ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Rab33a mediates anterograde vesicular transport for membrane exocytosis and axon outgrowth.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. 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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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
- Persistent PirB cleavage drives Golgi-directed trafficking deficits underlying neurodegeneration.Translational neurodegeneration · 2026Article
- LRRK2 and the fragile synapse: a molecular prelude to Parkinson's disease?The Biochemical journal · 2025Review
- Rab6-Mediated Polarized Transport of Synaptic Vesicle Precursors Is Essential for the Establishment of Neuronal Polarity and Brain Formation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- The Role of Rab GTPases in the development of genetic and malignant diseases.Molecular and cellular biochemistry · 2024Review
- The Role of Rab Proteins in Parkinson's Disease Synaptopathy.Biomedicines · 2022Review
- A drug-biomarker interaction model to predict the key targets of Scutellaria barbata D. Don in adverse-risk acute myeloid leukaemia.Molecular diversity · 2021Article
- Mechanosensitive axon outgrowth mediated by L1-laminin clutch interface.Biophysical journal · 2021Article
- Axonal Organelles as Molecular Platforms for Axon Growth and Regeneration after Injury.International journal of molecular sciences · 2021Review
- SCYL1 arginine methylation by PRMT1 is essential for neurite outgrowth via Golgi morphogenesis.Molecular biology of the cell · 2020Article
- LMTK1, a Novel Modulator of Endosomal Trafficking in Neurons.Frontiers in molecular neuroscience · 2020Article
- News about non-secretory exocytosis: mechanisms, properties, and functions.Journal of molecular cell biology · 2019Review
- Rab GTPases: Switching to Human Diseases.Cells · 2019Review
- Multitasking Rab Proteins in Autophagy and Membrane Trafficking: A Focus on Rab33b.International journal of molecular sciences · 2019Review
- Transcriptomic correlates of electrophysiological and morphological diversity within and across excitatory and inhibitory neuron classes.PLoS computational biology · 2019Article
- Epstein-Barr Virus dUTPase Induces Neuroinflammatory Mediators: Implications for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.Clinical therapeutics · 2019Article
- Dynamic balance between vesicle transport and microtubule growth enables neurite outgrowth.PLoS computational biology · 2019Article
- Rab33a and Rab33ba mediate the outgrowth of forebrain commissural axons in the zebrafish brain.Scientific reports · 2019Article
- Molecular basis of the functions of the mammalian neuronal growth cone revealed using new methods.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2019Review
- RAB37 interacts directly with ATG5 and promotes autophagosome formation via regulating ATG5-12-16 complex assembly.Cell death and differentiation · 2018Article
- Consequences of Rab GTPase dysfunction in genetic or acquired human diseases.Small GTPases · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Axon outgrowth requires plasma membrane expansion, which results from post-Golgi vesicular transport and fusion. However, the molecular mechanisms regulating post-Golgi vesicular trafficking for membrane expansion and axon outgrowth remain unclear. Here, we show that Rab33a expression became upregulated during axon outgrowth of cultured rat hippocampal neurons. Rab33a was preferentially localized to the Golgi apparatus and to synaptophysin-positive vesicles that are transported along the growing axon. Previous studies showed that synaptophysin is localized to post-Golgi vesicles transported by fast axonal transport in developing neurons. Reduction of Rab33a expression by RNAi (RNA interference) inhibited the anterograde transport of synaptophysin-positive vesicles, leading to their decrease in axonal tips. Furthermore, this treatment reduced membrane fusion of synaptophysin-positive vesicles at the growth cones and inhibited axon outgrowth. Overexpression of Rab33a, on the other hand, induced excessive accumulation of synaptophysin-positive vesicles and concurrent formation of surplus axons. These data suggest that Rab33a participates in axon outgrowth by mediating anterograde axonal transport of synaptophysin-positive vesicles and their concomitant fusion at the growth cones.
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Registered trials
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.