ArticleMolecular neurodegeneration2013
S-Nitrosylation of parkin as a novel regulator of p53-mediated neuronal cell death in sporadic Parkinson's disease.
Article in Molecular neurodegeneration, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 77 citations in OpenAlex.
- Article
- Neural cell state modulation bybioRxiv : the preprint server for biology · 2026Article
- Aberrant Protein S-Nitrosylation Mimics the Effect of Rare Genetic Mutations in Neurodegenerative Diseases.Journal of neurochemistry · 2026Review
- UQCRC1 deficiency impairs mitophagy via PINK1-dependent mechanisms in Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Oxidative/Nitrosative Stress, Apoptosis, and Redox Signaling: Key Players in Neurodegenerative Diseases.Journal of biochemical and molecular toxicology · 2025Review
- Discovery of a CK2α'-Biased ATP-Competitive Inhibitor from a High-Throughput Screen of an Allosteric-Inhibitor-Like Compound Library.ACS chemical neuroscience · 2024Article
- The Role of Protein S-Nitrosylation in Mitochondrial Quality Control in Central Nervous System Diseases.Aging and disease · 2024Review
- Identification of CK2α' selective inhibitors by the screening of an allosteric-kinase-inhibitor-like compound library.bioRxiv : the preprint server for biology · 2024Article
- Mitochondrial dysfunction in Parkinson's disease - a key disease hallmark with therapeutic potential.Molecular neurodegeneration · 2023Review
- Comparison of the Nitric Oxide Synthase Interactomes and S-Nitroso-Proteomes: Furthering the Case for Enzymatic S-Nitrosylation.Antioxidants & redox signaling · 2023Article
- Parkin regulates neuronal lipid homeostasis through SREBP2-lipoprotein lipase pathway-implications for Parkinson's disease.Human molecular genetics · 2023Article
- Nitric Oxide/Nitric Oxide Synthase System in the Pathogenesis of Neurodegenerative Disorders-An Overview.Antioxidants (Basel, Switzerland) · 2023Review
- Enhanced IRE1α Phosphorylation/Oligomerization-Triggered XBP1 Splicing Contributes to Parkin-Mediated Prevention of SH-SY5Y Cell Death under Nitrosative Stress.International journal of molecular sciences · 2023Article
- Cell Biology of Parkin: Clues to the Development of New Therapeutics for Parkinson's Disease.CNS drugs · 2022Review
- Decoding the Role of Familial Parkinson's Disease-Related Genes in DNA Damage and Repair.Aging and disease · 2022Article
- CBX3 accelerates the malignant progression of glioblastoma multiforme by stabilizing EGFR expression.Oncogene · 2022Article
- Parkin as a Molecular Bridge Linking Alzheimer's and Parkinson's Diseases?Biomolecules · 2022Review
- Protein Transnitrosylation Signaling Networks Contribute to Inflammaging and Neurodegenerative Disorders.Antioxidants & redox signaling · 2021Review
- Understanding the Potential of Genome Editing in Parkinson's Disease.International journal of molecular sciences · 2021Review
- SUV39H2 epigenetic silencing controls fate conversion of epidermal stem and progenitor cells.The Journal of cell biology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMutations in the gene encoding parkin, a neuroprotective protein with dual functions as an E3 ubiquitin ligase and transcriptional repressor of p53, are linked to familial forms of Parkinson's disease (PD). We hypothesized that oxidative posttranslational modification of parkin by environmental toxins may contribute to sporadic PD.
resultsWe first demonstrated that S-nitrosylation of parkin decreased its activity as a repressor of p53 gene expression, leading to upregulation of p53. Chromatin immunoprecipitation as well as gel-shift assays showed that parkin bound to the p53 promoter, and this binding was inhibited by S-nitrosylation of parkin. Additionally, nitrosative stress induced apoptosis in cells expressing parkin, and this death was, at least in part, dependent upon p53. In primary mesencephalic cultures, pesticide-induced apoptosis was prevented by inhibition of nitric oxide synthase (NOS). In a mouse model of pesticide-induced PD, both S-nitrosylated (SNO-)parkin and p53 protein levels were increased, while administration of a NOS inhibitor mitigated neuronal death in these mice. Moreover, the levels of SNO-parkin and p53 were simultaneously elevated in postmortem human PD brain compared to controls.
conclusionsTaken together, our data indicate that S-nitrosylation of parkin, leading to p53-mediated neuronal cell death, contributes to the pathophysiology of sporadic PD.
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