ArticleThe Biochemical journal2002
Cell-surface prion protein interacts with glycosaminoglycans.
Article in The Biochemical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 141 citations in OpenAlex.
- Prion protein regulates invasiveness in glioblastoma stem cells.BMC cancer · 2024Article
- Roles of prion proteins in mammalian development.Animal cells and systems · 2024Review
- The Multifaceted Functions of Prion Protein (PrPCancers · 2023Review
- Cellular prion protein offers neuroprotection in astrocytes submitted to amyloid β oligomer toxicity.Molecular and cellular biochemistry · 2023Article
- N-Terminal Regions of Prion Protein: Functions and Roles in Prion Diseases.International journal of molecular sciences · 2020Review
- Prion protein N1 cleavage peptides stimulate microglial interaction with surrounding cells.Scientific reports · 2020Article
- Shortening heparan sulfate chains prolongs survival and reduces parenchymal plaques in prion disease caused by mobile, ADAM10-cleaved prions.Acta neuropathologica · 2020Article
- The N-Terminal Polybasic Region of Prion Protein Is Crucial in Prion Pathogenesis Independently of the Octapeptide Repeat Region.Molecular neurobiology · 2020Article
- Structural Features of Heparin and Its Interactions With Cellular Prion Protein Measured by Surface Plasmon Resonance.Frontiers in molecular biosciences · 2020Article
- Binding between Prion Protein and Aβ Oligomers Contributes to the Pathogenesis of Alzheimer's Disease.Virologica Sinica · 2019Review
- Simulations of membrane-bound diglycosylated human prion protein reveal potential protective mechanisms against misfolding.Journal of neurochemistry · 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
- PrP Knockout Cells Expressing Transmembrane PrP Resist Prion Infection.Journal of virology · 2017Article
- Identification of Anti-prion Compounds using a Novel Cellular Assay.The Journal of biological chemistry · 2016Article
- Mutated but Not Deleted Ovine PrP(C) N-Terminal Polybasic Region Strongly Interferes with Prion Propagation in Transgenic Mice.Journal of virology · 2016Article
- Modulation of Glycosaminoglycans Affects PrPSc Metabolism but Does Not Block PrPSc Uptake.Journal of virology · 2015Article
- Cellular aspects of prion replication in vitro.Viruses · 2013Review
- Conserved roles of the prion protein domains on subcellular localization and cell-cell adhesion.PloS one · 2013Article
- The N-terminal, polybasic region of PrP(C) dictates the efficiency of prion propagation by binding to PrP(Sc).The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Allosteric function and dysfunction of the prion protein.Cellular and molecular life sciences : CMLS · 2012Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
We used ELISA and flow cytometry to study the binding of prion protein PrP to glycosaminoglycans (GAGs). We found that recombinant human PrP (rPrP) binds GAGs including chondroitin sulphate A, chondroitin sulphate B, hyaluronic acid, and heparin. rPrP binding to GAGs occurs via the N-terminus, a region known to bind divalent cations. Additionally, rPrP binding to GAGs is enhanced in the presence of Cu2+ and Zn2+, but not Ca2+ and Mn2+. rPrP binds heparin strongest, and the binding is inhibited by certain heparin analogues, including heparin disaccharide and sulphate-containing monosaccharides, but not by acetylated heparin. Full-length normal cellular prion protein (PrPC), but not N-terminally truncated PrPC species, from human brain bind GAGs in a similar Cu2+/Zn2+-enhanced fashion. We found that GAGs specifically bind to a synthetic peptide corresponding to amino acid residues 23-35 in the N-terminus of rPrP. We further demonstrated that while both wild-type PrPC and an octapeptide-repeat-deleted mutant PrP produced by transfected cells bound heparin at the cell surface, the PrP N-terminal deletion mutant and non-transfectant control failed to bind heparin. Binding of heparin to wild-type PrPC on the cell surface results in a reduction of the level of cell-surface PrPC. These results provide strong evidence that PrPC is a surface receptor for GAGs.
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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.