ArticleThe American journal of pathology2002
Parkin localizes to the Lewy bodies of Parkinson disease and dementia with Lewy bodies.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.
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Who cites it
100 citing papers in PubMed, 331 citations in OpenAlex.
- Alternative Translation Initiation in PRKN Delays the Onset of Parkinson's Disease and Offers a Therapeutic Target.Annals of neurology · 2026Article
- Canonical and alternate mechanisms that regulate ubiquitylation by the E3 ligase parkin.Biochemical Society transactions · 2025Review
- α-Synuclein Pathology in Synucleinopathies: Mechanisms, Biomarkers, and Therapeutic Challenges.International journal of molecular sciences · 2025Review
- The interplay between α-synuclein aggregation and necroptosis in Parkinson's disease: a spatiotemporal perspective.Frontiers in neuroscience · 2025Review
- Is There a Place for Lewy Bodies before and beyond Alpha-Synuclein Accumulation? Provocative Issues in Need of Solid Explanations.International journal of molecular sciences · 2024Review
- Ubiquitin Carboxyl-Terminal Hydrolase L1 and Its Role in Parkinson's Disease.International journal of molecular sciences · 2024Review
- Mitochondrial dysfunction in Parkinson's disease - a key disease hallmark with therapeutic potential.Molecular neurodegeneration · 2023Review
- Chronic carbon disulfide exposure induces parkinsonian pathology via α-synuclein aggregation and necrosome complex interaction.iScience · 2023Article
- Alpha-synuclein-associated changes in PINK1-PRKN-mediated mitophagy are disease context dependent.Brain pathology (Zurich, Switzerland) · 2023Article
- Targeted degradation of ⍺-synuclein aggregates in Parkinson's disease using the AUTOTAC technology.Molecular neurodegeneration · 2023Article
- Copper homeostasis and the ubiquitin proteasome system.Metallomics : integrated biometal science · 2023Review
- Concomitant protein pathogenesis in Parkinson's disease and perspective mechanisms.Frontiers in aging neuroscience · 2023Review
- Genetic insights into immune mechanisms of Alzheimer's and Parkinson's disease.Frontiers in immunology · 2023Review
- Understanding the Potential of Genome Editing in Parkinson's Disease.International journal of molecular sciences · 2021Review
- Age-associated insolubility of parkin in human midbrain is linked to redox balance and sequestration of reactive dopamine metabolites.Acta neuropathologica · 2021Article
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- Death-associated Protein Kinase 1 Phosphorylates α-Synuclein at Ser129 and Exacerbates Rotenone-induced Toxic Aggregation of α-Synuclein in Dopaminergic SH-SY5Y Cells.Experimental neurobiology · 2020Article
- Chaperones and Proteostasis: Role in Parkinson's Disease.Diseases (Basel, Switzerland) · 2020Review
- PINK1 and Parkin mitochondrial quality control: a source of regional vulnerability in Parkinson's disease.Molecular neurodegeneration · 2020Review
40 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 6 institutions in 3 countries.
Funding
Abstract
Mutations in alpha-synuclein (alpha S) and parkin cause heritable forms of Parkinson disease (PD). We hypothesized that neuronal parkin, a known E3 ubiquitin ligase, facilitates the formation of Lewy bodies (LBs), a pathological hallmark of PD. Here, we report that affinity-purified parkin antibodies labeled classical LBs in substantia nigra sections from four related human disorders: sporadic PD, inherited alphaS-linked PD, dementia with LBs (DLB), and LB-positive, parkin-linked PD. Anti-parkin antibodies also detected LBs in entorhinal and cingulate cortices from DLB brain and alphaS inclusions in sympathetic gangliocytes from sporadic PD. Double labeling with confocal microscopy of DLB midbrain sections revealed that approximately 90% of anti-alpha S-reactive LBs were also detected by a parkin antibody to amino acids 342 to 353. Accordingly, parkin proteins, including the 53-kd mature isoform, were present in affinity-isolated LBs from DLB cortex. Fluorescence resonance energy transfer and immunoelectron microscopy showed that alphaS and parkin co-localized within brainstem and cortical LBs. Biochemically, parkin appeared most enriched in cytosolic and postsynaptic fractions of adult rat brain, but also in purified, alpha S-rich presynaptic elements that additionally contained parkin's E2-binding partner, UbcH7. We conclude that parkin and UbcH7 are present with alphaS in subcellular compartments of normal brain and that parkin frequently co-localizes with alpha S aggregates in the characteristic LB inclusions of PD and DLB. These results suggest that functional parkin proteins may be required during LB formation.
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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.