| protein
| secreted protein, acidic and rich in cysteine, SPARC ( |
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full-length mTNX ( |
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Glypican-1 ( |
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connection between EMP2 and VEGFA |
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neuropilin-2, NRP2 ( |
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connective tissue growth factor, CTGF |
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SEMA3B |
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neuropilin-1, NRP1 ( and |
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HNRNPD and ELAVL1 ( |
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CTCF binds to the proximal promoter of VEGFA |
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HNRNPD regulates VEGFA expression, and it is an RGG peptide that suppresses VEGFA gene expression |
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EDN1 is potent lymphangiogenic factor that relies on the interplay with hypoxic microenvironment and with VEGFA, VEGFC, and FIGF |
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SP7 regulation of VEGFA is independent of HIF1A expression level 6) |
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FLT1 subunits modulate VEGFA activity predominantly by forming heterodimer receptors with KDR subunits and such heterodimers regulate endothelial cell homeostasis |
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HPSE is involved in hypoxia-induced neovascularization through promoting VEGFA expression |
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STAT1 inhibited VEGFA expression, while STAT3 promoted the expression of VEGFA |
|
cooperative regulation of VEGFA signaling by FHL1 and SMAD4 was evidenced, which may provide a novel regulation mechanism underlying cancer development and progression |
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caused translocation of PLEKHG5 from cell junctions, promoting junction disassembly |
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hypoxia-induced DDX6 reduction positively affects proangiogenic VEGFA expression |
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VEGFA inhibits EPHB4 and stimulates DLL4 expression in adult endothelial cells |
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VEGFA and PKC promote degradation-independent protein ubiquitination of FLNB to control intracellular trafficking of HDAC7 |
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PRKD2, mediated BCL6B gene expression by VEGFA stimulation |
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NF1 gene silencing induces upregulation of VEGFA expression in both Schwann and non-Schwann cells |
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VEGFA-induced sFLT1 upregulation can operate as a negative feedback system, which if modulated can become a novel therapeutic target for regulating pathological angiogenesis |
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major role of VEGFA in the regulation of RELN signaling, and DAB1 as a key molecule in the cross talk between reelin and VEGFA signaling pathways |
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LCK upregulates FOXP3 by tyrosine phosphorylation, resulting in decreased MMP9, SKP2, and VEGFA expression, and suppressed cellular invasion |
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MMP9 enhances PRKD2-mediated tumor angiogenesis by releasing extracellular matrix-bound VEGFA, increasing its bioavailability and angiogenesis |
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VEGFA activates EPOR and enhances VEGFR2-mediated pathological angiogenesis |
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FABP4 induction by VEGFA was reduced by blockade of DLL4 binding to NOTCH1 or inhibition of NOTCH1 signal transduction |
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ATF2 is likely functionally required for VEGFA-stimulated endothelial VCAM1 gene expression |
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EHMT2 is an epigenetic regulator of VEGFA alternative splicing |
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VEGFA induced interactions between NRP1 and GIPC1, a scaffold protein, and complex formation between GIPC1 and PLEKHG5, a RhoGEF |
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VEGFA/NRP1 stimulates GIPC1 and PLEKHG5 complex formation to promote RHOA activation and proliferation in skin cancer cells |
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overexpression of CASP5 can promote the angiogenesis significantly, possibly by inhibiting the ANGPT1/TEK pathway and promoting VEGFA pathway |
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FGF2 was superior, stimulating cell infiltration and angiogenesis better than TNFSF10 and VEGFA |
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DHX32 in colorectal cancer cells upregulated expression VEGFA at the transcription level through interacting with and stabilizing CTNNB1 |
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MDK is responsible for increased plasma levels of vascular endothelial growth factor A (VEGFA), necessary and sufficient to promote endothelial cell proliferation in growing collaterals |
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METTL3 regulates osteogenic differentiation and alternative splicing of VEGFA in bone marrow mesenchymal stem cells |
| Variant & Polymorphism
SNP
, other
| increasing the risk of vascular dementia |
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haplotype increasing the risk of neovascular age-related macular degeneration |
|
mutation gain of function provides neuroprotection in models of ALS, parkinson disease, in CNS and PNS injury, and in neuropathy and retinal degeneration |
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mutation loss of function increase risk of ALS |
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2578 C, -1154 G alleles, and the AAG haplotype are associated with ECD |
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rs4711751 on 6p12 near VEGFA associated with advanced age-related macular degeneration |
| 
|
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| that formation of blood vessels was abnormal, but not abolished, in heterozygous VEGF-deficient (VEGF+/-) mouse embryos and even more impaired in homozygous VEGF-deficient (VEGF-/-) T-ES embryos, resulting in death at mid-gestation | |
loss of a single VEGF allele is lethal in the mouse embryo between days 11 and 12 due to impairment of angiogenesis and blood-island formation |
|
Blood vessel invasion is almost completely suppressed, concomitant with impaired trabecular bone formation and expansion of hypertrophic chondrocyte zone in mice inactivated for Vegf |
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deletion of the hypoxia-response element in the Vegf mouse promotor reduced hypoxic Vegf expression in the spinal cord and caused adult-onset progressive motor neuron degeneration, reminiscent of amyotrophic lateral sclerosis |
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absence of the Vegf164 isoform caused birth defects in mice |
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lung-targeted VEGF(165) induced in mice through IL-13-dependent and -independent pathways, an asthma-like phenotype with inflammation, parenchymal and vascular remodeling, edema, mucus metaplasia, myocyte hyperplasia and airway hyper-responsiveness |
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In mouse cerebral cortex, microinjection of VEGF-A disrupted CLN-5 and OCLN and induced loss of barrier function |
