ArticleBrain pathology (Zurich, Switzerland)2019
A domain responsible for spontaneous conversion of bank vole prion protein.
Article in Brain pathology (Zurich, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 21 citations in OpenAlex.
- Enhanced Sensitivity of a Modified Quaking-Induced Conversion Diagnostic Test for the Broad Detection of Sporadic and Inherited Prion Diseases: A Retrospective Study.Annals of neurology · 2026Article
- The Phenotypic Spectrum of Sporadic Creutzfeldt-Jakob Disease Cortical Subtype.Annals of neurology · 2026Article
- Limited transmission of V180I genetic Creutzfeldt-Jakob disease in knock-in mice models.The Journal of general virology · 2026Article
- Transmission and Characterization of Creutzfeldt-Jakob Disease and Chronic Wasting Disease in the North American Deer Mouse.Viruses · 2025Article
- Cofactors facilitate bona fide prion misfolding in vitro but are not necessary for the infectivity of recombinant murine prions.PLoS pathogens · 2025Article
- Unsuccessful transmissions of atypical genetic Creutzfeldt-Jakob disease (PRNP p.T183A-129M) in transgenic mice.Acta neuropathologica · 2024Article
- The molecular determinants of a universal prion acceptor.PLoS pathogens · 2024Article
- Convergent generation of atypical prions in knockin mouse models of genetic prion disease.The Journal of clinical investigation · 2024Article
- Bona fide atypical scrapie faithfully reproduced for the first time in a rodent model.Acta neuropathologica communications · 2022Article
- A single amino acid residue in bank vole prion protein drives permissiveness to Nor98/atypical scrapie and the emergence of multiple strain variants.PLoS pathogens · 2022Article
- Identification of a homology-independent linchpin domain controlling mouse and bank vole prion protein conversion.PLoS pathogens · 2020Article
- Understanding Prion Strains: Evidence from Studies of the Disease Forms Affecting Humans.Viruses · 2019Review
- Recent advances on the molecular pathogenesis of prion diseases.Brain pathology (Zurich, Switzerland) · 2019Article
- Two distinct prions in fatal familial insomnia and its sporadic form.Brain communications · 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
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bank vole is a small rodent that shows high susceptibility to infection with diverse prion strains. To determine whether the increased susceptibility of bank voles to prion diseases can be attributed to the intrinsic nature of bank vole prion protein (PrP) or to host factors other than PrP, we produced transgenic mice overexpressing bank vole PrP. These transgenic mice spontaneously developed neurological illness with spongiform changes and the accumulation of abnormal PrP in the brain. Then, we produced transgenic mice overexpressing chimeric mouse/bank vole PrP, which differs from mouse PrP only at two residues located at the C-terminus, to determine the minimum essential domain for the induction of spontaneous generation of abnormal PrP. These transgenic mice also developed spontaneous neurological illness with spongiform changes and the accumulation of abnormal PrP in the brain. In addition, knock-in mice expressing bank vole PrP at the same level as that of wild-type mice did not develop spontaneous disease but showed high susceptibility to infection with diverse prion strains, similarly to bank voles. Taken together, these findings show that bank vole PrP has a high propensity for the conformational conversion both in spontaneous disease and in prion infection, probably due to the characteristic structural properties of the C-terminal domain.
Indexed as
Identifiers
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.