ArticleNature communications2025
Prion protein promotes copper toxicity in Wilson disease.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Cuprous Ions Binding to Cytosine and Guanine Oligonucleotides.Chembiochem : a European journal of chemical biology · 2026Article
- Copper Coordination to the Prion Fragment (95-126): Implications for Neurodegenerative Diseases.International journal of molecular sciences · 2026Article
- Copper in Human Health and Disease: Insights from Inherited Disorders.Physiology (Bethesda, Md.) · 2026Review
- [ModifiedNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- High copper levels induce oxidative stress and inflammatory processes in a cell culture model of Wilson's disease.Molecular and cellular biochemistry · 2026Article
- Tackling cuproptosis: from metabolic rewiring to therapeutic exploitation in cancer.Cellular & molecular immunology · 2026Review
- Deciphering Cu(II) EPR in biological buffers: Implications for copper protein studies.Journal of inorganic biochemistry · 2026Article
- Inactivation of Atp7b Copper Transporter in Intestinal Epithelial Cells Is Associated with Altered Lipid Processing and Cell Growth Machinery Independent from Hepatic Copper Accumulation and Severity of Liver Histology.The American journal of pathology · 2026Article
- Cuproptosis and Its Impact on Cardiovascular Health: Mechanisms and Therapeutic Opportunities.Cardiovascular toxicology · 2026Review
- Multiscale computational genomics in Wilson disease: from atomic dynamics to clinical prediction.Frontiers in genetics · 2026Review
- Some Properties of theInternational journal of molecular sciences · 2025Article
- Comparative review of copper-associated chronic hepatitis in dogs and Wilson disease in humans.Frontiers in veterinary science · 2025Review
Corrections and comments
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Authors and funding
26 authors.
Funding
Abstract
Copper (Cu) is a vitally important micronutrient, whose balance between essential and toxic levels requires a tightly regulated network of proteins. Dysfunction in key components of this network leads to the disruption of Cu homeostasis, resulting in fatal disorders such as Wilson disease, which is caused by mutations in the hepatic Cu efflux transporter ATP7B. Unfortunately, the molecular targets for normalizing Cu homeostasis in Wilson disease remain poorly understood. Here, using genome-wide screening, we identified the cellular prion protein (PrP) as an important mediator of Cu toxicity in WD. Loss of ATP7B stimulates hepatic expression of PrP, which promotes endocytic Cu uptake, leading to toxic Cu overload. Suppression of PrP significantly reduces Cu toxicity in cell and animal models of Wilson disease. These findings highlight the critical regulatory role of PrP in copper metabolism and open new avenues for exploring the therapeutic potential of PrP suppression in Wilson disease.
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