| Protein Name | Ras-Related Protein Rab-3A |
|---|---|
| Gene | [RAB3A](/genes/rab3a) |
| UniProt ID | [P20336](https://www.uniprot.org/uniprot/P20336) |
| Molecular Weight | 25 kDa |
| Subcellular Localization | Synaptic Vesicles, Presynaptic Terminal |
| Protein Family | RAB family |
| Gene Location | 19p13.2 |
RAB3A (Ras-Related Protein Rab-3A) is a synaptic vesicle-associated small GTPase that plays a central role in regulating neurotransmitter release[1][2]. As a member of the RAB GTPase family, RAB3A cycles between an active GTP-bound and inactive GDP-bound state, functioning as a molecular switch controlling synaptic vesicle trafficking, docking, and fusion. It is the most abundant RAB protein in synaptic vesicles and is essential for regulated exocytosis[3].
The RAB3 family includes four isoforms (RAB3A, RAB3B, RAB3C, and RAB3D) with distinct expression patterns. RAB3A is neuron-specific and enriched in presynaptic terminals, making it a key marker of synaptic vesicle cycling.
RAB3A has characteristic RAB GTPase features:
Post-translational lipid modifications (prenylation) anchor RAB3A to synaptic vesicle membranes[4]. The GTPase cycle is regulated by GTPase-activating proteins (GAPs) and guanine nucleotide exchange factors (GEFs).
RAB3A orchestrates the synaptic vesicle cycle:
RAB3A regulates release through interactions with:
RAB3A modulates forms of plasticity:
RAB3A dysfunction contributes to AD[5]:
RAB3A is implicated in PD:
RAB3A is a therapeutic target:
RAB3A in synaptic transmission (2018). Nature Reviews Neuroscience. 2018. ↩︎
RAB GTPases in neuronal function (2020). Physiological Reviews. 2020. ↩︎
RAB3A structure and function (2019). Journal of Biological Chemistry. 2019. ↩︎
Prenylation of RAB proteins (2021). Cellular and Molecular Life Sciences. 2021. ↩︎
Synaptic dysfunction in Alzheimer's disease (2022). Acta Neuropathologica. 2022. ↩︎