution of proteasomes and its role in synaptic function have been studied, whether proteasome activity regu...

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Detalles Bibliográficos
Autores principales: Otero, M.G., Bessone, I.F., Hallberg, A.E., Cromberg, L.E., De Rossi, M.C., Saez, T.M., Levi, V., Almenar-Queralt, A., Falzone, T.L.
Formato: JOUR
Materias:
Alzheimer disease
Amyloid precursor protein
Axonal transport
Lysosome
Proteasome
amyloid precursor protein
proteasome
animal cell
animal tissue
Article
cell membrane
controlled study
fluorescence analysis
Golgi complex
hippocampus
live cell imaging
lysosome
molecular interaction
mouse
nerve cell
nerve fiber transport
newborn
nonhuman
priority journal
protein aggregation
protein degradation
protein localization
protein metabolism
protein processing
protein transport
Western blotting
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_00219533_v131_n11_p_Otero
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

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