Caspase-3 cleavage of GGA3 stabilizes BACE: implications for Alzheimer's disease.
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.
Vassar
Robert
R
Department of Cell and Molecular Biology, Northwestern University, The Feinberg School of Medicine, Chicago, IL 60611-3006, USA. r-vassar@northwestern.edu
D020727:ADP-Ribosylation Factors / Q000378:metabolism*; D033942:Adaptor Proteins, Vesicular Transport / Q000378:metabolism*; D000544:Alzheimer Disease / Q000201:enzymology* / Q000503:physiopathology; D053829:Amyloid Precursor Protein Secretases / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000096:biosynthesis; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism*; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D016282:Aspartic Acid Endopeptidases / Q000378:metabolism*; D053148:Caspase 3 / Q000378:metabolism*; D006801:Humans; D011499:Protein Processing, Post-Translational / Q000502:physiology; D021381:Protein Transport / Q000502:physiology
D033942:Adaptor Proteins, Vesicular Transport; D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; C407306:GGA adaptor proteins; D053829:Amyloid Precursor Protein Secretases; D053148:Caspase 3; D016282:Aspartic Acid Endopeptidases; C509280:BACE1 protein, human; D020727:ADP-Ribosylation Factors