ArticleThe EMBO journal2001
Membrane topology influences N-glycosylation of the prion protein.
Article in The EMBO journal, 2001. 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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Who cites it
22 citing papers in PubMed, 77 citations in OpenAlex.
- BoDV-1 Infection Is Associated with Altered Prion Protein Glycoform Maturation and Reduced ETS1-MGAT5/GnTV Pathway Activity in Rat C6 Astroglial Cells.Microorganisms · 2026Article
- Partial Deletion of the Carboxyl-Terminal Signal Sequence of the Cellular Prion Protein Alters Protein Expression via Endoplasmic Reticulum-Associated Degradation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Topological confinement by a membrane anchor suppresses phase separation into protein aggregates: Implications for prion diseases.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Physiology of Cellular Prion Proteins in Reproduction.Development & reproduction · 2024Article
- Roles of prion proteins in mammalian development.Animal cells and systems · 2024Review
- Article
- Prion protein signaling induces M2 macrophage polarization and protects from lethal influenza infection in mice.PLoS pathogens · 2020Article
- PrP Knockout Cells Expressing Transmembrane PrP Resist Prion Infection.Journal of virology · 2017Article
- Prion protein "gamma-cleavage": characterizing a novel endoproteolytic processing event.Cellular and molecular life sciences : CMLS · 2016Article
- The glycan role in the glycopeptide immunogenicity revealed by atomistic simulations and spectroscopic experiments on the multiple sclerosis biomarker CSF114(Glc).Scientific reports · 2015Article
- The membrane-associated form of α(s1)-casein interacts with cholesterol-rich detergent-resistant microdomains.PloS one · 2014Article
- Efficient glycosylphosphatidylinositol (GPI) modification of membrane proteins requires a C-terminal anchoring signal of marginal hydrophobicity.The Journal of biological chemistry · 2012Article
- C-terminal hydrophobic region in human bone marrow stromal cell antigen 2 (BST-2)/tetherin protein functions as second transmembrane motif.The Journal of biological chemistry · 2011Article
- Prion protein interacts with BACE1 protein and differentially regulates its activity toward wild type and Swedish mutant amyloid precursor protein.The Journal of biological chemistry · 2011Article
- Effect of glycans and the glycophosphatidylinositol anchor on strain dependent conformations of scrapie prion protein: improved purifications and infrared spectra.Biochemistry · 2011Article
- Prion propagation in cells expressing PrP glycosylation mutants.Journal of virology · 2011Article
- Glypican-1 mediates both prion protein lipid raft association and disease isoform formation.PLoS pathogens · 2009Article
- Role of ADAMs in the ectodomain shedding and conformational conversion of the prion protein.The Journal of biological chemistry · 2009Article
- Minimotif miner 2nd release: a database and web system for motif search.Nucleic acids research · 2009Article
- Cellular prion protein regulates beta-secretase cleavage of the Alzheimer's amyloid precursor protein.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The glycosylation state of the glycosyl-phosphatidylinositol (GPI) anchored cellular prion protein (PrPC) can influence the formation of the disease form of the protein responsible for the neurodegenerative spongiform encephalopathies. We have investigated the role of membrane topology in the N-glycosylation of PrP by expressing a C-terminal transmembrane anchored form, PrP-CTM, an N-terminal transmembrane anchored form, PrP-NTM, a double-anchored form, PrP-DA, and a truncated form, PrPDeltaGPI, in human neuroblastoma SH-SY5Y cells. Wild-type PrP, PrP- CTM and PrP-DA were membrane anchored and present on the cell surface as glycosylated forms. In contrast, PrP-NTM, although membrane anchored and localized at the cell surface, was not N-glycosylated. PrPDeltaGPI was secreted from the cells into the medium in a hydrophilic form that was unglycosylated. The 4-fold slower rate at which PrPDeltaGPI was trafficked through the cell compared with wild-type PrP was due to the absence of the GPI anchor not the lack of N-glycans. Retention of PrPDeltaGPI in the endoplasmic reticulum did not lead to its glycosylation. These results indicate that C-terminal membrane anchorage is required for N-glycosylation of PrP.
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