Evidence map›Paper›PMID 33667547›Full record

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.

Anna S König, Nadine S Rösener, Lothar Gremer, Markus Tusche, Daniel Flender, Elke Reinartz, Wolfgang Hoyer, Philipp Neudecker, Dieter Willbold, Henrike Heise

Open access · goldAbstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.8field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. 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 · 2025
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  11. The Effect ofInternational journal of molecular sciences · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Anna S KönigInstitute of Biological Information Processing (IBI-7: Structural Biochemistry) and JuStruct: Jülich Center for Structural Biology, Forschungszentrum Jülich, Jülich, Germany; Institut für Physikalische Biologie, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany.
Nadine S RösenerInstitute of Biological Information Processing (IBI-7: Structural Biochemistry) and JuStruct: Jülich Center for Structural Biology, Forschungszentrum Jülich, Jülich, Germany; Institut für Physikalische Biologie, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany.
Lothar GremerInstitute of Biological Information Processing (IBI-7: Structural Biochemistry) and JuStruct: Jülich Center for Structural Biology, Forschungszentrum Jülich, Jülich, Germany; Institut für Physikalische Biologie, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany; Research Center for Molecular Mechanisms of Aging and Age-Related Diseases, Moscow Institute of Physics and Technology (State University), Dolgoprudny, Russia.
Markus TuscheInstitute of Biological Information Processing (IBI-7: Structural Biochemistry) and JuStruct: Jülich Center for Structural Biology, Forschungszentrum Jülich, Jülich, Germany.
Daniel FlenderInstitut für Physikalische Biologie, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany.
Elke ReinartzInstitut für Physikalische Biologie, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany.
Wolfgang HoyerInstitute of Biological Information Processing (IBI-7: Structural Biochemistry) and JuStruct: Jülich Center for Structural Biology, Forschungszentrum Jülich, Jülich, Germany; Institut für Physikalische Biologie, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany.
Philipp NeudeckerInstitute of Biological Information Processing (IBI-7: Structural Biochemistry) and JuStruct: Jülich Center for Structural Biology, Forschungszentrum Jülich, Jülich, Germany; Institut für Physikalische Biologie, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany.
Dieter WillboldInstitute of Biological Information Processing (IBI-7: Structural Biochemistry) and JuStruct: Jülich Center for Structural Biology, Forschungszentrum Jülich, Jülich, Germany; Institut für Physikalische Biologie, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany; Research Center for Molecular Mechanisms of Aging and Age-Related Diseases, Moscow Institute of Physics and Technology (State University), Dolgoprudny, Russia. Electronic address: d.willbold@fz-juelich.de.
Henrike HeiseInstitute of Biological Information Processing (IBI-7: Structural Biochemistry) and JuStruct: Jülich Center for Structural Biology, Forschungszentrum Jülich, Jülich, Germany; Institut für Physikalische Biologie, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany. Electronic address: h.heise@fz-juelich.de.
Forschungszentrum Jülich · DEHeinrich Heine University Düsseldorf · DEMoscow Institute of Physics and Technology · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Alzheimer DiseaseAmyloidAmyloid beta-PeptidesAnimalsCell LineHumansMagnetic Resonance SpectroscopyPrion ProteinsProtein MultimerizationProtein Structure, SecondaryRatsAmyloidAmyloid beta-PeptidesPrion ProteinsAlzheimer diseaseamyloid beta (Aβ)nuclear magnetic resonance (NMR)oligomerprion proteinsolid-state NMRsolution NMRstructural biology

Identifiers

PMID33667547
PMCPMC8042448
OpenAlexW3134472965

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Registered trials

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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.