ArticleCommunications biology2020
Augmentation of Bri2 molecular chaperone activity against amyloid-β reduces neurotoxicity in mouse hippocampus in vitro.
Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Emerging Roles of E3 Ligases and DUBs in Neurodegenerative Diseases.Molecular neurobiology · 2023Pooled it
- Mechanism-selective inhibition of α-synuclein aggregation by the chaperone-like BRICHOS domain.The Journal of biological chemistry · 2026Article
- Pathological mechanisms of motor dysfunction in familial Danish dementia: insights from a knock-in rat model.Journal of neuroinflammation · 2025Article
- Modeling Protein Aggregation Kinetics from NMR Data.Journal of molecular biology · 2025Review
- Chaperone-Mediated Regulation of Tau Phase Separation, Fibrillation, and Toxicity.Journal of the American Chemical Society · 2025Article
- Article
- Intravenous chaperone treatment of late-stage Alzheimer´s disease (AD) mouse model affects amyloid plaque load, reactive gliosis and AD-related genes.Translational psychiatry · 2024Article
- Cross-disorder and disease-specific pathways in dementia revealed by single-cell genomics.Cell · 2024Article
- Specific inhibition of α-synuclein oligomer generation and toxicity by the chaperone domain Bri2 BRICHOS.Protein science : a publication of the Protein Society · 2024Article
- Molecular basis for different substrate-binding sites and chaperone functions of the BRICHOS domain.Protein science : a publication of the Protein Society · 2024Article
- Treatment with BRICHOS domain helps to clarify issues with Alzheimer mouse models.EMBO molecular medicine · 2024Article
- Functional BRI2-TREM2 interactions in microglia: implications for Alzheimer's and related dementias.EMBO reports · 2024Article
- Myelin Basic Protein Attenuates Furin-Mediated Bri2 Cleavage and Postpones Its Membrane Trafficking.International journal of molecular sciences · 2024Article
- Secondary Modification of S100B Influences Anti Amyloid-β Aggregation Activity and Alzheimer's Disease Pathology.International journal of molecular sciences · 2024Article
- Identification of potential aggregation hotspots on Aβ42 fibrils blocked by the anti-amyloid chaperone-like BRICHOS domain.Nature communications · 2024Article
- Transfixed by transgenics: how pathology assumptions are slowing progress in Alzheimer's disease and related dementia research.EMBO molecular medicine · 2023Article
- Metal Binding of Alzheimer's Amyloid-β and Its Effect on Peptide Self-Assembly.Accounts of chemical research · 2023Article
- Identification of glycolytic proteins as binding partners of Bri2 BRICHOS domain.Journal of pharmaceutical and biomedical analysis · 2023Article
- A new kid in the folding funnel: Molecular chaperone activities of the BRICHOS domain.Protein science : a publication of the Protein Society · 2023Review
- Chaperone Activity and Protective Effect against Aβ-Induced Cytotoxicity ofPharmaceuticals (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Molecular chaperones play important roles in preventing protein misfolding and its potentially harmful consequences. Deterioration of molecular chaperone systems upon ageing are thought to underlie age-related neurodegenerative diseases, and augmenting their activities could have therapeutic potential. The dementia relevant domain BRICHOS from the Bri2 protein shows qualitatively different chaperone activities depending on quaternary structure, and assembly of monomers into high-molecular weight oligomers reduces the ability to prevent neurotoxicity induced by the Alzheimer-associated amyloid-β peptide 1-42 (Aβ42). Here we design a Bri2 BRICHOS mutant (R221E) that forms stable monomers and selectively blocks a main source of toxic species during Aβ42 aggregation. Wild type Bri2 BRICHOS oligomers are partly disassembled into monomers in the presence of the R221E mutant, which leads to potentiated ability to prevent Aβ42 toxicity to neuronal network activity. These results suggest that the activity of endogenous molecular chaperones may be modulated to enhance anti-Aβ42 neurotoxic effects.
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