ArticleFrontiers in cellular neuroscience2018
Contribution of the Endosomal-Lysosomal and Proteasomal Systems in Amyloid-β Precursor Protein Derived Fragments Processing.
Article in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Probiotics for Alzheimer's Disease: A Systematic Review.Nutrients · 2021Pooled it
- UPS-mediated P-glycoprotein regulation in Alzheimer's disease: pharmacological implications for the amyloid pathology.Molecular biology reports · 2026Review
- LAMP1 and LAMP2A localise to axonal organelles with distinct motility dynamics and partially overlapping molecular signatures in human neurons.Journal of cell science · 2026Article
- The multiple roles of chronic stress and glucocorticoids in Alzheimer's disease pathogenesis.Trends in neurosciences · 2024Review
- Genetic and chemical disruption of amyloid precursor protein processing impairs zebrafish sleep maintenance.iScience · 2024Article
- ARL6IP1 mediates small-molecule-induced alleviation of Alzheimer pathology through FXR1-dependent BACE1 translation initiation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The η-secretase-derived APP fragment ηCTF is localized in Golgi, endosomes and extracellular vesicles and contributes to Aβ production.Cellular and molecular life sciences : CMLS · 2023Article
- A Gating Mutation in Ryanodine Receptor Type 2 Rescues Phenotypes of Alzheimer's Disease Mouse Models by Upregulating Neuronal Autophagy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Lipoprotein Metabolism, Protein Aggregation, and Alzheimer's Disease: A Literature Review.International journal of molecular sciences · 2023Review
- Review
- The amyloid precursor protein: a converging point in Alzheimer's disease.Molecular neurobiology · 2022Review
- Mitochondrial Alterations in Neurons Derived from the Murine AppNL-F Knock-In Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2022Article
- Mechanism of Cellular Formation and In Vivo Seeding Effects of Hexameric β-Amyloid Assemblies.Molecular neurobiology · 2021Article
- The apolipoprotein receptor LRP3 compromises APP levels.Alzheimer's research & therapy · 2021Article
- Amyloid precursor protein glycosylation is altered in the brain of patients with Alzheimer's disease.Alzheimer's research & therapy · 2020Article
- Alix and Syntenin-1 direct amyloid precursor protein trafficking into extracellular vesicles.BMC molecular and cell biology · 2020Article
- Matrix Metalloproteinase 14 Mediates APP Proteolysis and Lysosomal Alterations Induced by Oxidative Stress in Human Neuronal Cells.Oxidative medicine and cellular longevity · 2020Article
- Contribution of the Endosomal-Lysosomal and Proteasomal Systems in Amyloid-β Precursor Protein Derived Fragments Processing.Frontiers in cellular neuroscience · 2018Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aβ peptides, the major components of Alzheimer's disease (AD) amyloid deposits, are released following sequential cleavages by secretases of its precursor named the amyloid precursor protein (APP). In addition to secretases, degradation pathways, in particular the endosomal/lysosomal and proteasomal systems have been reported to contribute to APP processing. However, the respective role of each of these pathways toward APP metabolism remains to be established. To address this, we used HEK 293 cells and primary neurons expressing full-length wild type APP or the β-secretase-derived C99 fragment (β-CTF) in which degradation pathways were selectively blocked using pharmacological drugs. APP metabolites, including carboxy-terminal fragments (CTFs), soluble APP (sAPP) and Aβ peptides were studied. In this report, we show that APP-CTFs produced from endogenous or overexpressed full-length APP are mainly processed by γ-secretase and the endosomal/lysosomal pathway, while in sharp contrast, overexpressed C99 is mainly degraded by the proteasome and to a lesser extent by γ-secretase.
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