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RAC1 — VAV3

Pathways - manually collected, often from reviews:

• KEGG Focal adhesion: VAV1/VAV2/VAV3 → RAC1/RAC2/RAC3 (protein-protein, activation)
• KEGG Natural killer cell mediated cytotoxicity: VAV1/VAV2/VAV3 → RAC1/RAC2/RAC3 (protein-protein, activation)
• KEGG B cell receptor signaling pathway: VAV1/VAV2/VAV3 → RAC1/RAC2/RAC3 (protein-protein, activation)
• KEGG Fc epsilon RI signaling pathway: VAV1/VAV2/VAV3 → RAC1/RAC2/RAC3 (protein-protein, activation)
• KEGG Fc gamma R-mediated phagocytosis: VAV1/VAV2/VAV3 → RAC1/RAC2 (protein-protein, activation)
• KEGG Leukocyte transendothelial migration: VAV1/VAV2/VAV3 → RAC1 (protein-protein, activation)
• KEGG Regulation of actin cytoskeleton: TIAM1/TIAM2/VAV1/VAV2/VAV3 → RAC1/RAC2/RAC3 (protein-protein, activation)
• KEGG Chemokine signaling pathway: VAV1/VAV2/VAV3 → RAC1/RAC2 (protein-protein, activation)
• NCI Pathway Database Integrins in angiogenesis: RAC1/GDP complex (RAC1) → VAV3 (VAV3) (modification, collaborate) Faccio et al., Nat Med 2005*
  Evidence: mutant phenotype, assay, other species
• NCI Pathway Database Regulation of RAC1 activity: RAC1/GDP complex (RAC1) → VAV3 (VAV3) (modification, collaborate) Aoki et al., Mol Biol Cell 2005*
  Evidence: assay
• NCI Pathway Database Osteopontin-mediated events: RAC1/GDP complex (RAC1) → VAV3 (VAV3) (modification, collaborate) Faccio et al., Nat Med 2005*
  Evidence: mutant phenotype, assay, other species
• NCI Pathway Database EPHA2 forward signaling: RAC1/GDP complex (RAC1) → Ephrin A1/EPHA2/VAV2-VAV3 complex (EFNA1-EPHA2-VAV2_VAV3) (modification, collaborate)
  Hunter et al., Mol Cell Biol 2006, Fang et al., J Biol Chem 2008
  Evidence: mutant phenotype, assay
• Reactome Reaction: RAC1 → VAV3 (reaction) Abe et al., J Biol Chem 2000, Zeng et al., Mol Cell Biol 2000, Chong et al., J Biol Chem 2001, Harrington et al., J Neurosci 2002, Parrini et al., Mol Cell 2002, Tybulewicz et al., Immunol Rev 2003, Marston et al., Nat Cell Biol 2003, Hall et al., Immunity 2006, Bos et al., Cell 2007, Garrett et al., Exp Cell Res 2007, Chrencik et al., J Mol Biol 2008*, Crespo et al., Nature 1997
• Reactome Reaction: RAC1 → VAV3 (indirect_complex) Tybulewicz et al., Immunol Rev 2003, Marston et al., Nat Cell Biol 2003, Bos et al., Cell 2007, Garrett et al., Exp Cell Res 2007
• WikiPathways Microglia Pathogen Phagocytosis Pathway: PLCG2/LAT/VAV1/VAV2/VAV3 → RAC1/RAC2/RAC3 (activation)
• WikiPathways Chemokine signaling pathway: VAV1/VAV2/VAV3 → RAC1/RAC2 (activation)

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: RAC1 — VAV3 (direct interaction, pull down) Movilla et al., Mol Cell Biol 1999*
• IRef Hprd Interaction: VAV3 — RAC1 (in vitro) Movilla et al., Mol Cell Biol 1999*
• IRef Ophid Interaction: RAC1 — VAV3 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Zeng et al., Mol Cell Biol 2000 (Cell Transformation, Neoplastic) : In vitro binding assays using glutathione S-transferase-fusion polypeptides containing the GTPase binding domains of Rok-alpha, Pak, or Ack revealed that overexpression of Vav3 in NIH 3T3 cells resulted in the activation of Rac-1 and Cdc42 whereas a deletion mutant lacking the N-terminal calponin homology and acidic region domains activated RhoA and Rac-1 but lost the ability to activate Cdc42
Inabe et al., J Exp Med 2002 : Here we report that Vav3 influences phosphoinositide 3-kinase (PI3K) function through Rac1 in that phosphatidylinositol-3,4,5-trisphosphate ( PIP3 ) generation was attenuated by loss of Vav3 or by expression of a dominant negative form of Rac1
Johmura et al., Immunity 2003 : By expression of Vav3 as a raft targeted construct, the defective Rac1 activation in Grb2- or BLNK-deficient B cells is restored
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
Rosenblatt et al., Endocr Relat Cancer 2011 (Breast Neoplasms) : Vav3 , a Rho guanine nucleotide exchange factor that activates Rac1 , was an upstream mediator, and P21/Cdc42/Rac1 activating kinase-1 ( Pak-1 ) was a downstream effector of Rac1 enhancement of ERa activity