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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Main Authors: Bustamante, Hianara A., Rivera-Dictter, Andrés, Cavieres, Viviana A., Muñoz, Vanessa C., González, Alexis, Lin, Yimo, Mardones, Gonzalo A., Burgos, Patricia V.
Formato: Artigo
Idioma:Inglês
Publicado em: Public Library of Science 2013
Assuntos:
Research Article
Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC3869756/
https://ncbi.nlm.nih.gov/pubmed/24376644
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1371/journal.pone.0083096
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