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

@inproceedings{Bustamante2013TurnoverOC,
  title={Turnover of C99 is Controlled by a Crosstalk between ERAD and Ubiquitin-Independent Lysosomal Degradation in Human Neuroglioma Cells},
  author={Hianara A. Bustamante and Andr{\'e}s Rivera-Dictter and Viviana A. Cavieres and Vanessa C. Mu{\~n}oz and Alexis Gonz{\'a}lez and Yimo Lin and Gonzalo A Mardones and Patricia V. Burgos},
  booktitle={PloS one},
  year={2013}
}
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 by γ-secretase to produce Aβ. Growing evidence indicates that high levels of C99/CTFβ are determinant for AD. Although it has been postulated that γ-secretase-independent pathways must control C99… CONTINUE READING

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