ArticleProceedings of the National Academy of Sciences of the United States of America2010
Prion protein interaction with stress-inducible protein 1 enhances neuronal protein synthesis via mTOR.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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
60 citing papers in PubMed, 103 citations in OpenAlex.
- XBP1s-Orchestrated Soluble Mediators: Participants of Oxidative Stress in Renal Ischemia-Reperfusion Injury Following Donation After Circulatory Death.Mediators of inflammation · 2026Review
- The role of the FKBP51-Hsp90 complex in Alzheimer's disease: An emerging new drug target.Cell stress & chaperones · 2024Review
- Novel therapeutic targets for major depressive disorder related to oxidative stress identified by integrative multi-omics and multi-trait study.Translational psychiatry · 2024Article
- Prion disease modelled in Drosophila.Cell and tissue research · 2023Review
- Genotype by environment interactions for chronic wasting disease in farmed US white-tailed deer.G3 (Bethesda, Md.) · 2022Article
- Propagation and Dissemination Strategies of Transmissible Spongiform Encephalopathy Agents in Mammalian Cells.International journal of molecular sciences · 2022Review
- Review
- Harnessing the Physiological Functions of Cellular Prion Protein in the Kidneys: Applications for Treating Renal Diseases.Biomolecules · 2021Review
- The Role of Cellular Prion Protein in Promoting Stemness and Differentiation in Cancer.Cancers · 2021Review
- PrPFrontiers in molecular neuroscience · 2021Review
- The Cellular Prion Protein-ROCK Connection: Contribution to Neuronal Homeostasis and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2021Review
- Cellular Prion Protein (PrPc): Putative Interacting Partners and Consequences of the Interaction.International journal of molecular sciences · 2020Review
- Increased levels of Stress-inducible phosphoprotein-1 accelerates amyloid-β deposition in a mouse model of Alzheimer's disease.Acta neuropathologica communications · 2020Article
- Show Me Your Friends and I Tell You Who You Are: The Many Facets of Prion Protein in Stroke.Cells · 2020Review
- STIP1 Tissue Expression Is Associated with Survival in Chemotherapy-Treated Bladder Cancer Patients.Pathology oncology research : POR · 2020Article
- Transcriptional signature of prion-induced neurotoxicity in a Drosophila model of transmissible mammalian prion disease.The Biochemical journal · 2020Article
- Emerging Role of Cellular Prion Protein in the Maintenance and Expansion of Glioma Stem Cells.Cells · 2019Review
- Prion Protein in Glioblastoma Multiforme.International journal of molecular sciences · 2019Review
- Hsp90 and Its Co-Chaperones in Neurodegenerative Diseases.International journal of molecular sciences · 2019Review
- The Protozoan Parasite Toxoplasma gondii Selectively Reprograms the Host Cell Translatome.Infection and immunity · 2018Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
Transmissible spongiform encephalopathies are fatal neurodegenerative diseases caused by the conversion of prion protein (PrP(C)) into an infectious isoform (PrP(Sc)). How this event leads to pathology is not fully understood. Here we demonstrate that protein synthesis in neurons is enhanced via PrP(C) interaction with stress-inducible protein 1 (STI1). We also show that neuroprotection and neuritogenesis mediated by PrP(C)-STI1 engagement are dependent upon the increased protein synthesis mediated by PI3K-mTOR signaling. Strikingly, the translational stimulation mediated by PrP(C)-STI1 binding is corrupted in neuronal cell lines persistently infected with PrP(Sc), as well as in primary cultured hippocampal neurons acutely exposed to PrP(Sc). Consistent with this, high levels of eukaryotic translation initiation factor 2alpha (eIF2alpha) phosphorylation were found in PrP(Sc)-infected cells and in neurons acutely exposed to PrP(Sc). These data indicate that modulation of protein synthesis is critical for PrP(C)-STI1 neurotrophic functions, and point to the impairment of this process during PrP(Sc) infection as a possible contributor to neurodegeneration.
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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.