ArticleHuman molecular genetics2014
In vitro screen of prion disease susceptibility genes using the scrapie cell assay.
Article in Human molecular genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Finding memo: versatile interactions of the VPS10p-Domain receptors in Alzheimer's disease.Molecular neurodegeneration · 2022Pooled it
- Genome-Wide Association Study of Leukocyte Traits Reveals Candidate Genes Associated With Immunity in Holstein Cattle From Southern China.Veterinary medicine and science · 2026Article
- RNA-seq analyses reveal the relevance of RNAs involved in ribosomal complex to induce mammalian prion protein aggregation and phase separationRNA biology · 2025Article
- Alzheimer's disease brain-derived tau extracts show differential processing and transcriptional effects in human astrocytes.iScience · 2025Article
- Human Genetic Evidence for New Targets in Prion Diseases: Opportunities and Challenges.Sub-cellular biochemistry · 2025Review
- Diminished Neuronal ESCRT-0 Function Exacerbates AMPA Receptor Derangement and Accelerates Prion-Induced Neurodegeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Heat shock protein Hspa13 regulates endoplasmic reticulum and cytosolic proteostasis through modulation of protein translocation.The Journal of biological chemistry · 2022Article
- Heterozygous loss of Zbtb38 leads to early embryonic lethality via the suppression of Nanog and Sox2 expression.Cell proliferation · 2022Article
- Propagation and Dissemination Strategies of Transmissible Spongiform Encephalopathy Agents in Mammalian Cells.International journal of molecular sciences · 2022Review
- FKBP52 in Neuronal Signaling and Neurodegenerative Diseases: A Microtubule Story.International journal of molecular sciences · 2022Review
- Development of prognostic models for survival and care status in sporadic Creutzfeldt-Jakob disease.Brain communications · 2022Article
- Decrease of neuronal FKBP4/FKBP52 modulates perinuclear lysosomal positioning and MAPT/Tau behavior during MAPT/Tau-induced proteotoxic stress.Autophagy · 2021Article
- Functional genomics screen identifies proteostasis targets that modulate prion protein (PrP) stability.Cell stress & chaperones · 2021Article
- Identification of novel risk loci and causal insights for sporadic Creutzfeldt-Jakob disease: a genome-wide association study.The Lancet. Neurology · 2020Article
- Modulation of Proteome Profile in AβPP/PS1 Mice Hippocampus, Medial Prefrontal Cortex, and Striatum by Palm Oil Derived Tocotrienol-Rich Fraction.Journal of Alzheimer's disease : JAD · 2019Article
- Regional protein expression in human Alzheimer's brain correlates with disease severity.Communications biology · 2019Article
- Transcriptomic Determinants of Scrapie Prion Propagation in Cultured Ovine Microglia.PloS one · 2016Article
- A systematic investigation of production of synthetic prions from recombinant prion protein.Open biology · 2015Article
- The emerging role of peptidyl-prolyl isomerase chaperones in tau oligomerization, amyloid processing, and Alzheimer's disease.Journal of neurochemistry · 2015Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Prion diseases (transmissible spongiform encephalopathies) are fatal neurodegenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in sheep and bovine spongiform encephalopathy in cattle. While genome-wide association studies in human and quantitative trait loci mapping in mice have provided evidence for multiple susceptibility genes, few of these have been confirmed functionally. Phenotyping mouse models is generally the method of choice. However, this is not a feasible option where many novel genes, without pre-existing models, would need to be tested. We have therefore developed and applied an in-vitro screen to triage and prioritize candidate modifier genes for more detailed future studies which is faster, far more cost effective and ethical relative to mouse bioassay models. An in vitro prion bioassay, the scrapie cell assay, uses a neuroblastoma-derived cell line (PK1) that is susceptible to RML prions and able to propagate prions at high levels. In this study, we have generated stable gene silencing and/or overexpressing PK1-derived cell lines to test whether perturbation of 14 candidate genes affects prion susceptibility. While no consistent differences were determined for seven genes, highly significant changes were detected for Zbtb38, Sorcs1, Stmn2, Hspa13, Fkbp9, Actr10 and Plg, suggesting that they play key roles in the fundamental processes of prion propagation or clearance. Many neurodegenerative diseases involve the accumulation of misfolded protein aggregates and 'prion-like' seeding and spread has been implicated in their pathogenesis. It is therefore expected that some of these prion-modifier genes may be of wider relevance in 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.