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CDC42 — VAV2

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: CDC42 → VAV2 (directlyIncreases, VAV2 Activity)
  Evidence: Cytoplasmic p120-catenin (p120) activates the RHO-family GTPases RAC1 and CDC42 (probably through the RHO guanine-nucleotide exchange factor (RHO-GEF) VAV2)
• KEGG T cell receptor signaling pathway: VAV1/VAV2/VAV3 → CDC42/RHOA (protein-protein, activation)
• KEGG Fc gamma R-mediated phagocytosis: VAV1/VAV2/VAV3 → CDC42 (protein-protein, activation)
• KEGG Leukocyte transendothelial migration: VAV1/VAV2/VAV3 → CDC42 (protein-protein, activation)
• KEGG Chemokine signaling pathway: VAV1/VAV2/VAV3 → CDC42 (protein-protein, activation)
• NCI Pathway Database ErbB1 downstream signaling: VAV2 (VAV2) → CDC42/GDP complex (CDC42) (modification, activates) Kurokawa et al., Mol Biol Cell 2004
  Evidence: assay
• NCI Pathway Database ErbB1 downstream signaling: VAV2 (VAV2) → CDC42/GTP complex (CDC42) (modification, activates) Kurokawa et al., Mol Biol Cell 2004
  Evidence: assay
• NCI Pathway Database Regulation of CDC42 activity: VAV2 (VAV2) → CDC42/GDP complex (CDC42) (modification, activates) Abe et al., J Biol Chem 2000, Liu et al., Mol Cell Biol 2000*, Tu et al., J Biol Chem 2003*, Aoki et al., Mol Biol Cell 2005*, Heo et al., Biochemistry 2005*
  Evidence: assay, physical interaction
• NCI Pathway Database Regulation of CDC42 activity: VAV2 (VAV2) → CDC42/GTP complex (CDC42) (modification, activates) Abe et al., J Biol Chem 2000, Liu et al., Mol Cell Biol 2000*, Tu et al., J Biol Chem 2003*, Aoki et al., Mol Biol Cell 2005*, Heo et al., Biochemistry 2005*
  Evidence: assay, physical interaction
• Reactome Reaction: VAV2 → CDC42 (reaction) Reid et al., J Biol Chem 1999, Schmidt et al., Genes Dev 2002, Jaffe et al., Annu Rev Cell Dev Biol 2005, Ramos-Morales et al., Oncogene 1995, Pasteris et al., Cell 1994, Hart et al., J Biol Chem 1994, Hart et al., J Biol Chem 1996, Zheng et al., J Biol Chem 1996, Van Aelst et al., Genes Dev 1997, Ren et al., J Biol Chem 1998
• WikiPathways Chemokine signaling pathway: VAV1/VAV2/VAV3 → CDC42 (activation)

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
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
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
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
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