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RHO — VEGFA

Text-mined interactions from Literome

Yourey et al., J Neurosci 2000 : After 7-9 d of treatment the VEGF-1 or VEGF-2, at a concentration of 10 ng/ml, induced a 200-300 % increase in rhodopsin protein and a 220 % increase in the number of rhodopsin-immunopositive cells
Chai et al., FASEB J 2004 (Stomach Ulcer) : Mechanistically, this study also revealed that VEGF promotes SRF expression and nuclear translocation and increases SRF binding activity to DNA in endothelial cells through both Rho-actin and MEK-ERK dependent signaling pathways
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
Takata et al., Mol Cancer Ther 2008 (Neovascularization, Pathologic) : Furthermore, hypoxia induced both vascular endothelial growth factor ( VEGF ) and VEGF receptor-2 expression through the Rho/ROCK/HIF-1alpha signaling in HUVECs
Birukova et al., Am J Physiol Lung Cell Mol Physiol 2008 : In contrast, 18 % CS further enhanced VEGF induced EC permeability, activation of Rho signaling, and formation of actin stress fibers and paracellular gaps
Kuno et al., Biochem Pharmacol 2009 : In order to investigate whether Rho-kinase is involved in the TGF-beta stimulated VEGF synthesis in these cells we examined the effects of Rho-kinase inhibitors on the VEGF synthesis ... Taken together, our results strongly suggest that Rho-kinase regulates TGF-beta stimulated VEGF synthesis via SAPK/JNK activation in osteoblasts