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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to VEGFA

CDH5 — VEGFA

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Rahimi et al., Mol Biol Cell 1999 : A role for cadherin-5 in regulation of vascular endothelial growth factor receptor 2 activity in endothelial cells
Lin et al., Mol Pharmacol 2003 : Of interest, resveratrol, at the dose of 1 or 2.5 muM, effectively abrogated VEGF mediated tyrosine phosphorylation of vascular endothelial (VE)-cadherin and its complex partner, beta-catenin ... In addition, antioxidant N-acetyl-cysteine was demonstrated to strongly inhibit VEGF mediated Src activation, VE-cadherin tyrosine phosphorylation, and HUVEC tube formation
Lambeng et al., Circ Res 2005 : In this model, Src inhibition impaired VEGF induced VE-cadherin phosphorylation, indicating that VE-cadherin phosphorylation was dependent on Src activation
Chang et al., Placenta 2005 : Induction of VE-cadherin in rat placental trophoblasts by VEGF through a NO-dependent pathway ... In explant culture, VEGF ( 0.01-1.0 ng/ml ) increased the protein abundance of VE-cadherin
Sulkowska et al., Tumori 2006 (Adenocarcinoma...) : Levels of VE-cadherin increase independently of VEGF in preoperative sera of patients with colorectal cancer
Wallez et al., Oncogene 2007 : Src kinase phosphorylates vascular endothelial-cadherin in response to vascular endothelial growth factor : identification of tyrosine 685 as the unique target site
Ali et al., J Pharmacol Sci 2006 : The novel Src kinase inhibitor M475271 inhibits VEGF induced vascular endothelial-cadherin and beta-catenin phosphorylation but increases their association ... The findings reveal pretreatment with M475271 significantly inhibits VEGF induced VE-cadherin and beta-catenin phosphorylation
Villasante et al., J Clin Endocrinol Metab 2007 (Ovarian Hyperstimulation Syndrome) : Culturing of HUVEC with high doses of E2 produced no significant changes in VE-cadherin concentration, but hCG and VEGF produced a significant increase in VE-cadherin release
Dalyot-Herman et al., Biochem Pharmacol 2009 : It did, however, inhibit VEGF induced phosphorylation of VE-cadherin and reduce the association of beta-catenin with VE-cadherin
Frank et al., Cancer Res 2011 (Melanoma...) : In vitro, VEGF induced the expression of CD144 in ABCB5 ( + ) subpopulations that constitutively expressed VEGFR-1 but not in ABCB5 ( - ) bulk populations that were predominantly VEGFR-1 ( - )
Chung et al., J Mol Med (Berl) 2013 (Neoplasms...) : Here, we show that CAPE suppressed VEGF induced proliferation, tube formation, migration, the formation of actin stress fibers and loss of VE-cadherin at cell-cell contacts in endothelial cells, indicating the inhibition of VEGF mediated VEGF receptor-2 (VEGFR-2) and its downstream signal activation in vitro
Zang et al., Cell Signal 2013 : Aberrant association between vascular endothelial growth factor receptor-2 and VE-cadherin in response to vascular endothelial growth factor-a in Shb-deficient lung endothelial cells
Rapraeger et al., FEBS J 2013 : We find that the Sdc1 coupled ternary receptor complex is required for VEGF signalling and for stimulation of vascular endothelial cell migration by vascular endothelial cadherin ( VE-cadherin ) engagement
Herr et al., Fertil Steril 2013 : This down-regulation was associated with changed rates of vascular permeability : hCG induced a VEGFA dependent down-regulation of VE-cadherin , nectin 2, and claudin 5, which increased the endothelial permeability in the coculture system
Hayashi et al., Nature communications 2013 : We conclude that the role of Tie2 in maintenance of vascular quiescence involves VE-PTP dependent dephosphorylation of VEGF receptor-2, and that VEGF receptor-2 activity regulates VE-cadherin tyrosine phosphorylation, endothelial cell polarity and lumen formation
Hebda et al., Cell communication and signaling : CCS 2013 : In this context, we have previously characterized that VEGF ( vascular endothelial growth factor ) leads to VE-cadherin phosphorylation, ß-arrestin2 recruitment and VE-cadherin internalization in mouse endothelial cells