ReviewMolecular and cellular neurosciences2015
Prion degradation pathways: Potential for therapeutic intervention.
Review in Molecular and cellular neurosciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
- Exposure of cells to prions induces prion strain-dependent changes in mitochondrial redox state and respiration.Journal of cell science · 2026Article
- CpG oligodeoxynucleotide reduces PrPMolecules and cells · 2026Article
- Theory and simulations of delayed stochastic and deterministic models of prion diseases.Journal of mathematical biology · 2026Article
- NOTCH3 CADASIL Variant Receptor Aggregation Requires NOTCH3 Wild-Type Receptors: Identification of Highly Selective Inhibitors That Block the Process.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Predicted high affinity binding of prion PRPC protein to Human Leukocyte Antigen (HLA).Journal of immunological sciences · 2026Article
- Molecular Mechanisms and Therapeutic Potential of Degron-Mediated Proteostasis Regulation in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2026Review
- Prions and protein aggregates as pathogens, self-propagating structures, biomarkers, and therapeutic targets.Microbiology and molecular biology reviews : MMBR · 2025Review
- New Therapeutic Modalities in Prion Diseases.Sub-cellular biochemistry · 2025Review
- Bovine spongiform encephalopathy: A review of current knowledge and challenges.Open veterinary journal · 2025Review
- Prion protein pathology in Ubiquilin 2 models of ALS.Neurobiology of disease · 2024Article
- Cytosolic GDH1 degradation restricts protein synthesis to sustain tumor cell survival following amino acid deprivation.The EMBO journal · 2021Article
- Therapeutic Assay with the Non-toxic C-Terminal Fragment of Tetanus Toxin (TTC) in Transgenic Murine Models of Prion Disease.Molecular neurobiology · 2021Article
- MicroRNAs in Prion Diseases-From Molecular Mechanisms to Insights in Translational Medicine.Cells · 2021Review
- A New Take on Prion Protein Dynamics in Cellular Trafficking.International journal of molecular sciences · 2020Review
- Identification of novel risk loci and causal insights for sporadic Creutzfeldt-Jakob disease: a genome-wide association study.The Lancet. Neurology · 2020Article
- Global analysis of protein degradation in prion infected cells.Scientific reports · 2020Article
- 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
- An Update on Autophagy in Prion Diseases.Frontiers in bioengineering and biotechnology · 2020Review
- Impairment of autophagy in scrapie-infected transgenic mice at the clinical stage.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Synthetic Prion Selection and Adaptation.Molecular neurobiology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Prion diseases are fatal neurodegenerative disorders. Pathology is closely linked to the misfolding of native cellular PrP(C) into the disease-associated form PrP(Sc) that accumulates in the brain as disease progresses. Although treatments have yet to be developed, strategies aimed at stimulating the degradation of PrP(Sc) have shown efficacy in experimental models of prion disease. Here, we describe the cellular pathways that mediate PrP(Sc) degradation and review possible targets for therapeutic intervention. This article is part of a Special Issue entitled 'Neuronal Protein'.
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What OpenQuestion holds
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.