ArticleBiochimica et biophysica acta2009
Cytoplasmic prion protein induces forebrain neurotoxicity.
Article in Biochimica et biophysica acta, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Copper Coordination to the Prion Fragment (95-126): Implications for Neurodegenerative Diseases.International journal of molecular sciences · 2026Article
- Soluble N-terminal region of prion protein causes rapid neurodegeneration in prion disease.Science advances · 2025Article
- Disease-Associated Q159X Mutant Prion Protein Is Sufficient to Cause Fatal Degenerative Disease in Mice.Molecular neurobiology · 2024Article
- Transgenic Overexpression of the Disordered Prion Protein N1 Fragment in Mice Does Not Protect Against Neurodegenerative Diseases Due to Impaired ER Translocation.Molecular neurobiology · 2020Article
- Transcriptional signature of prion-induced neurotoxicity in a Drosophila model of transmissible mammalian prion disease.The Biochemical journal · 2020Article
- The Sec61/SecY complex is inherently deficient in translocating intrinsically disordered proteins.The Journal of biological chemistry · 2017Article
- Prion protein inhibits fast axonal transport through a mechanism involving casein kinase 2.PloS one · 2017Article
- Functions of the cellular prion protein, the end of Moore's law, and Ockham's razor theory.Prion · 2016Article
- Prion-induced neurotoxicity: Possible role for cell cycle activity and DNA damage response.World journal of virology · 2015Review
- Intraperitoneal Infection of Wild-Type Mice with Synthetically Generated Mammalian Prion.PLoS pathogens · 2015Article
- Cytosolic PrP can participate in prion-mediated toxicity.Journal of virology · 2014Article
- De novo generation of infectious prions with bacterially expressed recombinant prion protein.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Prion disease: a tale of folds and strains.Brain pathology (Zurich, Switzerland) · 2013Review
- Structural features within the nascent chain regulate alternative targeting of secretory proteins to mitochondria.The EMBO journal · 2013Article
- Prion protein-mediated toxicity of amyloid-β oligomers requires lipid rafts and the transmembrane LRP1.The Journal of biological chemistry · 2013Article
- Highly neurotoxic monomeric α-helical prion protein.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
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- Interactions of prion protein with intracellular proteins: so many partners and no consequences?Cellular and molecular neurobiology · 2010Review
- Context-dependent perturbation of neural systems in transgenic mice expressing a cytosolic prion protein.NeuroImage · 2010Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The prion protein (PrP) is essential for the pathogenesis of prion disease. PrP has been detected in the cytosol of neurons and transgenic mice expressing PrP in the cytosol (cyPrP) under a pan-neuronal promoter developed rapid cerebellar granule neuron degeneration. Yet, it remains unclear whether cyPrP is capable to cause toxicity in other neuronal populations. Here, we report that transgenic mice expressing cyPrP in the forebrain neurons developed behavioral abnormalities including clasping and hyperactivity. These mice had reduced thickness in cortex and developed astrogliosis in hippocampal and cortical regions. Moreover, cyPrP in these mice was recognized by the A11 anti-oligomer antibody and was associated with the hydrophobic lipid core of membranes, indicating that cyPrP oligomer caused membrane perturbation contributes to cyPrP neurotoxicity. Together, our results clearly revealed that cyPrP is able to cause toxicity in different neuronal populations, supporting a role of cyPrP in PrP-mediated neurodegenerative disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.