ReviewPrion
Heterozygous inhibition in prion infection: the stone fence model.
Review in Prion. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed.
- Odocoileus virginianus PRNP sequencing reveals AF (QVeterinary research · 2026Article
- Allelic Interference in Prion Replication Is Modulated by the Convertibility of the Interfering PrPmBio · 2021Article
- Application of yeast to studying amyloid and prion diseases.Advances in genetics · 2020Review
- A domain responsible for spontaneous conversion of bank vole prion protein.Brain pathology (Zurich, Switzerland) · 2019Article
- Human prion diseases: surgical lessons learned from iatrogenic prion transmission.Neurosurgical focus · 2016Review
- Protective V127 prion variant prevents prion disease by interrupting the formation of dimer and fibril from molecular dynamics simulations.Scientific reports · 2016Article
- Role of the goat K222-PrP(C) polymorphic variant in prion infection resistance.Journal of virology · 2014Article
- Deciphering the pathogenesis of sporadic Creutzfeldt-Jakob disease with codon 129 M/V and type 2 abnormal prion protein.Acta neuropathologica communications · 2013Article
- Effects of polymorphisms in ovine and caprine prion protein alleles on cell-free conversion.Veterinary research · 2011Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human PrP gene (PRNP) has two major polymorphic codons: 129 for methionine (M) or valine (V) and 219 for glutamate (E) or lysine (K). The PRNP heterozygotes appear to be protected from sporadic CJD compared to the PRNP homozygotes. The molecular mechanism responsible for these protective effects of PRNP heterozygosity has remained elusive. In this review, we describe the inhibition of PrP conversion observed in a series of transmission studies using PRNP heterozygous animal models. In vCJD infection, the conversion incompetent human PrP 129V molecules showed an inhibitory effect on the conversion of human PrP 129M molecules in the 129M/V heterozygous mice. Furthermore, though the human PrP 219E and PrP 219K were both conversion competent in vCJD infection, these conversion competent PrP molecules showed an inhibitory effect in the 219E/K heterozygous animals. To explain this heterozygous inhibition, we propose a possible mechanism designated as the stone fence model.
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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.