ArticleCommunications biology2019
Partially oxidized DJ-1 inhibits α-synuclein nucleation and remodels mature α-synuclein fibrils in vitro.
Article in Communications biology, 2019. 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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Who cites it
14 citing papers in PubMed.
- VMAT2 dysfunction impairs vesicular dopamine uptake, driving its oxidation and α-synuclein pathology in DJ-1-linked Parkinson's neurons.Science advances · 2026Article
- Interaction Between α-Synuclein and DJ-1 in Parkinson's Disease.Brain sciences · 2025Review
- Redox modulatory role of DJ-1 in Parkinson's disease.Biogerontology · 2025Review
- Synaptic sabotage: How Tau and α-Synuclein undermine synaptic health.The Journal of cell biology · 2025Review
- The Sherpa hypothesis: Phenotype-Preserving Disordered Proteins stabilize the phenotypes of neurons and oligodendrocytes.NPJ systems biology and applications · 2023Article
- DJ-1 is not a deglycase and makes a modest contribution to cellular defense against methylglyoxal damage in neurons.Journal of neurochemistry · 2022Article
- Molecular Aspects of Insulin Aggregation and Various Therapeutic Interventions.ACS bio & med chem Au · 2022Review
- Review
- Article
- DJ-1 Acts as a Scavenger of α-Synuclein Oligomers and Restores Monomeric Glycated α-Synuclein.Biomolecules · 2021Article
- Molecular insights into α-synuclein interaction with individual human core histones, linker histone, and dsDNA.Protein science : a publication of the Protein Society · 2021Article
- Review
- The Role of DJ-1 in Cellular Metabolism and Pathophysiological Implications for Parkinson's Disease.Cells · 2021Review
- Keeping α-Synuclein at Bay: A More Active Role of Molecular Chaperones in Preventing Mitochondrial Interactions and Transition to Pathological States?Life (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DJ-1 is a deglycase enzyme which exhibits a redox-sensitive chaperone-like activity. The partially oxidized state of DJ-1 is active in inhibiting the aggregation of α-synuclein, a key protein associated with Parkinson's disease. The underlying molecular mechanism behind α-synuclein aggregation inhibition remains unknown. Here we report that the partially oxidized DJ-1 possesses an adhesive surface which sequesters α-synuclein monomers and blocks the early stages of α-synuclein aggregation and also restricts the elongation of α-synuclein fibrils. DJ-1 remodels mature α-synuclein fibrils into heterogeneous toxic oligomeric species. The remodeled fibers show loose surface topology due to a decrease in elastic modulus and disrupt membrane architecture, internalize easily and induce aberrant nitric oxide release. Our results provide a mechanism by which partially oxidized DJ-1 counteracts α-synuclein aggregation at initial stages of aggregation and provide evidence of a deleterious effect of remodeled α-synuclein species generated by partially oxidized DJ-1.
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