Academic Journal
The Neuronal tau protein blocks in vitro fibrillation of the amyloid-beta (A beta) peptide at the oligomeric stage
| العنوان: | The Neuronal tau protein blocks in vitro fibrillation of the amyloid-beta (A beta) peptide at the oligomeric stage |
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| المؤلفون: | Wallin, Cecilia, Hiruma, Yoshitaka, Warmlander, Sebastian K. T. S., Huvent, Isabelle, Jarvet, Juri, Abrahams, Jan Pieter, Graslund, Astrid, Lippens, Guy, Luo, Jinghui |
| المساهمون: | Department of Biochemistry and Biophysics, The Arrhenius Laboratories, Stockholm University, Divisions of Biochemistry, Netherlands Cancer Institute, Unité de Glycobiologie Structurale et Fonctionnelle - UMR 8576 (UGSF), Université de Lille-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS), Biozentrum Basel, Suisse, Université de Bâle = University of Basel = Basel Universität (Unibas), Laboratory of Biomolecular Research, Institut Paul Scherrer (IPS), Laboratoire d'Ingénierie des Systèmes Biologiques et des Procédés (LISBP), Institut National de la Recherche Agronomique (INRA)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS), Region Midi-Pyrenees, ERDF, SICOVAL, Alzheimer Foundation AF-642731, Swedish Research Council 2014-05867, department of Biology and Chemistry, Paul Scherrer Institute, ANR-11-INBS-0010,METABOHUB,Développement d'une infrastructure française distribuée pour la métabolomique dédiée à l'innovation(2011) |
| المصدر: | ISSN: 0002-7863. |
| بيانات النشر: | HAL CCSD American Chemical Society |
| سنة النشر: | 2018 |
| مصطلحات موضوعية: | alzheimers-disease, neurodegenerative diseases, atomic-resolution, catalytic cycle, alpha-synuclein, mouse model, aggregation, transmission, pathology, chaperone, [SDV]Life Sciences [q-bio] |
| الوصف: | In Alzheimer's disease, amyloid-beta (A beta) plaques and tau neurofibrillary tangles are the two pathological hallmarks. The co-occurrence and combined reciprocal pathological effects of A beta and tau protein aggregation have been observed in animal models of the disease. However, the molecular mechanism of their interaction remain unknown. Using a variety of biophysical measurements, we here show that the native full-length tau protein solubilizes the A beta(40) peptide and prevents its fibrillation. The tau protein delays the amyloid fibrillation of the A beta(40) peptide at substoichiometric ratios, showing different binding affinities toward the different stages of the aggregated A beta(40) peptides. The A beta monomer structure remains random coil in the presence of tau, as observed by nuclear magnetic resonance (NMR), circular dichroism (CD) spectroscopy and photoinduced cross-linking methods. We propose a potential interaction mechanism for the influence of tau on A beta fibrillation. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| Relation: | info:eu-repo/semantics/altIdentifier/pmid/29708745; PRODINRA: 447649; PUBMED: 29708745; WOS: 000438309400018 |
| DOI: | 10.1021/jacs.7b13623 |
| الاتاحة: | https://hal.science/hal-02154329 https://doi.org/10.1021/jacs.7b13623 |
| رقم الانضمام: | edsbas.F057BD9F |
| قاعدة البيانات: | BASE |
| DOI: | 10.1021/jacs.7b13623 |
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