ArticlePloS one2015
Strain-Dependent Effect of Macroautophagy on Abnormally Folded Prion Protein Degradation in Infected Neuronal Cells.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Prion propagation is controlled by a hierarchical network involving the nuclear Tfap2c and hnRNP K factors and the cytosolic mTORC1 complex.PLoS pathogens · 2026Article
- Contrasting roles of autophagy in cellular prion infection.Autophagy · 2025Article
- Novel anti-prion compounds screening in prion-infected cell culture model combined with surface plasmon resonance analysis.Scientific reports · 2025Article
- Therapeutic effect of curcumin derivative GT863 on prion-infected mice.Scientific reports · 2025Article
- Experimental and clinical tests of FDA-approved kinase inhibitors for the treatment of neurological disorders (update 2024).Exploration of drug science · 2025Article
- FDA-Approved Kinase Inhibitors in Preclinical and Clinical Trials for Neurological Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Pentosan polysulfate induces low-level persistent prion infection keeping measurable seeding activity without PrP-res detection in Fukuoka-1 infected cell cultures.Scientific reports · 2022Article
- From Cell Culture to Organoids-Model Systems for Investigating Prion Strain Characteristics.Biomolecules · 2021Review
- Administration of FK506 from Late Stage of Disease Prolongs Survival of Human Prion-Inoculated Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Article
- Novel Compounds Identified by Structure-Based Prion Disease Drug Discovery Using In Silico Screening Delay the Progression of an Illness in Prion-Infected Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Article
- From Seeds to Fibrils and Back: Fragmentation as an Overlooked Step in the Propagation of Prions and Prion-Like Proteins.Biomolecules · 2020Review
- An Update on Autophagy in Prion Diseases.Frontiers in bioengineering and biotechnology · 2020Review
- Type I interferon protects neurons from prions in in vivo models.Brain : a journal of neurology · 2019Article
- Autophagy pathways in the treatment of prion diseases.Current opinion in pharmacology · 2019Review
- Identification of Alprenolol Hydrochloride as an Anti-prion Compound Using Surface Plasmon Resonance Imaging.Molecular neurobiology · 2019Article
- Disulfide-crosslink scanning reveals prion-induced conformational changes and prion strain-specific structures of the pathological prion protein PrPThe Journal of biological chemistry · 2018Article
- Cellular mechanisms responsible for cell-to-cell spreading of prions.Cellular and molecular life sciences : CMLS · 2018Review
- Autophagy regulates exosomal release of prions in neuronal cells.The Journal of biological chemistry · 2018Article
- Structure-Based Drug Discovery for Prion Disease Using a Novel Binding Simulation.EBioMedicine · 2016Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prion diseases are neurodegenerative disorders caused by the accumulation of abnormal prion protein (PrPSc) in the central nervous system. With the aim of elucidating the mechanism underlying the accumulation and degradation of PrPSc, we investigated the role of autophagy in its degradation, using cultured cells stably infected with distinct prion strains. The effects of pharmacological compounds that inhibit or stimulate the cellular signal transduction pathways that mediate autophagy during PrPSc degradation were evaluated. The accumulation of PrPSc in cells persistently infected with the prion strain Fukuoka-1 (FK), derived from a patient with Gerstmann-Sträussler-Scheinker syndrome, was significantly increased in cultures treated with the macroautophagy inhibitor 3-methyladenine (3MA) but substantially reduced in those treated with the macroautophagy inducer rapamycin. The decrease in FK-derived PrPSc levels was mediated, at least in part, by the phosphatidylinositol 3-kinase/MEK signalling pathway. By contrast, neither rapamycin nor 3MA had any apparently effect on PrPSc from either the 22L or the Chandler strain, indicating that the degradation of PrPSc in host cells might be strain-dependent.
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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.