+ |
VEGFA | up-regulates
binding
|
KDR |
0.815 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-157100 |
|
|
Homo sapiens |
Macrophage, Monocyte |
pmid |
sentence |
17658244 |
Binding of vegf to the receptor induces dimerisation and autophosphorylation of specific intracellular tyrosine residues. Activation of intracellular cascades results in proliferation, migration, survival and increased permeability. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | VEGF Signaling |
+ |
VEGFA | up-regulates
binding
|
FLT1 |
0.839 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-121132 |
|
|
Homo sapiens |
Uveal Melanoma Cell |
pmid |
sentence |
14704231 |
Vegf exerts its action by binding to vegfr-1 and vegfr-2. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
HIF1A | up-regulates quantity
transcriptional regulation
|
VEGFA |
0.766 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256592 |
|
|
Homo sapiens |
|
pmid |
sentence |
8387214 |
Transcription of the human erythropoietin (EPO) gene is activated in Hep3B cells exposed to hypoxia. Hypoxia-inducible factor 1 (HIF-1) is a nuclear factor whose DNA binding activity is induced by hypoxia in Hep3B cells, and HIF-1 binds at a site in the EPO gene enhancer that is required for hypoxic activation of transcription. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | NOTCH Signaling |
+ |
MYC | up-regulates quantity by expression
transcriptional regulation
|
VEGFA |
0.475 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-259369 |
|
|
Mus musculus |
|
pmid |
sentence |
12368264 |
These defects are intrinsic to c-Myc, and are in part associated with a requirement for c-Myc for the expression of vascular endothelial growth factor (VEGF), as VEGF can partially rescue these defects. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | NOTCH Signaling |
+ |
HIC1 | down-regulates quantity by repression
transcriptional regulation
|
VEGFA |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254247 |
|
|
Homo sapiens |
MDA-MB-231 Cell |
pmid |
sentence |
24067369 |
HIC1 suppressing the VEGF and c-Myc promoter activity and the colony formation of MDA-MB 231 cells were STAT3-dependent. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
RUNX2 | up-regulates quantity by expression
transcriptional regulation
|
VEGFA |
0.459 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255084 |
|
|
Homo sapiens |
Thyroid Cancer Cell Line |
pmid |
sentence |
22641097 |
Effective silencing of Runx2 by short interfering RNA (siRNA) demonstrated downregulation of EMT-related molecules (SNAI2, SNAI3 and TWIST1), MMP2 and vasculogenic factors (VEGFA and VEGFC) in thyroid carcinoma cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MYOD/E12E47 | up-regulates quantity by expression
transcriptional regulation
|
VEGFA |
0.339 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-241545 |
|
|
Mus musculus |
|
pmid |
sentence |
18094043 |
we further demonstrate that the myogenic transcription factor, MyoD, and its heterodimeric binding proteins E12 and E47, up-regulate the expression of endogenous VEGF through direct interaction with the VEGF promoter. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Tissue: |
Skeletal Muscle |
+ |
ZMYND8 | down-regulates quantity by repression
transcriptional regulation
|
VEGFA |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-262041 |
|
|
Homo sapiens |
Prostate Cancer Cell Line |
pmid |
sentence |
27477906 |
Our quantitative ChIP experiments confirmed that ZMYND8 and JARID1D were co-localized at Slug, CD44, VEGFA, and EGFR genes (Figures 4F–4I). Our ChIP results also showed that ZMYND8 repressed and occupied other JARID1D target genes, such as the matrix metalloproteinase 1 (MMP1) and MMP3, that we previously reported |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MYOD1 | up-regulates quantity by expression
transcriptional regulation
|
VEGFA |
0.401 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-257598 |
|
|
Mus musculus |
|
pmid |
sentence |
18094043 |
We further demonstrate that the myogenic transcription factor, MyoD, and its heterodimeric binding proteins E12 and E47, up-regulate the expression of endogenous VEGF through direct interaction with the VEGF promoter. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Tissue: |
Skeletal Muscle |
Pathways: | NOTCH Signaling |
+ |
VEGFA | up-regulates
|
Angiogenesis |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252275 |
|
|
|
|
pmid |
sentence |
17326328 |
More than a dozen different proteins have been identified as angiogenic activators, including vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), angiogenin, transforming growth factor (TGF)-α, TGF-β, tumor necrosis factor (TNF)-α, platelet-derived endothelial growth factor, granulocyte colony-stimulating factor, placental growth factor, interleukin-8, hepatocyte growth factor, and epidermal growth factor |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256597 |
|
|
Homo sapiens |
|
pmid |
sentence |
16301830 |
VEGF as a key mediator of angiogenesis in cancer. |
|
Publications: |
2 |
Organism: |
, Homo Sapiens |
Pathways: | NOTCH Signaling, Pancreatic ductal adenocarcinoma (PDA) |
+ |
bevacizumab | down-regulates activity
binding
|
VEGFA |
0.4 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-259884 |
|
|
Homo sapiens |
Colorectal Cancer Cell |
pmid |
sentence |
15961063 |
Clinical trials with VEGF inhibitors in a variety of malignancies are ongoing. Recently, a humanized anti-VEGF monoclonal antibody (bevacizumab; Avastin) has been approved by the FDA as a first-line treatment for metastatic colorectal cancer in combination with chemotherapy. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
Aflibercept | down-regulates activity
chemical inhibition
|
VEGFA |
0.8 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-259386 |
|
|
Homo sapiens |
|
pmid |
sentence |
22813448 |
Aflibercept, a fusion protein with binding domains from native VEGF receptors, binds VEGF-A, VEGF-B, and placental growth factors 1 and 2 with high affinity.This soluble decoy receptor is produced by fusing all-human DNA sequences of the second immunoglobulin (Ig) domain of human VEGF receptor (VEGFR) 1 to the third Ig domain of human VEGFR-2, which then is fused to the Fc region of human IgG-1.2 Aflibercept binds to all VEGF-A and VEGF-B isoforms, as well as the highly related placental growth factor. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
VEGFA | up-regulates quantity by expression
transcriptional regulation
|
DLL4 |
0.487 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-196736 |
|
|
Homo sapiens |
|
pmid |
sentence |
22426001 |
Activation triggered by vegf-a (also known as vegf) has been shown to induce expression of thenotchligand dll4 in angiogenic vessels. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | NOTCH Signaling |
+ |
STAT3 | up-regulates quantity by expression
transcriptional regulation
|
VEGFA |
0.779 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-259456 |
|
|
Homo sapiens |
|
pmid |
sentence |
12545153 |
Stat3 directly regulated the promoter of the VEGF gene. Blockade of activated Stat3 by ectopic expression of dominant-negative Stat3 significantly inhibited VEGF expression, and the growth and metastasis of human pancreatic cancer cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Pancreatic ductal adenocarcinoma (PDA) |