Caspase-3 cleavage of GGA3 stabilizes BACE: implications for Alzheimer's disease

Neuron. 2007 Jun 7;54(5):671-3. doi: 10.1016/j.neuron.2007.05.018.

Abstract

BACE initiates the production of beta-amyloid (Abeta), the likely cause of Alzheimer's disease (AD). In this issue of Neuron, Tesco et al. show that during apoptosis caspase-3 cleaves the adaptor protein GGA3, which is required for BACE lysosomal degradation, consequently stabilizing BACE and elevating Abeta generation.

Publication types

  • Comment
  • Review

MeSH terms

  • ADP-Ribosylation Factors / metabolism*
  • Adaptor Proteins, Vesicular Transport / metabolism*
  • Alzheimer Disease / enzymology*
  • Alzheimer Disease / physiopathology
  • Amyloid Precursor Protein Secretases / metabolism*
  • Amyloid beta-Peptides / biosynthesis
  • Amyloid beta-Protein Precursor / metabolism*
  • Animals
  • Apoptosis / physiology
  • Aspartic Acid Endopeptidases / metabolism*
  • Caspase 3 / metabolism*
  • Humans
  • Protein Processing, Post-Translational / physiology
  • Protein Transport / physiology

Substances

  • Adaptor Proteins, Vesicular Transport
  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • GGA adaptor proteins
  • Amyloid Precursor Protein Secretases
  • Caspase 3
  • Aspartic Acid Endopeptidases
  • BACE1 protein, human
  • ADP-Ribosylation Factors