ArticleJournal of virology2000
Upregulation of the genes encoding lysosomal hydrolases, a perforin-like protein, and peroxidases in the brains of mice affected with an experimental prion disease.
Article in Journal of virology, 2000. 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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28 citing papers in PubMed, 65 citations in OpenAlex.
- Disrupting membranes, controlling cell fate: the role of pore-forming proteins in cell death and therapy.Apoptosis : an international journal on programmed cell death · 2025Review
- Article
- The Roles of Peroxiredoxin 6 in Brain Diseases.Molecular neurobiology · 2021Review
- Impairment of cerebellar long-term depression and GABAergic transmission in prion protein deficient mice ectopically expressing PrPLP/Dpl.Scientific reports · 2020Article
- Global analysis of protein degradation in prion infected cells.Scientific reports · 2020Article
- The cryo-EM structure of the acid activatable pore-forming immune effector Macrophage-expressed gene 1.Nature communications · 2019Article
- Macrophage-expressed perforins mpeg1 and mpeg1.2 have an anti-bacterial function in zebrafish.Journal of innate immunity · 2015Article
- Analysis of the hippocampal proteome in ME7 prion disease reveals a predominant astrocytic signature and highlights the brain-restricted production of clusterin in chronic neurodegeneration.The Journal of biological chemistry · 2014Article
- Article
- Peroxiredoxin 6 promotes upregulation of the prion protein (PrP) in neuronal cells of prion-infected mice.Cell communication and signaling : CCS · 2012Article
- Prion disease and the innate immune system.Viruses · 2012Review
- Functional genomics approach for identification of molecular processes underlying neurodegenerative disorders in prion diseases.Current genomics · 2012Article
- Methionine oxidation of Sup35 protein induces formation of the [PSI+] prion in a yeast peroxiredoxin mutant.The Journal of biological chemistry · 2011Article
- Effects of a brain-engraftable microglial cell line expressing anti-prion scFv antibodies on survival times of mice infected with scrapie prions.Cellular and molecular neurobiology · 2011Article
- Mutant prion protein expression is associated with an alteration of the Rab GDP dissociation inhibitor alpha (GDI)/Rab11 pathway.Molecular & cellular proteomics : MCP · 2010Article
- The ubiquitin-proteasome system in spongiform degenerative disorders.Biochimica et biophysica acta · 2008Review
- Chemically induced accumulation of GAGs delays PrP(Sc) clearance but prolongs prion disease incubation time.Cellular and molecular neurobiology · 2008Article
- Prion disease induced alterations in gene expression in spleen and brain prior to clinical symptoms.Advances and applications in bioinformatics and chemistry : AABC · 2008Article
- Differential expression of interferon responsive genes in rodent models of transmissible spongiform encephalopathy disease.Molecular neurodegeneration · 2007Article
- Prions: protein only or something more? Overview of potential prion cofactors.Journal of molecular neuroscience : MN · 2006Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In an attempt to identify the molecules involved in the pathogenesis of prion diseases, we performed cDNA subtraction on the brain tissues of mice affected with an experimental prion disease and the unaffected control. The genes identified as being upregulated in the prion-affected brain tissue included those encoding a series of lysosomal hydrolases (lysozyme M and both isoforms of beta-N-acetylhexosaminidase), a perforin-like protein (macrophage proliferation-specific gene-1 [MPS-1]), and an oxygen radical scavenger (peroxiredoxin). Dramatic increases in the expression level occurred at between 12 and 16 weeks after intracerebral inoculation of the prion, coinciding with the onset of spongiform degeneration. The proteinase K-resistant prion protein (PrP(Sc)) became detectable by immunoblotting well before 12 weeks, suggesting a causal relationship between this and the gene activation. Immunohistochemistry paired with in situ hybridization on sections of the affected brain tissue revealed that expression of the peroxiredoxin gene was detectable only in astrocytes and was noted throughout the affected brain tissue. On the other hand, the genes for the lysosomal hydrolases and MPS-1 were overexpressed exclusively by microglia, which colocalized with the spongiform morphological changes. A crucial role for microglia in the spongiform degeneration by their production of neurotoxic substances, and possibly via the aberrant activation of the lysosomal system, would have to be considered.
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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.