Regulated proteolysis induces aberrant phase transition of biomolecular condensates into aggregates; a protective role for the chaperone Clusterin.

chaperone, Clusterin intrinsically disoreded liquid-liquid phase separation neurodegeneration prion β-cleavage

Journal

Journal of molecular biology
ISSN: 1089-8638
Titre abrégé: J Mol Biol
Pays: Netherlands
ID NLM: 2985088R

Informations de publication

Date de publication:
28 Oct 2024
Historique:
received: 07 06 2024
revised: 22 10 2024
accepted: 23 10 2024
medline: 31 10 2024
pubmed: 31 10 2024
entrez: 30 10 2024
Statut: aheadofprint

Résumé

Several proteins associated with neurodegenerative diseases, such as the mammalian prion protein (PrP), undergo liquid-liquid phase separation (LLPS), which led to the hypothesis that condensates represent precursors in the formation of neurotoxic protein aggregates. However, the mechanisms that trigger aberrant phase separation are incompletely understood. In prion diseases, protease-resistant and infectious amyloid fibrils are composed of N-terminally truncated PrP, termed C2-PrP. C2-PrP is generated by regulated proteolysis (β-cleavage) of the cellular prion protein (PrP

Identifiants

pubmed: 39476948
pii: S0022-2836(24)00468-6
doi: 10.1016/j.jmb.2024.168839
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

168839

Informations de copyright

Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. The author is an Editorial Board Member/Editor-in-Chief/Associate Editor/Guest Editor for [Journal of Molecular Biology] and was not involved in the editorial review or the decision to publish this article.

Auteurs

Janine Kamps (J)

Department Biochemistry of Neurodegenerative Diseases, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Germany.

Patricia Yuste-Checa (P)

Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, Martinsried, Germany.

Fatemeh Mamashli (F)

Department Biochemistry of Neurodegenerative Diseases, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Germany.

Matthias Schmitz (M)

Department of Neurology, University Medical Center Göttingen, Germany.

Maria Georgina Herrera (M)

Department Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Germany.

Susana Margarida da Silva Correia (S)

Department of Neurology, University Medical Center Göttingen, Germany.

Kalpshree Gogte (K)

Department Biochemistry of Neurodegenerative Diseases, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Germany.

Verian Bader (V)

Department Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Germany.

Inga Zerr (I)

Department of Neurology, University Medical Center Göttingen, Germany.

F Ulrich Hartl (F)

Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, Martinsried, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.

Andreas Bracher (A)

Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, Martinsried, Germany.

Konstanze F Winklhofer (KF)

Department Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Germany; Cluster of Excellence RESOLV, Bochum, Germany.

Jörg Tatzelt (J)

Department Biochemistry of Neurodegenerative Diseases, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Germany; Cluster of Excellence RESOLV, Bochum, Germany. Electronic address: Joerg.Tatzelt@rub.de.

Classifications MeSH