Gene interactions and pathways from curated databases and text-mining

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RAC1 — VAV2

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Abe et al., J Biol Chem 2000 : Vav2 is an activator of Cdc42, Rac1 , and RhoA
Liu et al., Mol Cell Biol 2000 : Vav2 activates Rac1 , Cdc42, and RhoA downstream from growth factor receptors but not beta1 integrins ... Expression of a carboxy-terminal fragment of Vav2 decreased the elevation of Rac1 activity induced by epidermal growth factor, consistent with Vav2 mediating activation of Rac1 downstream from growth factor receptors
Marignani et al., J Cell Biol 2001 : Vav2 nucleotide exchange is Src dependent in vivo, since the coexpression of Vav2 and dominant negative Src, or treatment with the Src inhibitor PP2, blocks both Vav2 dependent Rac activation and lamellipodia formation
Servitja et al., J Biol Chem 2003 (Cell Transformation, Neoplastic) : Evidence of a role for Tiam1 and Vav2 in Rac activation by Src
Marcoux et al., Oncogene 2003 : EGF receptor mediates adhesion dependent activation of the Rac GTPase : a role for phosphatidylinositol 3-kinase and Vav2
Miller et al., Mol Endocrinol 2005 (Breast Neoplasms) : Activation of guanosine triphosphatase Rac-1 in Chinese hamster ovary transfectants required both Nek3 and Vav2 and was inhibited by the overexpression of a kinase inactivating Nek3 mutant
Aoki et al., Mol Biol Cell 2005 : Local phosphatidylinositol 3,4,5-trisphosphate accumulation recruits Vav2 and Vav3 to activate Rac1/Cdc42 and initiate neurite outgrowth in nerve growth factor stimulated PC12 cells ... Depletion of Vav2 and Vav3 by RNA interference significantly inhibited both Rac1/Cdc42 activation and the formation of short processes leading to neurite outgrowth ... At the NGF induced protrusions, local phosphatidylinositol 3,4,5-trisphosphate accumulation recruited Vav2 and Vav3 to activate Rac1 and Cdc42, and conversely, Vav2 and Vav3 were required for the local activation of PI3-kinase
Hunter et al., Mol Cell Biol 2006 : Overexpression of either Vav2 or Vav3 in primary microvascular endothelial cells promotes Rac1 activation, cell migration, and assembly in response to ephrin-A1 stimulation ... Conversely, loss of Vav2 and Vav3 GEFs inhibits Rac1 activation and ephrin-A1 induced angiogenic responses both in vitro and in vivo
Murata et al., J Neurosci 2006 : These results indicate that CD47 promotes development of dendrites and axons in hippocampal neurons in a manner dependent, at least in part, on activation of Cdc42 and Rac mediated by Src as well as by FRG and Vav2
Birukova et al., Exp Cell Res 2007 (Respiratory Distress Syndrome, Adult) : Both PGs caused cAMP mediated activation of PKA-, Epac/Rap1- and Tiam1/Vav2 dependent pathways of Rac1 activation and EC barrier regulation
Garrett et al., Exp Cell Res 2007 : VEGF induced Rac1 activation in endothelial cells is regulated by the guanine nucleotide exchange factor Vav2
Yi et al., Cell Physiol Biochem 2007 : Mechanism of homocysteine induced Rac1/NADPH oxidase activation in mesangial cells : role of guanine nucleotide exchange factor Vav2 ... This Vav2-siRNA also blocked Rac activation induced by C16-Ceramide ( C16-Cer ), an intermediate lipid product stimulated by Hcys ... These results suggest that Vav2 importantly contributes to Hcys induced increase in Rac1 activity and consequent activation of NADPH oxidase in RMCs via ceramide associated tyrosine phosphorylation
Lai et al., Oral Oncol 2008 (Carcinoma, Squamous Cell...) : Transfection of activated Vav2 into the immortalized keratinocyte cell line HaCat and a low-level expressing Vav2 invasive OSCC cell line resulted in increased GTP bound Rac1 and Cdc42 and increased invasion
Yi et al., Hypertension 2009 (Disease Models, Animal...) : In the rat kidneys with transfection of a dominant-active Vav2 variant ( onco-Vav2 ), we found that overexpression of Vav2 led to significant increases in Rac1 activity, superoxide production, and glomerular injury, which was similar to that induced by hyperhomocysteinemia
Duan et al., J Biol Chem 2010 : Inducible expression of a constitutively active form of Vav2 , a Rho GTPase guanine nucleotide exchange factor activated by receptor tyrosine kinases, in three-dimensional MEC culture activated Rac1 and Cdc42 ; Vav2 induction from early stages of culture impaired acinar morphogenesis, and induction in preformed acini disrupted the pre established acinar architecture and led to cellular outgrowths
Duan et al., J Biol Chem 2011 : Overexpression of constitutively active Vav2 activated Rac1/Cdc42 and reorganized junctional actin cytoskeleton ; these effects were suppressed by WT Cbl and enhanced by a ubiquitin ligase-deficient Cbl mutant
Maruvada et al., Infect Immun 2012 (Escherichia coli Infections...) : We further showed that the guanine nucleotide exchange factor Vav2 , not ß-Pix, was involved in E. coli K1-mediated Rac1 activation
Valls et al., J Cell Sci 2012 : Upon Wnt stimulation, Rac1 activation requires Rac1 and Vav2 binding to p120-catenin