Gene interactions and pathways from curated databases and text-mining

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FLT4 — VEGFA

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Baldwin et al., J Biol Chem 2001 : Human vascular endothelial growth factor-D ( VEGF-D ) binds and activates VEGFR-2 and VEGFR-3 , receptors expressed on vascular and lymphatic endothelial cells
Witmer et al., Invest Ophthalmol Vis Sci 2002 (Diabetic Retinopathy) : In diabetic eyes, expression of retinal VEGFR-2 and -3 is increased, mainly in leaky microvessels, and VEGF-A induces vascular expression of the VEGF-A receptor VEGFR-2 and the VEGF-C/D receptor VEGFR-3
Krishnan et al., Cancer Res 2003 (Lymphatic Metastasis...) : A number of clinical and experimental studies suggest that tumor induced lymphangiogenesis driven by vascular endothelial growth factor ( VEGF ) -C- and/or VEGF-D induced activation of VEGF receptor (VEGFR)-3 may promote metastasis to regional lymph nodes
Dixelius et al., J Biol Chem 2003 (Neovascularization, Pathologic) : Interestingly, VEGF-C stimulation of lymphatic endothelial cells also induced the formation of VEGFR-3/VEGFR-2 heterodimers, in which VEGFR-3 was phosphorylated only at three of the five sites while the two most carboxyl-terminal tyrosine residues appeared not to be accessible for the VEGFR-2 kinase
Orlandini et al., J Biol Chem 2006 : Moreover, in primary human osteoblasts, VEGF-D expression is under the control of VEGF, and inhibition of VEGF-D/VEGFR-3 signaling, by monoclonal antibodies or VEGFR-3 silencing, affects VEGF dependent osteoblast differentiation
Zhao et al., Br J Ophthalmol 2006 (Choroidal Neovascularization) : VEGF-A , but not glucose alone, stimulated VEGFR-3 mRNA expression
Kulkarni et al., Mech Dev 2009 : In vitro, endogenous and VEGF-A induced VEGFR-3 and podoplanin expression by human microvascular endothelial cells was reduced by siRNA to NFATc1, to levels comparable to reductions seen with siRNA to Prox-1
Mancinelli et al., Experimental biology and medicine (Maywood, N.J.) 2009 : We have shown that : ( i ) cholangiocytes express VEGFR-2 and VEGFR-3 ; ( ii ) VEGF-A and VEGF-C stimulate cholangiocyte proliferation via an autocrine mechanism ; and ( iii ) chronic administration of VEGF-A prevents cholangiocyte damage induced by hepatic artery ligation
Gavrilovskaya et al., J Virol 2012 : However, VEGF-C activation of LEC-specific VEGFR3 receptors blocked ANDV- and VEGF-A induced LEC permeability
Pajusola et al., Oncogene 1994 : Also, FLT4 did not interact with KDR in response to VEGF
Joukov et al., J Biol Chem 1998 : VEGF activates the endothelial VEGF receptors (VEGFR) 1 and 2, and VEGF-C activates VEGFR-3 and VEGFR-2