Neuroprotective Function of DJ-1 in Parkinson’s Disease
Open accessAbstract
Parkinson’s disease (PD) is caused by dopaminergic neuronal death in the substantia nigra, resulting in a reduced level of dopamine in the striatum. Oxidative stress and mitochondrial dysfunction are thought to be major causes of neurodegeneration in PD. Although genetic and environmental factors are thought to affect the onset of PD, precise mechanisms at the molecular level have not been elucidated. The DJ-1 gene is a causative gene for familial PD ( park7 ) and also an oncogene. DJ-1 has various functions, including transcriptional regulation, antioxidative stress reaction, and chaperone, protease, and mitochondrial regulation, and its activity is regulated by its oxidative status, especially that of cysteine 106 (C106) of DJ-1. Excess oxidation of DJ-1, which renders DJ-1 inactive, has been observed in patients with sporadic PD and Alzheimer’s disease, suggesting that DJ-1 also participates in the onset and pathogenesis of sporadic PD as well as familial PD. DJ-1 is also a stress sensor and its expression is increased upon various stresses, including oxidative stress. In this review, we describe functions of DJ-1 against oxidative stress and possible roles of DJ-1 in the pathogenesis of PD.
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PARK7 is reported to be involved in transcriptional regulation and complexes with processing bodies (P-bodies).
“PARK7 is reported to be involved in transcriptional regulation and complexes with processing bodies (P-bodies) suggesting that it may also play a central role in translational regulation as suggested by our PPI network (96,97).”
From Analysis of proteins that rapidly change upon mechanistic/mammalian target of rapamycin complex 1 (mTORC1) repression identifies parkinson protein 7 (PARK7) as a novel protein aberrantly expressed in tuberous sclerosis complex (TSC) (2016) · cites this paper as [96]
Section 2 identifies DJ-1 (PARK7) as participating in transcriptional regulation, and Section 3 describes its regulation of transcription factors. Neither the supplied passages nor searches of our copy for processing bodies and translational regulation support the claim that it complexes with P-bodies. The suggestion about a central role in translational regulation is framed as the citing authors’ inference, not a finding attributed to this source. (LLM, conf=0.85)
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Self-citationDJ-1 protects against dopamine toxicity
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Self-citation14-3-3 protein regulates Ask1 signaling and protects against diabetic cardiomyopathy
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Human DJ-1-specific Transcriptional Activation of Tyrosine Hydroxylase Gene
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Self-citationDJ-1 knock-down impairs astrocyte mitochondrial function
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Self-citationOxidized DJ-1 Interacts with the Mitochondrial Protein BCL-XL
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Self-citationA New Evolutionary Paradigm for the Parkinson Disease Gene DJ-1
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Self-citationSumoylation is critical for DJ‐1 to repress p53 transcriptional activity
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Self-citationExpression profiles of genes in DJ-1-knockdown and L166P DJ-1 mutant cells
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The Role of DJ-1 in Cellular Metabolism and Pathophysiological Implications for Parkinson’s Disease
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Atypical Ubiquitination and Parkinson’s Disease
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- Authors
- Ariga, H., Takahashi-Niki, K., Kato, I., Maita, H., Niki, T., & Iguchi-Ariga, S. M. M.
- Affiliations
- Hokkaido University (JP)
- Graduate School of Agriculture, Hokkaido University, Kita-ku, Sapporo 060-8589, Japan
- Corresponding author
- Ariga, Hiroyoshi
- ORCID
- Maita, Hiroshi
- Venue
- Oxidative Medicine and Cellular Longevity
- Publisher
- Wiley
- Published
- 2013
- Volume
- 2013
- Pages
- 1-9
- ISSN
- 1942-0994 (ISSN-L)
- 1942-0900
- PMC
- PMC3671546
- OpenAlex
- W1974927898
- Cited by
- 373
- References
- 117
- Citations by year
- 2026: 12 · 2025: 22 · 2024: 24 · 2023: 22 · 2022: 36 · 2021: 30 · 2020: 45 · 2019: 37 · 2018: 27 · 2017: 44 · 2016: 33 · 2015: 21 · 2014: 12 · 2013: 8
- FWCI
- 3.22
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Oxidative Medicine and Cellular Longevity (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- Hokkaido University Collection of Scholarly and Academic Papers (Hokkaido University) (submittedVersion)
- Funders
- National Institute of Biomedical Innovation
- Japan Society for the Promotion of Science (25830071, 25430059, 24650191, 23790970)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Keywords
- DJ-1, Parkinson's disease, neuroprotection, oxidative stress, mitochondrial dysfunction, dopaminergic neuron loss, substantia nigra, familial parkinsonism, sporadic Parkinson's disease, stress sensors, chaperone activity, protease function, transcriptional regulation
- MeSH terms
- Animals, Dopamine, Humans, Mitochondria, Parkinson Disease, Oncogene Proteins, Oxidative Stress, Neuroprotective Agents
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