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Gene Review

Vav3  -  vav 3 oncogene

Mus musculus

Synonyms: A530094I06Rik, AA986410, Guanine nucleotide exchange factor VAV3, Idd18.1, VAV-3
 
 
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Disease relevance of Vav3

 

High impact information on Vav3

  • Here we identify Vav3, a GDP-GTP exchange factor that stimulates Rho and Rac GTPases, as an essential factor regulating the homeostasis of the cardiovascular system [1].
  • Pharmacological studies with drugs targeting sympathetic and renin-angiotensin responses confirmed the causative role and hierarchy of these events in the development of the Vav3-null mouse phenotype [1].
  • These observations uncover the crucial role of Vav3 in the regulation of the sympathetic nervous system (SNS) and cardiovascular physiology, and reveal a signaling pathway that could be involved in the pathophysiology of human disease states involving tachycardia and sympathetic hyperactivity with unknown etiologies [1].
  • Vav3 proto-oncogene deficiency leads to sympathetic hyperactivity and cardiovascular dysfunction [1].
  • Moreover, we provide genetic and biochemical evidence for the role of Syk tyrosine kinase as a crucial upstream regulator of Vav3 in osteoclasts [2].
 

Biological context of Vav3

  • Here we identify Vav3, a Rho family guanine nucleotide exchange factor, as essential for stimulated osteoclast activation and bone density in vivo [2].
  • Comparison of these forms has revealed the interdomain interactions maintaining the inactive Vav3 state and the dynamic changes that the overall Vav3 structure undergoes upon tyrosine phosphorylation [3].
  • Over expression of Vav3 or Vav3-(6-10) resulted in an enhancement of cell motility [4].
  • Moreover, expression of Vav-3 alters cytokinesis, resulting in the formation of binucleated cells [5].
  • All of these responses need only the expression of the central region of Vav-3 encompassing the Dbl homology (DH), pleckstrin homology (PH), and zinc finger (ZF) domains but do not require the presence of the C-terminal SH3-SH2-SH3 regions [5].
 

Anatomical context of Vav3

 

Associations of Vav3 with chemical compounds

 

Other interactions of Vav3

  • Here we report the identification of Vav2 and Vav3 as guanine nucleotide exchange factors (GEFs) that link the EphA2 receptor to Rho family GTPase activation and angiogenesis [7].
  • Distinct role of phosphatidylinositol 3-kinase and Rho family GTPases in Vav3-induced cell transformation, cell motility, and morphological changes [4].
  • We report here the identification and characterization of a novel Vav family member, Vav-3 [5].
  • This phosphorylation event is conserved in Vav-2 and Vav-3, the other two members of the Vav family [8].
 

Analytical, diagnostic and therapeutic context of Vav3

  • Here, we have used single-particle electron microscopy to solve the structures of the inactive (unphosphorylated), active (phosphorylated), and constitutively active (N-terminally deleted) versions of the exchange factor Vav3 [3].

References

  1. Vav3 proto-oncogene deficiency leads to sympathetic hyperactivity and cardiovascular dysfunction. Sauzeau, V., Sevilla, M.A., Rivas-Elena, J.V., de Alava, E., Montero, M.J., López-Novoa, J.M., Bustelo, X.R. Nat. Med. (2006) [Pubmed]
  2. Vav3 regulates osteoclast function and bone mass. Faccio, R., Teitelbaum, S.L., Fujikawa, K., Chappel, J., Zallone, A., Tybulewicz, V.L., Ross, F.P., Swat, W. Nat. Med. (2005) [Pubmed]
  3. Global conformational rearrangements during the activation of the GDP/GTP exchange factor Vav3. Llorca, O., Arias-Palomo, E., Zugaza, J.L., Bustelo, X.R. EMBO J. (2005) [Pubmed]
  4. Distinct role of phosphatidylinositol 3-kinase and Rho family GTPases in Vav3-induced cell transformation, cell motility, and morphological changes. Sachdev, P., Zeng, L., Wang, L.H. J. Biol. Chem. (2002) [Pubmed]
  5. Biological and regulatory properties of Vav-3, a new member of the Vav family of oncoproteins. Movilla, N., Bustelo, X.R. Mol. Cell. Biol. (1999) [Pubmed]
  6. Vav family proteins are required for optimal regulation of PLCgamma2 by integrin alphaIIbbeta3. Pearce, A.C., McCarty, O.J., Calaminus, S.D., Vigorito, E., Turner, M., Watson, S.P. Biochem. J. (2007) [Pubmed]
  7. Essential role of Vav family guanine nucleotide exchange factors in EphA receptor-mediated angiogenesis. Hunter, S.G., Zhuang, G., Brantley-Sieders, D., Swat, W., Cowan, C.W., Chen, J. Mol. Cell. Biol. (2006) [Pubmed]
  8. Tyrosine phosphorylation mediates both activation and downmodulation of the biological activity of Vav. López-Lago, M., Lee, H., Cruz, C., Movilla, N., Bustelo, X.R. Mol. Cell. Biol. (2000) [Pubmed]
 
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