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Turnover of C99 is Controlled by a Crosstalk between ERAD and Ubiquitin-Independent Lysosomal Degradation in Human Neuroglioma Cells

Alzheimer’s disease (AD) is characterized by the buildup of amyloid-β peptides (Aβ) aggregates derived from proteolytic processing of the β-amyloid precursor protein (APP). Amyloidogenic cleavage of APP by β-secretase/BACE1 generates the C-terminal fragment C99/CTFβ that can be subsequently cleaved...

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Detalles Bibliográficos
Autores principales:	Bustamante, Hianara A., Rivera-Dictter, Andrés, Cavieres, Viviana A., Muñoz, Vanessa C., González, Alexis, Lin, Yimo, Mardones, Gonzalo A., Burgos, Patricia V.
Formato:	Online Artículo Texto
Lenguaje:	English
Publicado:	Public Library of Science 2013
Materias:	Research Article
Acceso en línea:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3869756/ https://www.ncbi.nlm.nih.gov/pubmed/24376644 http://dx.doi.org/10.1371/journal.pone.0083096

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