ArticleMolecular neurodegeneration2015
Loss of parkin promotes lipid rafts-dependent endocytosis through accumulating caveolin-1: implications for Parkinson's disease.
Article in Molecular neurodegeneration, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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31 citing papers in PubMed, 71 citations in OpenAlex.
- Improvements in high-yield detection and localisation of cholesterol in murine brains using water cluster beam secondary ion mass spectrometry.Analytical and bioanalytical chemistry · 2026Article
- Caveolae: Metabolic Platforms at the Crossroads of Health and Disease.International journal of molecular sciences · 2025Review
- Post-translational modifications in prion diseases.Frontiers in molecular neuroscience · 2024Review
- Impaired neuron differentiation in GBA-associated Parkinson's disease is linked to cell cycle defects in organoids.NPJ Parkinson's disease · 2023Article
- Review
- A breakdown in microglial metabolic reprogramming causes internalization dysfunction of α-synuclein in a mouse model of Parkinson's disease.Journal of neuroinflammation · 2022Article
- α-Synuclein at the Presynaptic Axon Terminal as a Double-Edged Sword.Biomolecules · 2022Review
- Fat and Protein Combat Triggers Immunological Weapons of Innate and Adaptive Immune Systems to Launch Neuroinflammation in Parkinson's Disease.International journal of molecular sciences · 2022Review
- Age-related increase in caveolin-1 expression facilitates cell-to-cell transmission of α-synuclein in neurons.Molecular brain · 2021Article
- Serum lipid profile among sporadic and familial forms of Parkinson's disease.NPJ Parkinson's disease · 2021Article
- The Role of Cholesterol in α-Synuclein and Lewy Body Pathology in GBA1 Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2021Review
- Caveolin-1 deficiency impairs synaptic transmission in hippocampal neurons.Molecular brain · 2021Article
- Dysfunction of Synaptic Vesicle Endocytosis in Parkinson's Disease.Frontiers in integrative neuroscience · 2021Review
- Blood Cholesterol Decreases as Parkinson's Disease Develops and Progresses.Journal of Parkinson's disease · 2021Article
- Lipid rafts and neurodegeneration: structural and functional roles in physiologic aging and neurodegenerative diseases.Journal of lipid research · 2020Review
- Cholesterol Metabolism in the Brain and Its Association with Parkinson's Disease.Experimental neurobiology · 2019Review
- SQSTM1/p62: A Potential Target for Neurodegenerative Disease.ACS chemical neuroscience · 2019Review
- The Role of Lipids in Parkinson's Disease.Cells · 2019Review
- Overview of Crosstalk Between Multiple Factor of Transcytosis in Blood Brain Barrier.Frontiers in neuroscience · 2019Review
- Ubiquitin C-terminal Hydrolase L1 Regulates Lipid Raft-dependent Endocytosis.Experimental neurobiology · 2018Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundParkinson's disease (PD) is characterized by progressive loss of midbrain dopaminergic neurons, resulting in motor dysfunctions. While most PD is sporadic in nature, a significant subset can be linked to either autosomal dominant or recessive mutations. PARK2, encoding the E3 ubiquitin ligase, parkin, is the most frequently mutated gene in autosomal recessive early onset PD. It has recently been reported that PD-associated gene products such as PINK1, α-synuclein, LRRK2, and DJ-1, as well as parkin associate with lipid rafts, suggesting that the dysfunction of these proteins in lipid rafts may be a causal factor of PD. Therefore here, we examined the relationship between lipid rafts-related proteins and parkin.
resultsWe identified caveolin-1 (cav-1), which is one of the major constituents of lipid rafts at the plasma membrane, as a substrate of parkin. Loss of parkin function was found to disrupt the ubiquitination and degradation of cav-1, resulting in elevated cav-1 protein level in cells. Moreover, the total cholesterol level and membrane fluidity was altered by parkin deficiency, causing dysregulation of lipid rafts-dependent endocytosis. Further, cell-to-cell transmission of α-synuclein was facilitated by parkin deficiency.
conclusionsOur results demonstrate that alterations in lipid rafts by the loss of parkin via cav-1 may be a causal factor of PD, and cav-1 may be a novel therapeutic target for PD.
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