ArticleCellular and molecular life sciences : CMLS2009
Inhibition of cholesterol recycling impairs cellular PrP(Sc) propagation.
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 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Contrasting roles of autophagy in cellular prion infection.Autophagy · 2025Article
- Treatment with efavirenz extends survival in a Creutzfeldt-Jakob disease model by regulating brain cholesterol metabolism.JCI insight · 2025Article
- Cholesterol and its reciprocal association with prion infection.Cell and tissue research · 2023Review
- Hepatitis B Virus Targets Lipid Transport Pathways to Infect Hepatocytes.Cellular and molecular gastroenterology and hepatology · 2023Article
- Endosomal sorting drives the formation of axonal prion protein endoggresomes.Science advances · 2021Article
- Oral administration of repurposed drug targeting Cyp46A1 increases survival times of prion infected mice.Acta neuropathologica communications · 2021Article
- The Role of Vesicle Trafficking Defects in the Pathogenesis of Prion and Prion-Like Disorders.International journal of molecular sciences · 2020Review
- From Seeds to Fibrils and Back: Fragmentation as an Overlooked Step in the Propagation of Prions and Prion-Like Proteins.Biomolecules · 2020Review
- Review
- Endogenous Brain Lipids Inhibit Prion Amyloid FormationJournal of virology · 2017Article
- Melanin or a Melanin-Like Substance Interacts with the N-Terminal Portion of Prion Protein and Inhibits Abnormal Prion Protein Formation in Prion-Infected Cells.Journal of virology · 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
- Efficient inhibition of infectious prions multiplication and release by targeting the exosomal pathway.Cellular and molecular life sciences : CMLS · 2015Article
- Anti-prion activity found in beetle grub hemolymph ofBiochemistry and biophysics reports · 2015Article
- The multivesicular body is the major internal site of prion conversion.Journal of cell science · 2015Article
- Review
- Gene expression profiling of brains from bovine spongiform encephalopathy (BSE)-infected cynomolgus macaques.BMC genomics · 2014Article
- Efficacy and mechanism of a glycoside compound inhibiting abnormal prion protein formation in prion-infected cells: implications of interferon and phosphodiesterase 4D-interacting protein.Journal of virology · 2014Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The infectious agent in prion diseases consists of an aberrantly folded isoform of the cellular prion protein (PrP(c)), termed PrP(Sc), which accumulates in brains of affected individuals. Studies on prion-infected cultured cells indicate that cellular cholesterol homeostasis influences PrP(Sc) propagation. Here, we demonstrate that the cellular PrP(Sc) content decreases upon accumulation of cholesterol in late endosomes, as induced by NPC-1 knock-down or treatment with U18666A. PrP(c) trafficking, lipid raft association, and membrane turnover are not significantly altered by such treatments. Cellular PrP(Sc) formation is not impaired, suggesting that PrP(Sc) degradation is increased by intracellular cholesterol accumulation. Interestingly, PrP(Sc) propagation in U18666A-treated cells was partially restored by overexpression of rab 9, which causes redistribution of cholesterol and possibly of PrP(Sc) to the trans-Golgi network. Surprisingly, rab 9 overexpression itself reduced cellular PrP(Sc) content, indicating that PrP(Sc) production is highly sensitive to alterations in dynamics of vesicle trafficking.
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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.