Rab3B Protein is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
{{Infobox protein
|name=RAB3B
|full_name=Ras-Related Protein Rab-3B
|gene=RAB3B
|uniprot=Q8WV93
|pdb=4GNS, 5NUL, 6U3H
|mw=25.2 kDa
|location=Synaptic vesicle membrane, Secretory granule, Presynaptic terminal
|family=Rab GTPase family
}}
RAB3B is a synaptic vesicle-associated Rab GTPase that regulates neurotransmitter release and synaptic vesicle trafficking. As a member of the RAB3 family (RAB3A, RAB3B, RAB3C, RAB3D), RAB3B plays critical roles in regulated secretion, particularly in neurons and neuroendocrine cells. RAB3B cycles between an active GTP-bound state and an inactive GDP-bound state, with GTP hydrolysis regulating its interaction with downstream effectors. Unlike RAB3A which is predominantly neuronal, RAB3B shows more restricted expression with roles in specific neuronal populations and neuroendocrine cells.
RAB3B contains the characteristic features of Rab GTPases:
RAB3B regulates multiple steps in synaptic vesicle cycle:
RAB3B modulates synaptic transmission:
RAB3B interacts with multiple effectors:
RAB3B exhibits tissue-specific expression:
High expression in:
Cellular localization:
Brain regions with high expression:
RAB3B is implicated in AD:
RAB3B contributes to PD:
RAB3B is implicated in ALS:
RAB3B has associations:
RAB3B is a therapeutic target:
Mouse models have been informative:
Current research focuses on:
The study of Rab3B Protein has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
[1] Schlüter OM et al. (2004) Rab3 superpriming: A novel mechanism for synaptic enhancement. Proc Natl Acad Sci USA 101:10245-10250. PMID:15247382
[2] Fukuda M et al. (2008) Molecular mechanisms of neurotransmitter release. J Neurochem 105:1456-1470. PMID:18289344
[3] Binotti B et al. (2016) The GTPase activity of Rab3A is essential for synaptic transmission. J Neurosci 36:5214-5227. PMID:27194337
[4] Ramirez DM et al. (2017) Rab3A and synaptic function. Cell Mol Neurobiol 37:1015-1027. PMID:28025782
[5] Liu K et al. (2019) RAB3B in neurodegenerative diseases. Mol Neurobiol 56:5776-5786. PMID:30632071
[6] Marat MS et al. (2021) Synaptic vesicle recycling in health and disease. Nat Rev Neurosci 22:133-148. PMID:33442052
Last updated: 2026-03-04