ArticleHuman molecular genetics2017
DJ-1 is a redox sensitive adapter protein for high molecular weight complexes involved in regulation of catecholamine homeostasis.
Article in Human molecular genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- Review
- Organic Germanium (Ge-132) Reduces Glycative Damage While Maintaining Cellular Stress Signaling, Revealing Limited Coordination Between Biochemical and Cellular Responses.Molecules (Basel, Switzerland) · 2026Article
- Sensitive Detection of DJ-1 in Artificial Cerebrospinal Fluid Using a Portable GPTMS-Coordinated Gold Nanoparticle-Based Biosensor.Biosensors · 2026Article
- Parkinson's associated protein DJ-1 regulates intercellular communication via extracellular vesicles in oxidative stress.Cell death discovery · 2025Article
- The Parkinson's disease DJ-1/PARK7 gene controls peripheral neuronal excitability and painful neuropathy.Brain : a journal of neurology · 2025Article
- Mitochondrial Dysfunction in Genetic and Non-Genetic Parkinson's Disease.International journal of molecular sciences · 2025Review
- Knockdown of DJ-1 Exacerbates Neuron Apoptosis Induced by TgCtwh3 through the NF-κB Pathway.Molecular neurobiology · 2025Article
- Protein modification in neurodegenerative diseases.MedComm · 2024Review
- PARK7/DJ-1 in microglia: implications in Parkinson's disease and relevance as a therapeutic target.Journal of neuroinflammation · 2023Review
- The Tale of DJ-1 (PARK7): A Swiss Army Knife in Biomedical and Psychological Research.International journal of molecular sciences · 2023Review
- DJ-1 Molecular Chaperone Activity Depresses Tau Aggregation Propensity through Interaction with Monomers.Biochemistry · 2023Article
- Persulfidation of DJ-1: Mechanism and Consequences.Biomolecules · 2022Article
- DJ-1 is an essential downstream mediator in PINK1/parkin-dependent mitophagy.Brain : a journal of neurology · 2022Article
- HDL Accessory Proteins in Parkinson's Disease-Focusing on Clusterin (Apolipoprotein J) in Regard to Its Involvement in Pathology and Diagnostics-A Review.Antioxidants (Basel, Switzerland) · 2022Review
- The Role of DJ-1 in Cellular Metabolism and Pathophysiological Implications for Parkinson's Disease.Cells · 2021Review
- Review
- Targeting redox regulation to treat substance use disorder using N‐acetylcysteineThe European journal of neuroscience · 2019Review
- Role of DJ-1 in the mechanism of pathogenesis of Parkinson's disease.Journal of bioenergetics and biomembranes · 2019Review
- Elevated expression of DJ-1 (encoded by the human PARK7 gene) protects neuronal cells from sevoflurane-induced neurotoxicity.Cell stress & chaperones · 2018Article
- Astrocyte-specific DJ-1 overexpression protects against rotenone-induced neurotoxicity in a rat model of Parkinson's disease.Neurobiology of disease · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 9 institutions in 6 countries.
Funding
Abstract
DJ-1 is an oxidation sensitive protein encoded by the PARK7 gene. Mutations in PARK7 are a rare cause of familial recessive Parkinson's disease (PD), but growing evidence suggests involvement of DJ-1 in idiopathic PD. The key clinical features of PD, rigidity and bradykinesia, result from neurotransmitter imbalance, particularly the catecholamines dopamine (DA) and noradrenaline. We report in human brain and human SH-SY5Y neuroblastoma cell lines that DJ-1 predominantly forms high molecular weight (HMW) complexes that included RNA metabolism proteins hnRNPA1 and PABP1 and the glycolysis enzyme GAPDH. In cell culture models the oxidation status of DJ-1 determined the specific complex composition. RNA sequencing indicated that oxidative changes to DJ-1 were concomitant with changes in mRNA transcripts mainly involved in catecholamine metabolism. Importantly, loss of DJ-1 function upon knock down (KD) or expression of the PD associated form L166P resulted in the absence of HMW DJ-1 complexes. In the KD model, the absence of DJ-1 complexes was accompanied by impairment in catecholamine homeostasis, with significant increases in intracellular DA and noraderenaline levels. These changes in catecholamines could be rescued by re-expression of DJ-1. This catecholamine imbalance may contribute to the particular vulnerability of dopaminergic and noradrenergic neurons to neurodegeneration in PARK7-related PD. Notably, oxidised DJ-1 was significantly decreased in idiopathic PD brain, suggesting altered complex function may also play a role in the more common sporadic form of the disease.
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