ArticleBrain : a journal of neurology2019
Parkin interacting substrate zinc finger protein 746 is a pathological mediator in Parkinson's disease.
Article in Brain : a journal of neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Nilotinib in Parkinson's disease: A systematic review and meta-analysis.Frontiers in aging neuroscience · 2022Pooled it
- The 201 Trial: a placebo-controlled randomized phase 2 study of safety and tolerance of the c-Abl kinase inhibitor risvodetinib in untreated Parkinson's disease.Nature aging · 2026Trial
- A Phase I, Randomized, SAD, MAD, and PK Study of Risvodetinib in Older Adults and Parkinson's Disease.Journal of Parkinson's disease · 2024Trial
- Molecular mechanisms underlying FCCP-induced mitophagy in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Neuronal titration of Snca via enhancer disruption mitigates disease onset in a Parkinson's disease mouse model.Brain : a journal of neurology · 2026Article
- Neuronal PARIS-STAT3 axis drives tau pathology and glial activation in Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- PARL stabilizes mitochondrial BCL-2 via Nur77-mediated scaffolding as a therapeutic strategy for Parkinson's disease.Cell death & disease · 2025Article
- Gut microbial production of imidazole propionate drives Parkinson's pathologies.Nature communications · 2025Article
- Regulation of Apoptotic Pathways by MicroRNAs: A Therapeutic Strategy for Alzheimer's Disease.Molecular neurobiology · 2025Review
- Nanozymes: Innovative Therapeutics in the Battle Against Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Preclinical studies and transcriptome analysis in a model of Parkinson's disease with dopaminergic ZNF746 expression.Molecular neurodegeneration · 2025Article
- Emerging targets of α-synuclein spreading in α-synucleinopathies: a review of mechanistic pathways and interventions.Molecular neurodegeneration · 2025Review
- α-Synuclein pathology as a target in neurodegenerative diseases.Nature reviews. Neurology · 2025Review
- Aplp1 interacts with Lag3 to facilitate transmission of pathologic α-synuclein.Nature communications · 2024Article
- Role of NLRP3 in Parkinson's disease: Specific activation especially in dopaminergic neurons.Heliyon · 2024Review
- Heat Shock Response and Heat Shock Proteins: Current Understanding and Future Opportunities in Human Diseases.International journal of molecular sciences · 2024Review
- Liquid-liquid phase separation and conformational strains ofFrontiers in molecular neuroscience · 2024Review
- Proximity proteomic analysis of the NRF family reveals the Parkinson's disease protein ZNF746/PARIS as a co-complexed repressor of NRF2.Science signaling · 2023Article
- PARIS undergoes liquid-liquid phase separation and poly(ADP-ribose)-mediated solidification.EMBO reports · 2023Article
- Chiisanoside Mediates the Parkin/ZNF746/PGC-1α Axis by Downregulating MiR-181a to Improve Mitochondrial Biogenesis in 6-OHDA-Caused Neurotoxicity Models In Vitro and In Vivo: Suggestions for Prevention of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Article
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Authors and funding
22 authors at 2 institutions in 1 country.
Funding
Abstract
α-Synuclein misfolding and aggregation plays a major role in the pathogenesis of Parkinson's disease. Although loss of function mutations in the ubiquitin ligase, parkin, cause autosomal recessive Parkinson's disease, there is evidence that parkin is inactivated in sporadic Parkinson's disease. Whether parkin inactivation is a driver of neurodegeneration in sporadic Parkinson's disease or a mere spectator is unknown. Here we show that parkin in inactivated through c-Abelson kinase phosphorylation of parkin in three α-synuclein-induced models of neurodegeneration. This results in the accumulation of parkin interacting substrate protein (zinc finger protein 746) and aminoacyl tRNA synthetase complex interacting multifunctional protein 2 with increased parkin interacting substrate protein levels playing a critical role in α-synuclein-induced neurodegeneration, since knockout of parkin interacting substrate protein attenuates the degenerative process. Thus, accumulation of parkin interacting substrate protein links parkin inactivation and α-synuclein in a common pathogenic neurodegenerative pathway relevant to both sporadic and familial forms Parkinson's disease. Thus, suppression of parkin interacting substrate protein could be a potential therapeutic strategy to halt the progression of Parkinson's disease and related α-synucleinopathies.
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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.