ArticleJournal of molecular neuroscience : MN2013
Parkinson's disease-associated DJ-1 mutations increase abnormal phosphorylation of tau protein through Akt/GSK-3β pathways.
Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 34 citations in OpenAlex.
- Lithium mitigates hippocampal tau pathology in a rodent model of traumatic brain injury.Acta neuropathologica communications · 2025Article
- Traditional Chinese Medicine-derived formulations and extracts modulating the PI3K/AKT pathway in Alzheimer's disease.Frontiers in pharmacology · 2025Review
- Genetic forms of tauopathies: inherited causes and implications of Alzheimer's disease-like TAU pathology in primary and secondary tauopathies.Journal of neurology · 2024Review
- Gut Microbial Metabolome and Dysbiosis in Neurodegenerative Diseases: Psychobiotics and Fecal Microbiota Transplantation as a Therapeutic Approach-A Comprehensive Narrative Review.International journal of molecular sciences · 2023Review
- The Molecular Mechanisms of the Relationship between Insulin Resistance and Parkinson's Disease Pathogenesis.Nutrients · 2023Review
- Deficiency of Parkinson's Related Protein DJ-1 Alters Cdk5 Signalling and Induces Neuronal Death by Aberrant Cell Cycle Re-entry.Cellular and molecular neurobiology · 2023Article
- Effectiveness of Recombinant Human Growth Hormone Therapy for Children With Phelan-McDermid Syndrome: An Open-Label, Cross-Over, Preliminary Study.Frontiers in psychiatry · 2022Article
- Repurposing GLP-1 Receptor Agonists for Parkinson's Disease: Current Evidence and Future Opportunities.Pharmaceutical medicine · 2021Article
- ROS networks: designs, aging, Parkinson's disease and precision therapies.NPJ systems biology and applications · 2020Article
- GSK-3β Contributes to Parkinsonian Dopaminergic Neuron Death: Evidence From Conditional Knockout Mice and Tideglusib.Frontiers in molecular neuroscience · 2020Article
- Inhibition of SIRT2 by Targeting GSK3β-Mediated Phosphorylation Alleviates SIRT2 Toxicity in SH-SY5Y Cells.Frontiers in cellular neuroscience · 2019Article
- The Role of Insulin/IGF-1/PI3K/Akt/GSK3β Signaling in Parkinson's Disease Dementia.Frontiers in neuroscience · 2018Review
- Regulation of Signal Transduction by DJ-1.Advances in experimental medicine and biology · 2017Article
- Glycogen Synthase Kinase-3 (GSK-3)-Targeted Therapy and Imaging.Theranostics · 2016Review
- Coffee and caffeine potentiate the antiamyloidogenic activity of melatonin via inhibition of Aβ oligomerization and modulation of the Tau-mediated pathway in N2a/APP cells.Drug design, development and therapy · 2015Article
- The associations between Parkinson's disease and cancer: the plot thickens.Translational neurodegeneration · 2015Review
- Tau protein modifications and interactions: their role in function and dysfunction.International journal of molecular sciences · 2014Review
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4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Hyperphosphorylated tau protein is the main component of neurofibrillary tangles found in Alzheimer's disease and Parkinson's disease (PD). Mutations in DJ-1 have been identified as the causative gene for Parkinson's disease 7 (PARK7)-linked PD. DJ-1L166P and DJ-1D149A, two types of DJ-1 mutations, are most commonly studied as the loss-of-function mutations responsible for early-onset familial PD. Whether mutations in DJ-1 result in tauopathy is as yet unknown. In this study, we found that the L166P and D149A mutant isoforms of DJ-1 associated with familial PD cause tau phosphorylation at Ser202, Ser262, and PHF1 (396/404) sites in neuroblastoma 2a cells. Glycogen synthase kinase (GSK)-3β phosphorylation at serine 9 (Ser9) decreases around 50 % in DJ-1L166P- or DJ-1D149A-transfected cells, while there is no change in total levels of GSK-3β. Our results also indicate that overexpression of DJ-1L166P or DJ-1D149A leads to a significant decrease in the level of phosphorylation of Akt at Thr308, which plays a critical role in phosphorylating GSK-3β at Ser9 and inhibiting its kinase activity. Importantly, insulin, the activator for Akt, effectively attenuates the reduced phosphorylation level of GSK-3β at Ser9 induced by DJ-1L166P. Neither the expression of cyclin-dependent kinase 5 nor the level of PP2A activity was found to have changed, suggesting that the familial PD-associated DJ-1L166P and DJ-1D149A mutations increase tau phosphorylation by increasing the activity of GSK-3β. Finally, we found that administration of lithium chloride, a well-known GSK-3β inhibitor, resulted in decreased levels of phosphorylated tau in DJ-1L166P-transfected cells.
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