ArticleThe Journal of biological chemistry
Structural details of amyloid β oligomers in complex with human prion protein as revealed by solid-state MAS NMR spectroscopy.
Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 37 citations in OpenAlex.
- In vitro, cellular and in vivo studies of amyloid oligomers structure and toxicity: Challenges and advances.Protein science : a publication of the Protein Society · 2026Review
- 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
- Aggregation dynamics of a 150 kDa Aβ42 oligomer: Insights from cryo electron microscopy and multimodal analysis.Computational and structural biotechnology journal · 2024Article
- Aggregation Dynamics of a 150 kDa Aβ42 Oligomer: Insights from Cryo Electron Microscopy and Multimodal Analysis.bioRxiv : the preprint server for biology · 2024Article
- Elucidation of the Role of Lipids in Late Endosomes on the Aggregation of Insulin.ACS chemical neuroscience · 2023Article
- Length and saturation of fatty acids in phosphatidylserine determine the rate of lysozyme aggregation simultaneously altering the structure and toxicity of amyloid oligomers and fibrils.Protein science : a publication of the Protein Society · 2023Article
- Anchorless risk or released benefit? An updated view on the ADAM10-mediated shedding of the prion protein.Cell and tissue research · 2023Review
- Differentiation of subnucleus-sized oligomers and nucleation-competent assemblies of the Aβ peptide.Biophysical journal · 2023Article
- Unveiling the Potential of Polyphenols as Anti-Amyloid Molecules in Alzheimer's Disease.Current neuropharmacology · 2023Review
- Amyloid oligomers as on-pathway precursors or off-pathway competitors of fibrils.Frontiers in molecular biosciences · 2023Review
- The Effect ofInternational journal of molecular sciences · 2022Article
- Melatonin: Regulation of Prion Protein Phase Separation in Cancer Multidrug Resistance.Molecules (Basel, Switzerland) · 2022Review
- Biological Functions of the Intrinsically Disordered N-Terminal Domain of the Prion Protein: A Possible Role of Liquid-Liquid Phase Separation.Biomolecules · 2021Review
- Aβ receptors specifically recognize molecular features displayed by fibril ends and neurotoxic oligomers.Nature communications · 2021Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human PrP (huPrP) is a high-affinity receptor for oligomeric amyloid β (Aβ) protein aggregates. Binding of Aβ oligomers to membrane-anchored huPrP has been suggested to trigger neurotoxic cell signaling in Alzheimer's disease, while an N-terminal soluble fragment of huPrP can sequester Aβ oligomers and reduce their toxicity. Synthetic oligomeric Aβ species are known to be heterogeneous, dynamic, and transient, rendering their structural investigation particularly challenging. Here, using huPrP to preserve Aβ oligomers by coprecipitating them into large heteroassemblies, we investigated the conformations of Aβ(1-42) oligomers and huPrP in the complex by solid-state MAS NMR spectroscopy. The disordered N-terminal region of huPrP becomes immobilized in the complex and therefore visible in dipolar spectra without adopting chemical shifts characteristic of a regular secondary structure. Most of the well-defined C-terminal part of huPrP is part of the rigid complex, and solid-state NMR spectra suggest a loss in regular secondary structure in the two C-terminal α-helices. For Aβ(1-42) oligomers in complex with huPrP, secondary chemical shifts reveal substantial β-strand content. Importantly, not all Aβ(1-42) molecules within the complex have identical conformations. Comparison with the chemical shifts of synthetic Aβ fibrils suggests that the Aβ oligomer preparation represents a heterogeneous mixture of β-strand-rich assemblies, of which some have the potential to evolve and elongate into different fibril polymorphs, reflecting a general propensity of Aβ to adopt variable β-strand-rich conformers. Taken together, our results reveal structural changes in huPrP upon binding to Aβ oligomers that suggest a role of the C terminus of huPrP in cell signaling. Trapping Aβ(1-42) oligomers by binding to huPrP has proved to be a useful tool for studying the structure of these highly heterogeneous β-strand-rich assemblies.
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