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Gene Review

Rab3a  -  RAB3A, member RAS oncogene family

Mus musculus

Synonyms: Ras-related protein Rab-3A
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Psychiatry related information on Rab3a

  • Spontaneous activity in normal home cage settings was unaffected but Rab3a(-/-) mice showed increased motor activity when the home cage was equipped with a wheel [1].
  • Rab3a(-/-) mice showed normal acquisition but moderately impaired platform reversal learning in the water maze including reference memory and episodic-like memory tasks [1].
  • Since Rab3a constitutive knockout mice react to novel stimuli with hyperactivity, a further search for association of RAB3A DNA variants with other neurobehavioral disorders such as attention deficit/hyperactivity disorder appears justified [2].

High impact information on Rab3a

  • Rab3a is the most abundant Rab (ras-associated binding) protein in the brain and has a regulatory role in synaptic vesicle trafficking [3].
  • Mice with a targeted loss-of-function mutation in Rab3a have defects in Ca(2+)-dependent synaptic transmission: the number of vesicles released in response to an action potential is greater than in wildtype mice, resulting in greater synaptic depression and the abolishment of CA3 mossy-fiber long term potentiation [3].
  • Sequence analysis of Rab3a identified a point mutation in the conserved amino acid (Asp77Gly) within the GTP-binding domain of this protein in earlybird mutants, resulting in significantly reduced levels of Rab3a protein [3].
  • The peptide response can be accelerated by GDP-beta S, suggesting that Rab3a peptides compete with endogenous Rab3 proteins for a binding site on a target effector protein, which causes fusion on activation [4].
  • We have found that synthetic oligopeptides, corresponding to part of the effector domain of Rab3a, stimulate complete exocytotic degranulation, similar to that induced by GTP-gamma S [4].

Biological context of Rab3a


Anatomical context of Rab3a

  • Among the 60 different Rab proteins described in mammals, Rab3a is the most abundant in brain, where it is involved in synaptic vesicle fusion and neurotransmitter release [1].

Regulatory relationships of Rab3a

  • The goals of this study were to analyse possible behavioral consequences of the lack of synaptic plasticity in the mossy fiber pathway using a broad battery of sensitive behavioral measures that has been used previously to analyse the behavior of Gdi1 mice lacking a protein thought to regulate Rab3a [1].

Other interactions of Rab3a

  • On the other hand, the phenotypic changes in the Rab3a(-/-) mice bore no relation to the behavioral changes as observed in the Gdi1 mice [1].
  • A Northern analysis revealed that the rab23 mRNA is predominantly expressed in the brain, which places the protein, together with Rab3a and Rab15, in the group of small GTPases characteristic of the nervous system [6].


  1. Mice deficient for the synaptic vesicle protein Rab3a show impaired spatial reversal learning and increased explorative activity but none of the behavioral changes shown by mice deficient for the Rab3a regulator Gdi1. D'Adamo, P., Wolfer, D.P., Kopp, C., Tobler, I., Toniolo, D., Lipp, H.P. Eur. J. Neurosci. (2004) [Pubmed]
  2. DNA variants in the human RAB3A gene are not associated with autism. D'Adamo, P., Bacchelli, E., Blasi, F., Lipp, H.P., Toniolo, D., Maestrini, E. Genes Brain Behav. (2004) [Pubmed]
  3. Mutations in Rab3a alter circadian period and homeostatic response to sleep loss in the mouse. Kapfhamer, D., Valladares, O., Sun, Y., Nolan, P.M., Rux, J.J., Arnold, S.E., Veasey, S.C., Bućan, M. Nat. Genet. (2002) [Pubmed]
  4. Exocytotic fusion is activated by Rab3a peptides. Oberhauser, A.F., Monck, J.R., Balch, W.E., Fernandez, J.M. Nature (1992) [Pubmed]
  5. Investigation by transient transfection of the effects on regulated exocytosis of Rab3a. Holz, R.W., Senter, R.A., Uhler, M.D. Meth. Enzymol. (1995) [Pubmed]
  6. Isolation of a mouse cDNA encoding Rab23, a small novel GTPase expressed predominantly in the brain. Olkkonen, V.M., Peterson, J.R., Dupree, P., Lütcke, A., Zerial, M., Simons, K. Gene (1994) [Pubmed]
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