ArticleInternational journal of biomedical science : IJBS2006
Regulation of prion protein expression: a potential site for therapeutic intervention in the transmissible spongiform encephalopathies.
Article in International journal of biomedical science : IJBS, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed.
- Accurate genomic predictions for chronic wasting disease in North American elk.G3 (Bethesda, Md.) · 2026Article
- Exploring the Biological Connection Between Tau and PrPMolecular neurobiology · 2025Review
- Roles of prion proteins in mammalian development.Animal cells and systems · 2024Review
- Characterization of Amyloid-β Deposits in Bovine Brains.Journal of Alzheimer's disease : JAD · 2016Article
- Translation of the prion protein mRNA is robust in astrocytes but does not amplify during reactive astrocytosis in the mouse brain.PloS one · 2014Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Transmissible Spongiform Encephalopathies (TSEs) are a group of rare neurodegenerative diseases, which can be transmitted between members of the same species and possibly across different species. The link between the emergence of Bovine Spongiform Encephalopathy (BSE) and the new variant form of Creutzfedlt Jakob Disease (vCJD) has been the cause of much public concern. vCJD is the most widely known of the human TSEs but by no means the most common; inherited and sporadic forms are much more prevalent. The agent responsible for these diseases is a conformationally altered form of a normal cell surface glycoprotein, called the prion protein (PrP). The normal isoform must be present for the disease to progress, and disease incubation time decreases with increased PrP expression. There is still no cure for any of these diseases but recent advances in the understanding of how prion protein expression is regulated at the genetic level, and of exogenous factors modulating expression levels, may provide new insights into potential therapeutic targets for disease management by down regulation of cellular PrP levels.
Indexed as
Identifiers
23674999PMC3614639What OpenQuestion holds
Registered trials
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