Gene interactions and pathways from curated databases and text-mining

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KDR — PDGFC

Pathways - manually collected, often from reviews:

  • KEGG Focal adhesion: EGF/FIGF/HGF/IGF1/PDGFA/PDGFB/PDGFC/PDGFD/PGF/VEGFA/VEGFB/VEGFC → EGFR/ERBB2/FLT1/FLT4/IGF1R/KDR/MET/PDGFRA/PDGFRB (protein-protein, activation)
  • WikiPathways Focal Adhesion-PI3K-Akt-mTOR-signaling pathway: EFNA1/FGF1/FGF11/FGF10/EFNA2/EGF/FGF12/CSF1/ANGPT4/ANGPT2/ANGPT1/VEGFA/EFNA3/EFNA4/EFNA5/FGF14/FGF19/FGF17/FGF18/FGF2/FGF3/FGF4/FGF6/FGF7/FGF8/FGF9/FIGF/HGF/IGF1/INS/INS/KITLG/VEGFC/VEGFB/PDGFB/PGF/PDGFA/NGF/PDGFC/FGF21/FGF22/PDGFD/FGF20/FGF16 → FGFR2/KDR/INSR/FGFR3/IGF1R/KIT/FGFR1/EPHA2/EGFR/CSF1R/FGFR4/FLT1/FLT4/NGFR/MET/PDGFRA/PDGFRB/TEK (activation)
  • WikiPathways Focal Adhesion: EGF/FIGF/HGF/IGF1/PDGFA/PDGFB/PGF/PDGFC/PDGFD/VEGFA/VEGFB/VEGFC → BLK/EGFR/ERBB2/FGR/FLT1/HCK/IGF1R/KDR/MET/PDGFRA/PDGFRB/PTK6/SRMS/TXK/TESK2/STYK1/TNK2/TNK1 (activation)

Text-mined interactions from Literome

Ishida et al., J Cell Physiol 2001 : Since VEGF-E is a specific activator of flk-1 while PlGF specifically activates only flt-1, SMC migration induced by VEGF ( 165 ) is likely to be mediated primarily through the flk-1 receptor
Mayr-Wohlfart et al., Bone 2002 : An in vitro kinase assay failed to demonstrate activation of VEGFR-2 upon stimulation with either VEGF-E or VEGF-A, consistent with the idea that the effect of VEGF-A on primary human osteoblasts is mediated via VEGFR-1
Shibuya et al., Endothelium : journal of endothelial cell research 2006 : Interestingly, activation of VEGFR2 via VEGF-E in vivo results in a strong angiogenic response in mice, with minor effects on inflammation and hypervascular permeability compared with VEGF-A, suggesting that VEGF-E is a useful tool for proangiogenic therapy in ischemic diseases
Shibuya et al., J Biochem Mol Biol 2006 (Atherosclerosis...) : Interestingly, the activation of VEGFR2 via VEGF-E in vivo results in a strong angiogenic response in mice with minor side effects such as inflammation compared with VEGF-A, suggesting VEGF-E to be a novel material for pro-angiogenic therapy
Heckman et al., Cancer Res 2008 (Neovascularization, Pathologic) : In human endothelial cells, cediranib inhibited VEGF-E induced phosphorylation of VEGFR-2 and VEGF-C156S induced phosphorylation of VEGFR-3 at concentrations of < /=1nmol/L and inhibited activation of downstream signaling molecules