Gene interactions and pathways from curated databases and text-mining

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FLT1 — VEGFA

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Tufro et al., J Am Soc Nephrol 1999 : In late fetal kidneys ( E19 ), immunoreactive VEGF was detected in glomerular epithelial and tubular cells, whereas Flt-1 and Flk-1 were expressed in contiguous endothelial cells ... VEGF induced upregulation of Flk-1 and Flt-1 expression, as assessed by Western blot analysis
Aoki et al., Blood 1999 (Lymphoma, Non-Hodgkin) : Two of the PEL cell lines expressed the VEGF/VPF receptor Flt-1 , but VEGF/VPF did not stimulate proliferation in these cells
Warner et al., Biochem J 2000 : It has also been difficult to demonstrate VEGF induced phosphorylation of Flt1 , which has led to speculation that KDR may be the more important receptor for the mitogenic action of VEGF on endothelial cells
Kroll et al., Z Kardiol 2000 (Cardiovascular Diseases) : VEGF-A stimulates many actions of endothelial cells including proliferation, migration, and nitric oxide release via binding to and activation of the two primarily endothelial-specific receptor-tyrosine kinases KDR and Flt-1
Sato et al., Ann N Y Acad Sci 2000 : VEGF stimulated the expression of transcription factor Ets-1 as well as matrix metalloproteinase-1 (MMP-1) and Flt-1 in HUVECs
Suzuma et al., J Biol Chem 2000 : VEGF activated the tyrosine receptor phosphorylation of KDR and Flt1 and increased the binding of phosphatidylinositol 3-kinase ( PI3-kinase ) p85 subunit to KDR and Flt1, both of which could mediate CTGF gene induction
Abbott et al., Dev Dyn 2000 : VEGFR1 may be primarily responsible for binding of VEGF to yolk sac and embryonic tissues, as masking VEGFR2 did not reduce VEGF binding in those areas, and it is interesting that major structural defects were also not found in those regions
Aoki et al., Leukemia & lymphoma 2001 (Herpesviridae Infections...) : Two of the PEL cell lines express the VEGF/VPF receptor Flt-1 , but VEGF did not stimulate proliferation in these cells
Wulff et al., J Clin Endocrinol Metab 2001 : Luteal Flt mRNA expression is dependent upon VEGF, and VEGF inhibition results in abortive increases in expression of VEGF, angiopoietin-2, and Tie-2
Deroanne et al., Oncogene 2002 : TSA inhibited in a dose dependent and reversible fashion the VEGF induced expression of VEGF receptors, VEGFR1 , VEGFR2, and neuropilin-1
Koolwijk et al., Angiogenesis 2001 : Involvement of VEGFR-2 ( kdr/flk-1 ) but not VEGFR-1 ( flt-1 ) in VEGF-A and VEGF-C induced tube formation by human microvascular endothelial cells in fibrin matrices in vitro ... These data indicate that VEGF-A or VEGF-C activation of the VEGFR-2, and not of VEGFR-1 , is involved in the formation of capillary-like tubular structures of hMVEC in 3D fibrin matrices used as a model of repair associated or pathological angiogenesis in vitro
Witmer et al., Invest Ophthalmol Vis Sci 2002 (Diabetic Retinopathy) : Initial vascular VEGF signaling may act primarily through VEGFR-1
Zhao et al., Circulation 2002 (Arteriosclerosis...) : Soluble FLT-1 can suppress VEGF activity both by sequestering VEGF and by functioning as a dominant negative inhibitor of VEGF receptors
Bernatchez et al., J Cell Biochem 2002 : In contrast, stimulation of PAEC-Flt-1 and PAEC-NRP-1 with VEGF-A or VEGF-C did not induce proliferation, migration, or PAF synthesis
Hoshida et al., Pancreas 2002 (Neovascularization, Pathologic...) : The soluble form of flt-1 VEGF receptor inhibits VEGF activity in a dominant negative manner
Itokawa et al., Mol Cancer Ther 2002 (Neovascularization, Pathologic) : SU5416 inhibited cell migration of human vascular endothelial cells expressing both Flt-1 and KDR in response to VEGF and also inhibited the cell migration in response to placenta growth factor ( PIGF ), a specific ligand for Flt-1
Zhang et al., Am J Reprod Immunol 2003 : We found that up-regulation of the expression of MMPs was induced by FN and VEGF through the focal adhesion kinase ( FAK ) /mitogen activated protein kinase ( MAPK ) and Flt-1/p38SAPK/MAPKAPK2 signaling pathways, respectively
Lissbrant et al., Prostate 2004 : The testosterone stimulated increase in epithelial cell proliferation was unaffected by flt ( 1-3 ) IgG, but endothelial and epithelial cell apoptosis were increased in the anti-VEGF compared to the vehicle treated groups
Kobayashi et al., FASEB J 2004 : The c-Cbl/CD2AP complex regulates VEGF induced endocytosis and degradation of Flt-1 ( VEGFR-1 )
Takeda et al., Circ Res 2004 : In conclusion, EPAS1 promotes Flt-1 gene expression and induces mRNA expression of VEGF , Flk-1, and Tie2, leading to enhancement of mature angiogenesis in vivo
Huckle et al., J Cell Biochem 2004 : Alternative Flt-1 RNA processing, involving retention of intron 13 and the use of intronic cleavage-polyadenylation signals, produces a secreted form of Flt-1 , `` sFlt-1, '' that binds VEGF with high affinity and can inhibit VEGF signaling
Chen et al., Biochem Biophys Res Commun 2005 : In addition, 11,11'-dideoxyverticillin decreased VEGF secretion by MDA-MB-468 breast cancer cells, and significantly suppressed VEGF induced tyrosine phosphorylation of Flt-1 and KDR/Flk-1
Singh et al., Invest Ophthalmol Vis Sci 2005 (Anoxia...) : Flt24K suppressed VEGF expression by 30.8 % ( P = 0.042 ), leukocytes by 25.8 % ( P < 0.001 ), and neovascularization by 49.5 % ( P = 0.015 )
Wey et al., Cancer 2005 (Neoplasm Invasiveness...) : VEGFR-1 stimulation by VEGF-A or VEGF-B was found to promote migration in both cell lines
Aldridge et al., Biochem Biophys Res Commun 2005 (Bone Resorption) : We have shown that VEGF induces osteoclast differentiation through its action on VEGFR1
Wang et al., Int J Cancer 2006 (Carcinoma...) : Using real-time PCR, we found that VEGF , at 20 ng/ml, significantly increased the expression of VEGFR-1 and VEGFR-2 by approximately 4-fold and 31-fold, respectively, compared to untreated control ( p < 0.05 )
Krysiak et al., Circ Res 2005 (Pre-Eclampsia) : Soluble vascular endothelial growth factor receptor-1 ( sFLT-1 ) mediates downregulation of FLT-1 and prevents activated neutrophils from women with preeclampsia from additional migration by VEGF ... VEGF dependent FLT-1 expression is regulated by changing FLT-1-promoter activity
Cai et al., J Biol Chem 2006 (Neovascularization, Pathologic) : PEDF was also able to inhibit VEGF induced phosphorylation of VEGFR-1
Kumai et al., J Cereb Blood Flow Metab 2007 (Brain Ischemia) : Our goal in this study was to explore protective effects of gene transfer of soluble flt-1 ( sFlt-1 ), a natural inhibitor of VEGF , on focal brain ischemia
Hirokoshi et al., Nephron. Clinical practice 2007 (Pre-Eclampsia) : Here, we determined the ratio of serum concentration of soluble fms-like tyrosine kinase 1 ( sFlt-1 ), a natural inhibitor of pro-angiogenic vascular endothelial growth factor ( VEGF ) relative to angiopoietin-2 (Ang-2), a natural antagonist of angiopoietin-1 (Ang-1) involved in promoting angiogenesis in the presence of VEGF, in women with preeclampsia
Lee et al., PLoS Med 2007 (Breast Neoplasms...) : This study provides, to our knowledge for the first time, evidence of a unique survival system in breast cancer cells by which VEGF can act as an internal autocrine ( intracrine ) survival factor through its binding to VEGFR1
Chandrasekaran et al., J Mol Graph Model 2007 : In an attempt to identify the binding site for SPARC on VEGF, we hypothesized that this binding site could overlap at least partially the binding site of VEGF receptor 1 (VEGFR-1), as SPARC acts by preventing VEGF induced phosphorylation of VEGFR-1
Banerjee et al., Biochemistry 2008 (Breast Neoplasms) : We found that VEGF-A 165 induces hAOSMC migration parallel with the induction of NRP-1 and VEGFR1 expressions and their associations along with the activation of PI3K/Akt
Jacobsen et al., J Bone Miner Res 2008 : To test the hypothesis that DO is strictly dependent on vascualrization, we inhibited vascular endothelial growth factor ( VEGF ) activity by antibody blockade of both receptors VEGFR1 ( Flt-1 ) and VEGFR2 ( Flk-1 ) or only VEGFR2 ( Flk-1 ) in a previously developed murine tibia DO model
Krum et al., Exp Neurol 2008 (Brain Injuries...) : VEGF signaling is regulated mainly through its two primary receptors : flk-1 ( KDR/VEGF-R2 ) is expressed on vascular endothelium and some neurons and flt-1 ( VEGF-R1 ) in the CNS, is expressed predominantly by activated astrocytes
Kimura et al., Cancer Sci 2008 (Colonic Neoplasms...) : On the other hand, the three dihydroxystilbenes had no effect on VEGFR-1 and-2 expression, and VEGF induced VEGFR-1 phosphorylation in HUVECs
Rodewald et al., Hum Reprod 2009 (Ovarian Hyperstimulation Syndrome) : The increased permeability in the presence of LGCs and hCG was inhibited when VEGF was blocked by Flt-1Fc ( P < 0.05 )
Horta et al., J Mol Graph Model 2009 : VEGF activates both Flt-1 and KDR
Krejca et al., Med Sci Monit 2010 : Outside stenting of the vein graft decreases VEGF-A expression and induces significant down-regulation of VEGFR-1 in the intimal and medial layers after the re-endothelialization period ... These findings indicate that outside stenting of the vein graft decreases VEGF-A expression and induces significant down-regulation of VEGFR-1 in the intima and media after the re-endothelialization
Genetos et al., Bone 2010 : This suggests that VEGF induction of Annexin A2 is not mediated via VEGF-R1 agonism alone but by VEGF-R1 and Neuropilin-1 or Neuropilin-2 heterodimers
Lee et al., Cancer Res 2010 (Carcinoma, Renal Cell...) : VEGF induced greater phosphorylation of VEGFR-2 in lung ECs and of VEGFR-1 in liver ECs
Ozgurtas et al., Hormone research in pædiatrics 2011 : A soluble truncated form of VEGFR-1 ( sVEGFR-1 ) binds to VEGF as strongly as full-length VEGFR-1 and inhibits VEGF activity
Brave et al., Mol Cancer Ther 2011 : Cediranib inhibited VEGF-A stimulated VEGFR-1 activation in AG1-G1-Flt1 cells ( IC ( 50 ) = 1.2 nmol/L ) ... VEGF-A induced greatest phosphorylation of VEGFR-1 at tyrosine residues Y1048 and Y1053 ; this was reversed by cediranib
Forsten-Williams et al., BMC systems biology 2011 : VEGF also binds to extracellular matrix ( ECM ) and neuropilin ( NP ), a cell surface glycoprotein that enhances VEGF binding to VEGFR2 while inhibiting VEGF-VEGFR1 interactions
Cai et al., J Biol Chem 2011 (Neovascularization, Pathologic) : We have reported previously that pigment epithelium derived factor (PEDF) can, via ?-secretase mediated events, inhibit VEGF induced angiogenesis in microvascular endothelial cells by both ( a ) cleavage and intracellular translocation of a C-terminal fragment of VEGF receptor-1 (VEGFR1) and ( b ) inhibition of VEGF induced phosphorylation of VEGFR1
Le Roux et al., J Am Soc Nephrol 2012 (Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis) : Here, we observed a marked increase in serum levels of soluble Flt1 ( sFlt1 ), a potent inhibitor of vascular endothelial growth factor , in patients with active ANCA associated vasculitis compared with patients during remission and other controls
Takahashi et al., Biol Pharm Bull 2011 (Neoplasms) : VEGF-A activates VEGFR-1 and VEGFR-2, whereas VEGF-B and PlGF bind to only VEFGR-1
Dellinger et al., PloS one 2011 : In vitro experiments with primary human dermal lymphatic endothelial cells ( LECs ) demonstrate that blocking VEGF-A activation of VEGFR2, not VEGFR1 , significantly inhibits VEGF-A induced proliferation and migration of LECs
Avraham-Lubin et al., Stem Cell Rev 2012 (Disease Models, Animal...) : VEGF signaling mediated by Flt-1 induces early neural and sustained astrocytic differentiation of stem cells elutriated from adult bone-marrow, with significant contribution to stabilization retinal architecture following ischemic injury
Woollard et al., Prostate 2013 (Lymphatic Metastasis...) : These results suggest that activation of VEGFR-1 by VEGF-A within the carcinoma, and activation of lymphatic endothelial cell VEGFR-3 by VEGF-D within the adjacent benign stroma may be important signaling mechanisms involved in the progression and subsequent metastatic spread of prostate cancer
Gennari-Moser et al., Hypertension 2013 (Pre-Eclampsia) : In rats, overexpression of soluble fms-like tyrosine kinase-1 , an endogenous VEGF inhibitor , led to adrenocortical capillary rarefaction and fall in aldosterone concentrations that correlated inversely with soluble fms-like tyrosine kinase-1 levels
Zheng et al., J Ethnopharmacol 2013 : tPNS ( 100µg/ml ) significantly enhanced the mRNA expression level of VEGF-A and Kdr compared to the control group, while they had no obvious effect on the expression of Flt-1
Saito et al., FEBS Lett 2013 (MAP Kinase Signaling System) : VEGF-A induces its negative regulator, soluble form of VEGFR-1 , by modulating its alternative splicing
Sato et al., J Clin Invest 1995 (Graves Disease) : VEGF , a secretable angiogenesis factor, subsequently stimulates Flt receptors on endothelial cells in a paracrine manner, leading to their proliferation and producing hypervascularity of the thyroid gland, as seen in patients with Graves ' disease
Waltenberger et al., J Biol Chem 1994 : KDR was found to undergo ligand induced autophosphorylation in intact cells, and both Flt1 and KDR were phosphorylated in vitro in response to VEGF , however, KDR much more efficiently than Flt1
Pajusola et al., Oncogene 1994 : Also, FLT4 did not interact with KDR in response to VEGF
Lee et al., Proc Natl Acad Sci U S A 1996 : Flt1 and Flk1 have been shown to play key roles in vascular development ; these two receptors bind and are activated by vascular endothelial growth factor ( VEGF )
Albini et al., Nat Med 1996 (Neovascularization, Pathologic) : Endothelial cell stimulation by Tat occurs in the absence of activation of FLT-1 , another VEGF-A tyrosine kinase receptor
Barleon et al., Cancer Res 1997 : VEGF stimulated FLT-1 mRNA expression was inhibited by actinomycin D
Landgren et al., Oncogene 1998 : We furthermore examined induction of protein levels of plasminogen activator (PA), which was evident in the PlGF stimulated Flt 1 cells, but not in the VEGF stimulated KDR cells
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
Oyama et al., J Immunol 1998 : Thus, NF-kappa B plays an important role in maturation of HPCs to DC, and VEGF activation of the Flt-1 receptor is able to block the activation of NF-kappa B in this system