ArticleNeurobiology of aging2021
Mutations in the COPI coatomer subunit α-COP induce release of Aβ-42 and amyloid precursor protein intracellular domain and increase tau oligomerization and release.
Article in Neurobiology of aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 20 citations in OpenAlex.
- Conditional knockout mouse model demonstrates that Copa expression is required for viability in development and adulthood.Biochemical and biophysical research communications · 2025Article
- Targeting COPA to Enhance Erdafitinib Sensitivity in FGFR-Altered Bladder Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- COPI coatomer subunit α-COP interacts with the RNA binding protein Nucleolin via a C-terminal dilysine motif.Human molecular genetics · 2023Article
- COPI-regulated mitochondria-ER contact site formation maintains axonal integrity.Cell reports · 2023Article
- Depletion of COPI in cancer cells: the role of reactive oxygen species in the induction of lipid accumulation, noncanonical lipophagy and apoptosis.Molecular biology of the cell · 2022Article
- Adamantinomatous craniopharyngioma cyst fluid can trigger inflammatory activation of microglia to damage the hypothalamic neurons by inducing the production of β-amyloid.Journal of neuroinflammation · 2022Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Understanding the cellular processes that lead to Alzheimer's disease (AD) is critical, and one key lies in the genetics of families with histories of AD. Mutations a complex known as COPI were found in families with AD. The COPI complex is involved in protein processing and trafficking. Intriguingly, several recent publications have found components of the COPI complex can affect the metabolism of pathogenic AD proteins. We reduced levels of the COPI subunit α-COP, altering maturation and cleavage of amyloid precursor protein (APP), resulting in decreased release of Aβ-42 and decreased accumulation of the AICD. Depletion of α-COP reduced uptake of proteopathic Tau seeds and reduces intracellular Tau self-association. Expression of AD-associated mutant α-COP altered APP processing, resulting in increased release of Aβ-42 and increased intracellular Tau aggregation and release of Tau oligomers. These results show that COPI coatomer function modulates processing of both APP and Tau, and expression of AD-associated α-COP confers a toxic gain of function, resulting in potentially pathogenic changes in both APP and Tau.
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