VEGFA

Protein VEGFA

Identifiers
HGNC:12680
vascular endothelial growth factor A
HUGO:VEGFA hgnc_id:HGNC:12680 HGNC:12680 ENTREZ:7422 UNIPROT:P15692
HUGO:VEGFA, HGNC:12680, ENTREZ:7422, GENECARDS:GC06P043737, UNIPROT:P15692
HUGO:VEGFA HGNC:12680 ENTREZ:7422 UNIPROT:P15692
HUGO:VEGFA

Maps_Modules
HMC:TUMOR_PROMOTING_INFLAMMATION
HMC:ACTIVATING_INVASION_AND_METASTASIS
Cancer Associated Fibroblasts / GROWTH_FACTORS_PRODUCTION
Cancer Associated Fibroblasts / TREG_MODULATORS
EMT Senescence / EMT_REGULATORS
EMT Senescence / ECM
Innate Immunity / IMMUNOSUPPRESSIVE_CYTOKINE_PATHWAYS
Innate Immunity / TUMOR_GROWTH

References
PMID:22064427
CASCADE:IL6
PMID:24346288
IL-6 promoted VEGF expression by fibroblasts but not by cancer cell lines
PMID:12629515; PMID:11960372
Probably IL6 induces VEGF expression in fibroblasts via STAT3 pathway (data from non fibroblasts only)
PMID:16572188; PMID:9753319
Vascular endothelial growth factor (VEGF, also known as vascular permeability factor (VPF)) has a central role in the emergence of the reactive stroma27. VEGF can be released by cancer cells themselves, but fibroblasts and inflammatory cells are the principal source of host-derived VEGF28. VEGF induces microvascular permeability, which leads to the extravasation of plasma proteins such as fibrin, which in turn attract an influx of fibroblasts, inflammatory cells and endothelial cells27, 29, 30. These cells produce ECM that is rich in fibronectin and type I collagen, both of which are conducive to initiating tumour angiogenesis
PMID:26201938
The expression levels of cytokine genes, including those for IL6, CXCL8, TNF, TGFB1, and VEGFA, were higher in CAFs. T cell proliferation was suppressed more by CAFs or their supernatants than by NFs.
PMID:19414323
overexpression of VEGF activity in tumours can lead to increased infiltration of TReg cells and MDSCs, which as discussed above are key cell types that trigger immunosuppression.
PMID:9157999
VEGF increased the level of ETS1 mRNA in human umbifical vein endothelial cells and lung microvascular endothelial cells over 5-fold.
Protein levels were shown to increase concordantly.
PMID:15111329
VEGF is a predominant angiogenic factor that mediates ocular neovascularization.
VEGF is increased by hypoxia, which is one of the primary stimuli for ocular neovascularization.
VEGF induces Ets-1 expression in bovine retinal endothelial cells and its expression is PKC/ERK pathway-dependent.
Ets-1 up-regulation is involved in the development of retinal neovascularization, and inhibition of Ets-1 may be beneficial in the treatment of ischemic ocular diseases
PMID:11166270
VEGF stands for the vascular Endothelial Growth Factor family of ligands and receptors is crucial for vascular development and neovascularization in physiological and pathological processes in both embryos, and in adults
PMID:13678960
VEGFs belong to a family of homodimeric glycoproteins that containts five members (VEGF-A, B, C, D, and Placenta growth factor PLGF).
VEGFs bind to 3 different VEGF-receptor tyrosine kinases (VEGFR-1, 2, 3).
Upon ligation, VEGF-receptors dimerize, autophosphorylate and, thereby transduce signals that direct cellular functions.
PMID:10022831
PMID:15501236
VEGFA is a homodimer that exists in five different isoforms comprising 121, 145, 165, 189, and 206 amino acids per chain.
The isoforms differ in their ability to bind heparan sulfate proteoglycans in the extracellular matrix (ECM).
In adult Endothelial cells, VEGFA exhibits high affinity binding to tyrosine kinase receptors, VEGFR1 and VEGFR2.
Although ECs express both receptors, recent findings suggest that only VEGFR2 is able to mediate angiogenic effects of VEGFA
DENDRITIC_CELL
MACROPHAGE
MDSC
MAST_CELL
CASCADE:VEGFA
CASCADE:LACTIC
CASCADE:MIF
CASCADE:IL4
CASCADE:TLR2_4
CASCADE:CSF2
CASCADE:IFNAB
NEUTROPHIL
PMID:15573129, PMID:8837607
Vascular endothelial growth factor (VEGF) was the first tumour-derived factor shown to inhibit DC differentiation.
The involvement of VEGF in tumour-induced defects in DC differentiation was indicated by in vitro experiments in which neutralizing VEGF-specific antibody abrogated the negative effect of tumour-cell-conditioned medium on the differentiation of DCs from HPCs.
(VEGF) inhibit the activation of NF-B by blocking IB phosphorylation55, 101, 102, possibly through activation of STAT3 (signal transducer and activator of transcription 3). Recent data have shown that STAT3 might also bind p65 subunits of NF-B, thereby directly inhibiting NF-B activity
PMID:9570538
VEGF inhibits TNF-?? inducible activation of NF-??B in HPC, resulting in inhibition of DC differentiation
The presence of VEGF significantly decreased the specific DNA binding of NF-kappa B as early as 30 min after induction with TNF-alpha. This was followed on days 7 to 10 by decreases in the mRNA for RelB and c-Rel, two subunits of NF-kappa B.
PMID:16002046
Vascular endothelial growth factor impairs the functional ability of dendritic cells through Id pathways.
PMID:17086423
Vascular endothelial growth factor inhibits the function of
human mature dendritic cells mediated by VEGF receptor-2 (KDR)
PMID:23390297, PMID:22461508
MIF signaling induces angiogenesis probavly via upregulation of MMP9, VEGF expression in macrophages and activates tumor invasion
PMID:21372296
HMGB1 induces the production of angiogenic factors VEGF, and TGFB1 by macrophage via TLR4-dependent mechanisms.
PMID:15099563
Mast cells produce heparin, interleukin-8 (IL-8) and vascular
endothelial cell growth factor (VEGF), which induce
neovascularization,
PMID:15520864
MC-derived Ang-1 and VEGF-A promotes
growth of plasmocytomas by stimulating neovascularization.

Modifications:
In compartment: INNATE_IMMUNE_CELL_Cytosol

VEGFA@INNATE_IMMUNE_CELL_Cytosol

In compartment: default

VEGFA@default

Participates in complexes:
In compartment: INNATE_IMMUNE_CELL_Membrane

In compartment: default

VEGFA:trVEGFR1*@default

Participates in reactions:
As Reactant or Product:

As Catalyser: