ArticleInternational journal of molecular sciences2021
The C-Terminal Domain of LRRK2 with the G2019S Substitution Increases Mutant A53T α-Synuclein Toxicity in Dopaminergic Neurons In Vivo.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Role of LRRK2 in physiological activities, diseases, and therapy.Chinese medical journal · 2026Review
- An Inducible Luminescent System to Explore Parkinson's Disease-Associated Genes.International journal of molecular sciences · 2024Article
- AAV-based vectors for human diseases modeling in laboratory animals.Frontiers in medicine · 2024Review
- Characterisation of functional deficits induced by AAV overexpression of alpha-synuclein in rats.Current research in neurobiology · 2023Article
- Adeno-Associated Viruses for Modeling Neurological Diseases in Animals: Achievements and Prospects.Biomedicines · 2022Review
- Time-Course of Alterations in the Endocannabinoid System after Viral-Mediated Overexpression of α-Synuclein in the Rat Brain.Molecules (Basel, Switzerland) · 2022Article
- Sequential or Simultaneous Injection of Preformed Fibrils and AAV Overexpression of Alpha-Synuclein Are Equipotent in Producing Relevant Pathology and Behavioral Deficits.Journal of Parkinson's disease · 2022Article
- The Small Molecule Alpha-Synuclein Aggregator, FN075, Enhances Alpha-Synuclein Pathology in Subclinical AAV Rat Models.Biomolecules · 2021Article
- Translocation of TMEM175 Lysosomal Potassium Channel to the Plasma Membrane by Dynasore Compounds.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
22 authors at 2 institutions in 1 country.
Funding
Abstract
Alpha-synuclein (α-syn) and leucine-rich repeat kinase 2 (LRRK2) play crucial roles in Parkinson's disease (PD). They may functionally interact to induce the degeneration of dopaminergic (DA) neurons via mechanisms that are not yet fully understood. We previously showed that the C-terminal portion of LRRK2 (ΔLRRK2) with the G2019S mutation (ΔLRRK2
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Registered trials
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