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CDC42 — VEGFA
Pathways - manually collected, often from reviews:
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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
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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
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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
SanĂger 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 )