ArticlePrion2012
Unraveling the neuroprotective mechanisms of PrP (C) in excitotoxicity.
Article in Prion, 2012. 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, 20 citations in OpenAlex.
- Exploring the Biological Connection Between Tau and PrPMolecular neurobiology · 2025Review
- Impaired Synaptic Plasticity Mechanisms in Alzheimer's Disease.Metabolic brain disease · 2025Review
- New Light on Prions: Putative Role of PrPInternational journal of molecular sciences · 2024Review
- Cellular prion protein offers neuroprotection in astrocytes submitted to amyloid β oligomer toxicity.Molecular and cellular biochemistry · 2023Article
- Cellular prion protein activates Caspase 3 for apoptotic defense mechanism in astrocytes.Molecular and cellular biochemistry · 2021Article
- Tau Protein as a New Regulator of Cellular Prion Protein Transcription.Molecular neurobiology · 2020Article
- Review
- Implications of peptide assemblies in amyloid diseases.Chemical Society reviews · 2017Review
- Expression of Reactive Oxygen Species-Related Transcripts in Egyptian Children With Autism.Biomarker insights · 2017Article
- RNA sequencing and proteomics approaches reveal novel deficits in the cortex ofMolecular autism · 2017Article
- Review
- Functions of the cellular prion protein, the end of Moore's law, and Ockham's razor theory.Prion · 2016Article
- Involvement of PrP(C) in kainate-induced excitotoxicity in several mouse strains.Scientific reports · 2015Article
- Anchorless 23-230 PrPC interactomics for elucidation of PrPC protective role.Molecular neurobiology · 2014Article
- Gene expression resulting from PrPC ablation and PrPC overexpression in murine and cellular models.Molecular neurobiology · 2014Review
- Lack of influence of prion protein gene expression on kainate-induced seizures in mice: studies using congenic, coisogenic and transgenic strains.Neuroscience · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Knowledge of the natural roles of cellular prion protein (PrP (C) ) is essential to an understanding of the molecular basis of prion pathologies. This GPI-anchored protein has been described in synaptic contacts, and loss of its synaptic function in complex systems may contribute to the synaptic loss and neuronal degeneration observed in prionopathy. In addition, Prnp knockout mice show enhanced susceptibility to several excitotoxic insults, GABAA receptor-mediated fast inhibition was weakened, LTP was modified and cellular stress increased. Although little is known about how PrP (C) exerts its function at the synapse or the downstream events leading to PrP (C) -mediated neuroprotection against excitotoxic insults, PrP (C) has recently been reported to interact with two glutamate receptor subunits (NR2D and GluR6/7). In both cases the presence of PrP (C) blocks the neurotoxicity induced by NMDA and Kainate respectively. Furthermore, signals for seizure and neuronal cell death in response to Kainate in Prnp knockout mouse are associated with JNK3 activity, through enhancing the interaction of GluR6 with PSD-95. In combination with previous data, these results shed light on the molecular mechanisms behind the role of PrP (C) in excitotoxicity. Future experimental approaches are suggested and discussed.
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Registered trials
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