ArticleJournal of biomedical research2016
Retrograde trafficking of VMAT2 and its role in protein stability in non-neuronal cells.
Article in Journal of biomedical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Retromer-targeted therapy for neurodegenerative diseases.Molecular neurodegeneration · 2026Review
- Emergent glutamate & dopamine dysfunction in VPS35NPJ Parkinson's disease · 2025Article
- Structural determinants specific for retromer protein sorting nexin 5 in regulating subcellular retrograde membrane trafficking.Journal of biomedical research · 2023Article
- SNX5 targets a monoamine transporter to the TGN for assembly into dense core vesicles by AP-3.The Journal of cell biology · 2022Article
- The needs of a synapse-How local organelles serve synaptic proteostasis.The EMBO journal · 2022Review
- Retromer dependent changes in cellular homeostasis and Parkinson's disease.Essays in biochemistry · 2021Review
- Elucidating the Relationship Between Diabetes Mellitus and Parkinson's Disease UsingFrontiers in neuroscience · 2020Review
- Interdependency Between Autophagy and Synaptic Vesicle Trafficking: Implications for Dopamine Release.Frontiers in molecular neuroscience · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence suggests that the impaired neuroprotection of vesicular monoamine transporter 2 (VMAT2) contributes to the pathogenesis of Parkinson's disease. That has been linked to aberrant subcellular retrograde trafficking as strongly indicated by recent genomic studies on familial Parkinson's diseases. However, whether VMAT2 function is regulated by retrograde trafficking is unknown. By using biochemistry and cell biology approaches, we have shown that VMAT2 was stringently localized to the trans-Golgi network and underwent retrograde trafficking in non-neuronal cells. The transporter also interacted with the key component of retromer, Vps35, biochemically and subcellularly. Using specific siRNA, we further showed that Vps35 depletion altered subcellular localization of VMAT2. Moreover, siRNA-mediated Vps35 knockdown also decreased the stability of VMAT2 as demonstrated by the reduced half-life. Thus, our work suggested that altered vesicular trafficking of VMAT2 may play a vital role in neuroprotection of the transporter as well as in the pathogenesis of Parkinson's disease.
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Registered trials
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