◀ Back to VEGFA

CDC42 — VEGFA

Pathways - manually collected, often from reviews:

• NCI Pathway Database Signaling events mediated by VEGFR1 and VEGFR2: CDC42/GDP complex (CDC42) → VEGFR2 (dimer)/VEGFA (dimer)/Fyn/NCK1-2/PAK2 complex (KDR-VEGFA-FYN-NCK2_NCK1-PAK2) (modification, collaborate)
  Lamalice et al., Oncogene 2004, Lamalice et al., J Biol Chem 2006
  Evidence: mutant phenotype
• Reactome Reaction: VEGFA → CDC42 (reaction) Gatti et al., J Biol Chem 1999, Chong et al., J Biol Chem 2001, Renkema et al., Mol Cell Biol 2002, Gerhardt et al., J Cell Biol 2003, Lamalice et al., J Biol Chem 2006
• Reactome Reaction: VEGFA → CDC42 (indirect_complex) Gatti et al., J Biol Chem 1999, Chong et al., J Biol Chem 2001, Renkema et al., Mol Cell Biol 2002, Gerhardt et al., J Cell Biol 2003, Lamalice et al., J Biol Chem 2006

Text-mined interactions from Literome

Soga et al., Exp Cell Res 2001 : VEGF signaling required Rac activation during chemotaxis, and Rac and Cdc42 were activated during haptotaxis on type I collagen
Lamalice et al., Oncogene 2004 : Phosphorylation of tyrosine 1214 on VEGFR2 is required for VEGF induced activation of Cdc42 upstream of SAPK2/p38 ... Here, we found that VEGF increased by twofold the activity of the small GTPase Cdc42 and that the expression of two different constitutively active forms of Cdc42 ( Cdc42 V12 and Cdc42 L61 ) led to a marked increase in the formation of stress fibers that was sensitive to SAPK2/p38 inhibition by SB203580 ... Using a site-specific mutant of the major autophosphorylation site Y1214 on VEGFR2, we found that the mutant Y1214F inhibited the activation of both Cdc42 and SAPK2/p38 in response to VEGF
Saníger et al., J Cell Biochem 2006 : These findings indicate that Rho oncoprotein endogenously activated regulates VEGF expression through a transcriptional mechanism, and that the c-Jun kinase activity is a mediator in the expression of VEGF induced by Rac1 and Cdc42 oncoproteins, but not of that induced by RhoA
Kusuhara et al., PloS one 2012 : Arhgef15 promotes retinal angiogenesis by mediating VEGF induced Cdc42 activation and potentiating RhoJ inactivation in endothelial cells ... Of 9 RhoGEFs which were highly expressed in retinal ECs, we show that Arhgef15 acted as an EC-specific GEF to mediate VEGF induced Cdc42 activation and potentiated RhoJ inactivation, thereby promoting actin polymerization and cell motility
Ma et al., PloS one 2013 : Here, we determined that activated Rac1/Cdc42 in MCF-7 breast cancer cells could decrease p53 protein levels and increase VEGF secretion to promote proliferation and tube formation of human umbilical vein endothelial cells ( HUVECs )