ArticleAntioxidants & redox signaling2012
Redox proteomics analyses of the influence of co-expression of wild-type or mutated LRRK2 and Tau on C. elegans protein expression and oxidative modification: relevance to Parkinson disease.
Article in Antioxidants & redox signaling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 52 citations in OpenAlex.
- Groundbreaking Insights Into SIRT1/NRF2-Mediated Ferroptosis Inhibition by Resveratrol in Parkinson's Disease Models.CNS neuroscience & therapeutics · 2025Article
- Mechanisms of autophagy-lysosome dysfunction in neurodegenerative diseases.Nature reviews. Molecular cell biology · 2024Review
- LRRK2 regulates production of reactive oxygen species in cell and animal models of Parkinson's disease.Science translational medicine · 2024Article
- Biliverdin Reductase-A integrates insulin signaling with mitochondrial metabolism through phosphorylation of GSK3β.Redox biology · 2024Article
- Dynamic Changes of BVRA Protein Levels Occur in Response to Insulin: A Pilot Study in Humans.International journal of molecular sciences · 2023Article
- The interplay among oxidative stress, brain insulin resistance and AMPK dysfunction contribute to neurodegeneration in type 2 diabetes and Alzheimer disease.Free radical biology & medicine · 2021Review
- Non-Rodent Genetic Animal Models for Studying Tauopathy: Review ofInternational journal of molecular sciences · 2021Review
- mTOR in Alzheimer disease and its earlier stages: Links to oxidative damage in the progression of this dementing disorder.Free radical biology & medicine · 2021Review
- Stress Responses in Down Syndrome Neurodegeneration: State of the Art and Therapeutic Molecules.Biomolecules · 2021Review
- The emerging roles of vacuolar-type ATPase-dependent Lysosomal acidification in neurodegenerative diseases.Translational neurodegeneration · 2020Review
- Proteostasis Failure in Neurodegenerative Diseases: Focus on Oxidative Stress.Oxidative medicine and cellular longevity · 2020Review
- Disturbance of redox homeostasis in Down Syndrome: Role of iron dysmetabolism.Free radical biology & medicine · 2018Review
- Biological Activities, Health Benefits, and Therapeutic Properties of Avenanthramides: From Skin Protection to Prevention and Treatment of Cerebrovascular Diseases.Oxidative medicine and cellular longevity · 2018Review
- Regulation of autophagy, mitochondrial dynamics, and cellular bioenergetics by 4-hydroxynonenal in primary neurons.Autophagy · 2017Article
- Disorders of lysosomal acidification-The emerging role of v-ATPase in aging and neurodegenerative disease.Ageing research reviews · 2016Review
- High ω3-polyunsaturated fatty acids in fat-1 mice prevent streptozotocin-induced Purkinje cell degeneration through BDNF-mediated autophagy.Scientific reports · 2015Article
- Comparative Proteomic Analysis of Carbonylated Proteins from the Striatum and Cortex of Pesticide-Treated Mice.Parkinson's disease · 2015Article
- An investigation of the molecular mechanisms engaged before and after the development of Alzheimer disease neuropathology in Down syndrome: a proteomics approach.Free radical biology & medicine · 2014Article
- New insight into neurodegeneration: the role of proteomics.Molecular neurobiology · 2014Review
- Mitochondrial dysfunction driven by the LRRK2-mediated pathway is associated with loss of Purkinje cells and motor coordination deficits in diabetic rat model.Cell death & disease · 2014Article
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Authors and funding
15 authors at 8 institutions in 2 countries.
Funding
Abstract
aimsThe human LRRK2 gene has been identified as the most common causative gene of autosomal-dominantly inherited and idiopathic Parkinson disease (PD). The G2019S substitution is the most common mutation in LRRK2. The R1441C mutation also occurs in cases of familial PD, but is not as prevalent. Some cases of LRRK2-based PD exhibit Tau pathology, which suggests that alterations on LRRK2 activity affect the pathophysiology of Tau. To investigate how LRRK2 might affect Tau and the pathophysiology of PD, we generated lines of C. elegans expressing human LRRK2 [wild-type (WT) or mutated (G2019S or R1441C)] with and without V337M Tau. Expression and redox proteomics were used to identify the effects of LRRK2 (WT and mutant) on protein expression and oxidative modifications.
resultsCo-expression of WT LRRK2 and Tau led to increased expression of numerous proteins, including several 60S ribosomal proteins, mitochondrial proteins, and the V-type proton ATPase, which is associated with autophagy. C. elegans expressing mutant LRRK2 showed similar changes, but also showed increased protein oxidation and lipid peroxidation, the latter indexed as increased protein-bound 4-hydroxy-2-nonenal (HNE). INNOVATION: Our study brings new knowledge about the possible alterations induced by LRRK2 (WT and mutated) and Tau interactions, suggesting the involvement of G2019S and R1441C in Tau-dependent neurodegenerative processes.
conclusionThese results suggest that changes in LRRK2 expression or activity lead to corresponding changes in mitochondrial function, autophagy, and protein translation. These findings are discussed with reference to the pathophysiology of PD.
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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.