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Updated: Jun 16, 2026

Purification of Ubiquitinated p53 Proteins from Mammalian Cells
Published on: March 21, 2022
p53 is regulated by and regulates members of the gamma-secretase complex
Frédéric Checler1, Julie Dunys, Raphaelle Pardossi-Piquard
1Institut de Pharmacologie Moléculaire et Cellulaire et Institut de NeuroMédecine Moléculaire, UMR6097 CNRS/UNSA, Valbonne, France. checler@ipmc.cnrs.fr
Abstract:
Amyloid beta-peptides is the generic term for a set of hydrophobic peptides that accumulate in Alzheimer's disease (AD)-affected brains. These amyloid-beta peptide fragments are mainly generated by an enzymatic machinery referred to as gamma-secretase complex that is built up by the association of four distinct proteins, namely presenilin 1 (PS1) or PS2, nicastrin, Aph-1 and Pen-2. AD is also characterized by exacerbated cell death that appears linked to the tumor suppressor p53. Interestingly, all members of the gamma-secretase complex control p53-dependent cell death. On the other hand, p53 appears to be able to regulate directly or indirectly the expression and transcription of PS1, PS2 and Pen-2. This review will focus on the functional cross-talk between the members of the gamma-secretase complex and p53 and will discuss the putative implication of this oncogene in AD pathology.
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