ArticleCellular and molecular life sciences : CMLS2009
Activation and repression of prion protein expression by key regions of intron 1.
Article in Cellular and molecular life sciences : CMLS, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 10 citations in OpenAlex.
- Copper chaperone antioxidant 1: multiple roles and a potential therapeutic target.Journal of molecular medicine (Berlin, Germany) · 2023Review
- CpG site DNA methylation patterns reveal a novel regulatory element in the mouse prion protein gene.The Journal of veterinary medical science · 2017Article
- IGF-1-induced enhancement of PRNP expression depends on the negative regulation of transcription factor FOXO3a.PloS one · 2013Article
- Role of the cellular prion protein in the neuron adaptation strategy to copper deficiency.Cellular and molecular neurobiology · 2012Article
- Transcriptional regulation of the beta-synuclein 5'-promoter metal response element by metal transcription factor-1.PloS one · 2011Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of the prion protein is necessary for infection with prion diseases. Altered expression levels may play an important role in susceptibility to infection. Therefore, understanding the mechanisms that regulate prion protein expression is of great importance. It was previously shown that expression of the prion protein is to some degree regulated by an alternative promoter within intron 1. Studies using GFP and luciferase reporter systems were undertaken to determine key sites for the repression and activation of expression of the prion protein driven by intron 1. We identified a region within intron 1 sufficient to drive prion protein expression. Our findings highlight two potential repressor regions. Both regions have binding sites for the known repressor Hes-1. Hes-1 overexpression caused a dramatic decrease in PrP protein expression. Additionally, we have identified Atox-1 as a transcription factor that upregulates prion protein expression. These findings clearly indicate that intron 1 plays a key role in regulation of prion protein expression levels.
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Registered trials
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