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RAC1 — VEGFA
Pathways - manually collected, often from reviews:
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
Ikeda et al., Circ Res 2005
(Ischemia) :
In this study, we show that overexpression of dominant negative ARF6 [ ARF6 ( T27N ) ] almost completely inhibits
VEGF induced
Rac1 activation, ROS production, and VEGFR2 autophosphorylation in ECs
Dentelli et al., Oncogene 2005
(Neoplasm Invasiveness...) :
Engagement of IL-3 receptor beta common ( IL-3R beta c ) contributes to both IL-3- and
VEGF induced
Rac1 activation, cell migration and in vitro tube-like structure formation as shown by the expression of the dominant negative IL-3R beta c construct ( Delta455 )
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
Lee et al., Clin Cancer Res 2006
(Carcinoma, Hepatocellular...) :
Rac induced the transcriptional activation of
VEGF by direct interaction with hypoxia-inducible factor-1alpha ( HIF-1alpha ) expression
Garrett et al., Exp Cell Res 2007
:
VEGF induced
Rac1 activation in endothelial cells is regulated by the guanine nucleotide exchange factor Vav2 ... The goal of this study was to identify the GEF responsible for activating
Rac1 in
response to
VEGF stimulation ... We have found that
VEGF stimulates biphasic activation of
Rac1 and for these studies we focused on the peak of activation that occurs at 30 min. Inhibition of VEGFR-2 signaling blocks VEGF induced Rac1 activation ... Additionally, we show that depleting endothelial cells of endogenous Vav2 with siRNA prevents
VEGF induced
Rac1 activation
Miao et al., Arterioscler Thromb Vasc Biol 2008
:
Moreover, D88N-Hsp90 abolished
VEGF stimulated
Rac activation and suppressed VEGF induced stress fiber formation
Yokomori et al., Liver Int 2009
:
Rac1 activity increased progressively to 17 h in cells cultured without VEGF, but markedly
increased at 7 h in the presence of
VEGF
Peng et al., Acta Diabetol 2010
(Diabetic Nephropathies) :
Using an integrated in vitro approach, we investigated whether the
effect of
VEGF on endothelial cell permeability involves
Rac1 GTPase activation and tight junction disassembly
Miura et al., Exp Cell Res 2010
(Corneal Neovascularization) :
Consistent with these observations, rhChM-I was found to significantly reduce the activity of Rac1/Cdc42 during cell spreading, and the
VEGF-A induced
Rac1 activity but not its basal activity in quiescent cells
Monaghan-Benson et al., Am J Pathol 2010
(Choroidal Neovascularization...) :
We found that
vascular endothelial growth factor induced the activation of
Rac1 and of NADPH oxidase in cultured human choroidal endothelial cells ... Taken together, these results indicate that
vascular endothelial growth factor activates
Rac1 upstream from NADPH oxidase in human choroidal endothelial cells and increases generation of reactive oxygen species, contributing to choroidal neovascularization
Oshikawa et al., Am J Physiol Heart Circ Physiol 2012
(MAP Kinase Signaling System) :
Depletion of endogenous p66Shc with short interfering RNA inhibits
VEGF induced
Rac1 activity and ROS production
Kearns et al., Am J Physiol Lung Cell Mol Physiol 2012
(Emphysema) :
Our data show that the uptake of apoptotic cells by murine AMs and human monocyte derived macrophages is inhibited by depletion of
VEGF and that VEGF
activates Rac1
Zang et al., Cell Signal 2013
:
VEGF-A stimulated extracellular-signal regulated kinase, Akt and
Rac1 activities in the wild-type cells whereas no such responses were noted in the knockout cells
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 )