ArticleFrontiers in cellular neuroscience2015
The prion protein constitutively controls neuronal store-operated Ca(2+) entry through Fyn kinase.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Mitochondrial CaScientific reports · 2024Article
- Neuronal Store-Operated Calcium Channels.Molecular neurobiology · 2023Review
- SOD1 in ALS: Taking Stock in Pathogenic Mechanisms and the Role of Glial and Muscle Cells.Antioxidants (Basel, Switzerland) · 2022Review
- Article
- Melatonin: Regulation of Prion Protein Phase Separation in Cancer Multidrug Resistance.Molecules (Basel, Switzerland) · 2022Review
- Regulation of Endoplasmic Reticulum-Mitochondria Tethering and CaInternational journal of molecular sciences · 2021Article
- Accumulation of cellular prion protein within β-amyloid oligomer plaques in aged human brains.Brain pathology (Zurich, Switzerland) · 2021Article
- Interaction between Aβ and Tau in the Pathogenesis of Alzheimer's Disease.International journal of biological sciences · 2021Review
- ALS-Associated SOD1(G93A) Decreases SERCA Pump Levels and Increases Store-Operated CaInternational journal of molecular sciences · 2019Article
- Binding between Prion Protein and Aβ Oligomers Contributes to the Pathogenesis of Alzheimer's Disease.Virologica Sinica · 2019Review
- The Link of the Prion Protein with CaInternational journal of molecular sciences · 2019Review
- The Prion Protein Regulates Synaptic Transmission by Controlling the Expression of Proteins Key to Synaptic Vesicle Recycling and Exocytosis.Molecular neurobiology · 2019Article
- Prion acute synaptotoxicity is largely driven by protease-resistant PrPSc species.PLoS pathogens · 2018Article
- Neuronal pathophysiology featuring PrPPrion · 2018Article
- α-synuclein interacts with PrPNature neuroscience · 2017Article
- Generation and validation of novel adeno-associated viral vectors for the analysis of CaScientific reports · 2017Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prion protein (PrP(C)) is a cell surface glycoprotein mainly expressed in neurons, whose misfolded isoforms generate the prion responsible for incurable neurodegenerative disorders. Whereas PrP(C) involvement in prion propagation is well established, PrP(C) physiological function is still enigmatic despite suggestions that it could act in cell signal transduction by modulating phosphorylation cascades and Ca(2+) homeostasis. Because PrP(C) binds neurotoxic protein aggregates with high-affinity, it has also been proposed that PrP(C) acts as receptor for amyloid-β (Aβ) oligomers associated with Alzheimer's disease (AD), and that PrP(C)-Aβ binding mediates AD-related synaptic dysfunctions following activation of the tyrosine kinase Fyn. Here, use of gene-encoded Ca(2+) probes targeting different cell domains in primary cerebellar granule neurons (CGN) expressing, or not, PrP(C), allowed us to investigate whether PrP(C) regulates store-operated Ca(2+) entry (SOCE) and the implication of Fyn in this control. Our findings show that PrP(C) attenuates SOCE, and Ca(2+) accumulation in the cytosol and mitochondria, by constitutively restraining Fyn activation and tyrosine phosphorylation of STIM1, a key molecular component of SOCE. This data establishes the existence of a PrP(C)-Fyn-SOCE triad in neurons. We also demonstrate that treating cerebellar granule and cortical neurons with soluble Aβ(1-42) oligomers abrogates the control of PrP(C) over Fyn and SOCE, suggesting a PrP(C)-dependent mechanizm for Aβ-induced neuronal Ca(2+) dyshomeostasis.
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