ArticleMolecular neurodegeneration2015
α-synuclein interacts with SOD1 and promotes its oligomerization.
Article in Molecular neurodegeneration, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- FGFRL1: Structure, Molecular Function, and Involvement in Human Disease.Current issues in molecular biology · 2025Review
- Parkinson-like wild-type superoxide dismutase 1 pathology induces nigral dopamine neuron degeneration in a novel murine model.Acta neuropathologica · 2025Article
- Superoxide dismutase: a key target for the neuroprotective effects of curcumin.Molecular and cellular biochemistry · 2024Review
- PINK1 is a target of T cell responses in Parkinson's disease.bioRxiv : the preprint server for biology · 2024Article
- A Mouse Model to Test Novel Therapeutics for Parkinson's Disease: an Update on the Thy1-aSyn ("line 61") Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Crossroads between copper ions and amyloid formation in Parkinson's disease.Essays in biochemistry · 2022Article
- Synucleinopathy in Amyotrophic Lateral Sclerosis: A Potential Avenue for Antisense Therapeutics?International journal of molecular sciences · 2022Review
- CNS Redox Homeostasis and Dysfunction in Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- Ingenuity pathway analysis ofFrontiers in molecular neuroscience · 2022Article
- NEK1-mediated retromer trafficking promotes blood-brain barrier integrity by regulating glucose metabolism and RIPK1 activation.Nature communications · 2021Article
- Crosstalk Between Alpha-Synuclein and Other Human and Non-Human Amyloidogenic Proteins: Consequences for Amyloid Formation in Parkinson's Disease.Journal of Parkinson's disease · 2020Review
- Oxidative stress in the aging substantia nigra and the etiology of Parkinson's disease.Aging cell · 2019Review
- SQSTM1/p62: A Potential Target for Neurodegenerative Disease.ACS chemical neuroscience · 2019Review
- Redox Mechanisms in Neurodegeneration: From Disease Outcomes to Therapeutic Opportunities.Antioxidants & redox signaling · 2019Review
- Dysregulation of a novel miR-1825/TBCB/TUBA4A pathway in sporadic and familial ALS.Cellular and molecular life sciences : CMLS · 2018Article
- Differential induction of mutant SOD1 misfolding and aggregation by tau and α-synuclein pathology.Molecular neurodegeneration · 2018Article
- Commentary: Immunochemical Markers of the Amyloid Cascade in the Hippocampus in Motor Neuron Diseases.Frontiers in neurology · 2017Article
- Neuronal hemoglobin in mitochondria is reduced by forming a complex with α-synuclein in aging monkey brains.Oncotarget · 2016Article
- Commentary: alpha-synuclein interacts with SOD1 and promotes its oligomerization.Journal of neurology & neuromedicine · 2016Article
- Dysregulation of Ubiquitin-Proteasome System in Neurodegenerative Diseases.Frontiers in aging neuroscience · 2016Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundParkinson's disease (PD) and amyotrophic lateral sclerosis (ALS) are both neurodegenerative diseases leading to impaired execution of movement. α-Synuclein plays a central role in the pathogenesis of PD whereas Cu, Zn superoxide dismutase (SOD1) is a key player in a subset of familial ALS cases. Under pathological conditions both α-synuclein and SOD1 form oligomers and fibrils. In this study we investigated the possible molecular interaction of α-synuclein and SOD1 and its functional and pathological relevance.
resultsUsing a protein-fragment complementation approach and co-IP, we found that α-synuclein and SOD1 physically interact in living cells, human erythrocytes and mouse brain tissue. Additionally, our data show that disease related mutations in α-synuclein (A30P, A53T) and SOD1 (G85R, G93A) modify the binding of α-synuclein to SOD1. Notably, α-synuclein accelerates SOD1 oligomerization independent of SOD1 activity.
conclusionThis study provides evidence for a novel interaction of α-synuclein and SOD1 that might be relevant for neurodegenerative diseases.
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Registered trials
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.