ArticleThe Journal of biological chemistry2009
Prion-induced activation of cholesterogenic gene expression by Srebp2 in neuronal cells.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Regulation of Neuronal Senescence byBiology · 2026Article
- Treatment with efavirenz extends survival in a Creutzfeldt-Jakob disease model by regulating brain cholesterol metabolism.JCI insight · 2025Article
- Article
- Human Genetic Evidence for New Targets in Prion Diseases: Opportunities and Challenges.Sub-cellular biochemistry · 2025Review
- Cholesterol and its reciprocal association with prion infection.Cell and tissue research · 2023Review
- Protein-lipid interactions and protein anchoring modulate the modes of association of the globular domain of the Prion protein and Doppel protein to model membrane patches.Frontiers in bioinformatics · 2023Article
- Propagation and Dissemination Strategies of Transmissible Spongiform Encephalopathy Agents in Mammalian Cells.International journal of molecular sciences · 2022Review
- What is the role of lipids in prion conversion and disease?Frontiers in molecular neuroscience · 2022Review
- Volatile Anesthetic Sevoflurane Precursor 1,1,1,3,3,3-Hexafluoro-2-Propanol (HFIP) Exerts an Anti-Prion Activity in Prion-Infected Culture Cells.Neurochemical research · 2021Article
- Large-scale lipidomic profiling identifies novel potential biomarkers for prion diseases and highlights lipid raft-related pathways.Veterinary research · 2021Article
- Oral administration of repurposed drug targeting Cyp46A1 increases survival times of prion infected mice.Acta neuropathologica communications · 2021Article
- Dimerization of the cellular prion protein inhibits propagation of scrapie prions.The Journal of biological chemistry · 2018Article
- Immunization of cervidized transgenic mice with multimeric deer prion protein induces self-antibodies that antagonize chronic wasting disease infectivity in vitro.Scientific reports · 2017Article
- Prion infection impairs lysosomal degradation capacity by interfering with rab7 membrane attachment in neuronal cells.Scientific reports · 2016Article
- Screening and Identification of APOC1 as a Novel Potential Biomarker for Differentiate ofFrontiers in microbiology · 2016Article
- Application of "Omics" Technologies for Diagnosis and Pathogenesis of Neurological Infections.Current neurology and neuroscience reports · 2015Review
- Article
- Review
- Assessing proteinase K resistance of fish prion proteins in a scrapie-infected mouse neuroblastoma cell line.Viruses · 2014Article
- Gene expression profiling of brains from bovine spongiform encephalopathy (BSE)-infected cynomolgus macaques.BMC genomics · 2014Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prion diseases are neurodegenerative diseases associated with the accumulation of a pathogenic isoform of the host-encoded prion protein. The cellular responses to prion infection are not well defined. By performing microarray analysis on cultured neuronal cells infected with prion strain 22L, in the group of up-regulated genes we observed predominantly genes of the cholesterol pathway. Increased transcript levels of at least nine enzymes involved in cholesterol synthesis, including the gene for the rate-limiting hydroxymethylglutaryl-CoA reductase, were detected. Up-regulation of cholesterogenic genes was attributable to a prion-dependent increase in the amount and activity of the sterol regulatory element-binding protein Srebp2, resulting in elevated levels of total and free cellular cholesterol. The up-regulation of cholesterol biosynthesis appeared to be a characteristic response of neurons to prion challenge, as cholesterogenic transcripts were also elevated in persistently infected GT-1 cells and prion-exposed primary hippocampal neurons but not in microglial cells and primary astrocytes. These results convincingly demonstrate that prion propagation not only depends on the availability of cholesterol but that neuronal cells themselves respond to prions with specific up-regulation of cholesterol biosynthesis.
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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.