ArticleJournal of virology2004
Scrapie protein degradation by cysteine proteases in CD11c+ dendritic cells and GT1-1 neuronal cells.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 50 citations in OpenAlex.
- Prions and protein aggregates as pathogens, self-propagating structures, biomarkers, and therapeutic targets.Microbiology and molecular biology reviews : MMBR · 2025Review
- Review
- Excess α-synuclein compromises phagocytosis in iPSC-derived macrophages.Scientific reports · 2017Article
- Cystatin F is a biomarker of prion pathogenesis in mice.PloS one · 2017Article
- Transcriptomic Determinants of Scrapie Prion Propagation in Cultured Ovine Microglia.PloS one · 2016Article
- The Good, the Bad, and the Ugly of Dendritic Cells during Prion Disease.Journal of immunology research · 2015Review
- Uptake and degradation of protease-sensitive and -resistant forms of abnormal human prion protein aggregates by human astrocytes.The American journal of pathology · 2014Article
- A specific population of abnormal prion protein aggregates is preferentially taken up by cells and disaggregated in a strain-dependent manner.Journal of virology · 2013Article
- Alternative fates of newly formed PrPSc upon prion conversion on the plasma membrane.Journal of cell science · 2013Article
- Prion protein misfolding, strains, and neurotoxicity: an update from studies on Mammalian prions.International journal of cell biology · 2013Review
- Prion disease and the innate immune system.Viruses · 2012Review
- Prion propagation, toxicity and degradation.Nature neuroscience · 2012Review
- Dissociation of infectivity from seeding ability in prions with alternate docking mechanism.PLoS pathogens · 2011Article
- Spreading of prions from the immune to the peripheral nervous system: a potential implication of dendritic cells.Histochemistry and cell biology · 2010Article
- Inhibition of cholesterol recycling impairs cellular PrP(Sc) propagation.Cellular and molecular life sciences : CMLS · 2009Article
- Prions hijack tunnelling nanotubes for intercellular spread.Nature cell biology · 2009Article
- Specific biarsenical labeling of cell surface proteins allows fluorescent- and biotin-tagging of amyloid precursor protein and prion proteins.Molecular biology of the cell · 2009Article
- Oral scrapie infection modifies the homeostasis of Peyer's patches' dendritic cells.Histochemistry and cell biology · 2007Article
- The tyrosine kinase inhibitor imatinib mesylate delays prion neuroinvasion by inhibiting prion propagation in the periphery.Journal of neurovirology · 2007Article
- Inhibitors of the mitogen-activated protein kinase kinase 1/2 signaling pathway clear prion-infected cells from PrPSc.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dendritic cells (DC) of the CD11c(+) myeloid phenotype have been implicated in the spread of scrapie in the host. Previously, we have shown that CD11c(+) DC can cause a rapid degradation of proteinase K-resistant prion proteins (PrP(Sc)) in vitro, indicating a possible role of these cells in the clearance of PrP(Sc). To determine the mechanisms of PrP(Sc) degradation, CD11c(+) DC that had been exposed to PrP(Sc) derived from a neuronal cell line (GT1-1) infected with scrapie (ScGT1-1) were treated with a battery of protease inhibitors. Following treatment with the cysteine protease inhibitors (2S,3S)-trans-epoxysuccinyl-L-leucylamido-3-methylbutane (E-64c), its ethyl ester (E-64d), and leupeptin, the degradation of PrP(Sc) was inhibited, while inhibitors of serine and aspartic and metalloproteases (aprotinin, pepstatin, and phosphoramidon) had no effect. An endogenous degradation of PrP(Sc) in ScGT1-1 cells was revealed by inhibiting the expression of cellular PrP (PrP(C)) by RNA interference, and this degradation could also be inhibited by the cysteine protease inhibitors. Our data show that PrP(Sc) is proteolytically cleaved preferentially by cysteine proteases in both CD11c(+) DC and ScGT1-1 cells and that the degradation of PrP(Sc) by proteases is different from that of PrP(C). Interference by protease inhibitors with DC-induced processing of PrP(Sc) has the potential to modify prion spread, clearance, and immunization in a host.
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