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This study provides evidence that germline polymorphisms in VEGFR1, KRAS and ITGAV genes are associated with prognosis in stages II-III colon cancer patients. As stage and tumor location are correlated with prognosis, future genetic studies should stratify colon cancer patients according to these parameters.
VEGFR1 was expressed predominantly neuronally and was significantly reduced in Alzheimer's disease (AD). The downregulation of VEGFR1 may represent a pro-angiogenic response to the hypoperfusion. However, the relative increase in sVEGFR1 would be expected to have an anti-angiogenic effect which may be a factor in AD.
these results indicate that sFlt-1 up-regulation by VEGF may be mediated by the VEGF/Flt-1 and/or VEGF/KDR signaling pathways.
Serum sFlt-1 can be used as a prognostic marker to predict the occurrence of complications of preeclampsia.
The ratio of sFlt-1/sEGFR could be used as a novel candidate biochemical marker in monitoring the severity of preterm preeclampsia. sEndoglin and sEGFR may be involved in the pathogenesis of small for gestational age in preterm preelampsia.
A contingent strategy of measuring the sFlt-1/PlGF ratio at 24-28weeks in women previously selected by clinical factors and uterine artery Doppler enables an accurate prediction of preeclampsia/fetal growth restriction.
dynamic regulation of mVEGFR1 stability and turnover in blood vessels impacts angiogenesis
Study shows that soluble VEGF receptor 1 (sVEGFR-1/ soluble fms-like tyrosine kinase 1 [sFlt-1]) showed a cytotoxic effect on BeWo cells. Results suggest that sFLT-1 could be therapeutic for malignant tumors.
A single measurement of sFlt-1/PlGF ratio at third trimester to predict pre-eclampsia and intrauterine growth retardation occurring after 34weeks of pregnancy.
sFlt1 was produced in significant amounts by preeclamptic peripheral blood mononuclear leukocytes, and ex vivo studies show that the placenta induces this over-expression. In contrast, exposure to PBMCs appears to decrease sFlt1 production by preeclamptic placenta.
The levels of sFlt-1, PlGF, and the sFlt-1/PlGF ratio in pre-eclamptic women with an onset at < 32 weeks were sig- ni fi cantly di ff erent from those in women with an onset at >/=32-33 weeks.
These results showed that arginase controlled sFlt-1 elevation to some extent.
These results suggest that VM formation is increased by EBVLMP1 via VEGF/VEGFR1 signaling and provide additional information to clarify the role of EBVLMP1 in nasopharyngeal carcinoma (NPC)pathophysiology
An sFlt-1:PlGF ratio above 655 is not predictive of impaired perinatal outcomes, and insufficiently reliable for predicting outcomes in cases with clinical signs of preeclampsia.
The maternal sFlt-1 to PlGF ratio in women with hypertensive disorders in pregnancy carries prognostic value for the development of preeclampsia.
VEGFA activates VEGFR1 homodimers and AKT, leading to a cytoprotective response, whilst abluminal VEGFA induces vascular leakage via VEGFR2 homodimers and p38
metformin's dual effect in hyperglycemia-chemical hypoxia is mediated by direct effect on VEGFR1/R2 leading to activation of cell migration through MMP16 and ROCK1 upregulation, and inhibition of apoptosis by increase in phospho-ERK1/2 and FABP4, components of VEGF signaling cascades
Additionally, LVsFlt1MSCs inhibited tumor growth and prolonged survival in an hepatocellular carcinoma (HCC)mouse model via systemic injection. Overall, the present study was designed to investigate the potential of LVsFlt1MSCs for antiangiogenesis gene therapy in HCC.
Review of the role of dysregulation at the Fms-like tyrosine kinase 1 locus in the fetal genome (likely in the placenta) in conferring genetic predisposition to preeclampsia.
VEGF and VEGFR1 levels in different regions of the normal and preeclampsia placentae.
sFlt1 role in the venous sprouting and spinal cord vascularization.
we determined that radial glia control this process via the Vegf decoy receptor sFlt1: sflt1 mutants exhibit the venous over-sprouting observed in radial glia-ablated larvae, and sFlt1 overexpression rescues it. Genetic mosaic analyses show that sFlt1 function in trunk endothelial cells can limit their over-sprouting.
Flt1-tyrosine kinase (TK) activity contributed significantly in endothelial cells survival and vascular development during embryo angiogenesis in zebrafish by engaging PI3K/Akt pathway.
Elevated Notch signaling downstream of perturbed VEGF signaling contributes to aberrant flt-1(-/-) blood vessel formation.
Data indicate that the increase in FLT1/sFLT1 protein levels upon miR-10 knockdown inhibited the angiogenic behavior of endothelial cells largely by antagonizing vascular endothelial growth factor receptor 2 signaling.
excessive sFlt1 and lack of eNOS synergistically induce hepatic dysfunction and thrombocytopenia, suggesting a novel role for VEGF and nitric oxide signaling in hepatocyte-endothelial cross-talk in health and in liver injury states.
Motor neurons control blood vessel patterning by an autocrine mechanism that titrates motor neuron-derived VEGF via their own expression of sFlt1.
inducible endothelial genetic deletion of Neuropilin1 (Nrp1) and Vascular endothelial growth factor receptor 1 (Vegfr1; also known as Flt1) renders mice resistant to diet-induced obesity.
findings identified a novel function of the VEGFR1 signaling in avoiding over-expression of Arginase 1 potentially to maintain the proper innate immune response.
Results show that Flt1 heterozygosity causes embryonic edema with enhanced vascular permeability. It can also be a risk factor for embryonic lethality in combination with other mutations causing non-lethal vascular phenotype.
Our study suggests that "migration" of the placenta is derived from placental degeneration at the caudal part of the placenta, and sFlt-1 plays a role in this placental degeneration.
This is the first report demonstrating the spatiotemporal expression patterns of Flk1 and Flt1 in the coronary vascular system during development and after MI; thus, this study suggests that these factors have distinct and important functions in coronary angiogenesis.
sFlt-1 overexpression in Padi4(-/-) mice resulted in dramatically lower inflammatory and thrombotic response, which was accompanied by significant reduction in pregnancy losses. Inhibition of NETosis may serve as a novel target in disorders of impaired placentation.
endothelial dysfunction due to high circulating sFLT1 may be the primary event leading to enhanced vasoconstrictor sensitivity that is characteristic of preeclampsia
Flt1 has a role in blood vessel anastomosis during angiogenesis
Esomeprazole decreased blood pressure in a transgenic mouse model where human sFlt-1 was overexpressed in placenta. PPIs upregulated endogenous antioxidant defenses and decreased cytokine secretion from placental tissue and endothelial cells.
First-in-class selective PET tracers for imaging VEGFR-1 and VEGFR-2 were constructed and successfully validated in an orthotopic murine tumor model.
these results suggest that VEGFR1 signaling plays a role in regulating the balance between macrophage phenotypes in streptozotocin -induced diabetic wounds, prevents impaired diabetic wound healing, and promotes angiogenesis/lymphangiogenesis.
These data therefore support a tightly controlled, paracrine signaling mechanism of VEGF-B to VEGFR1.
Flt1/VEGF-A signalling has stage-specific effects on vascular morphogenesis.
IL-35 treatment reduced collagen-induced arthritis via inhibiting vascular endothelial growth factor and its receptors
the VEGFR-1 tyrosine kinase signaling has an effect on angiogenesis.
data suggest that sFlt-1 may have a therapeutic effect on AS, resulting from suppression of VEGF signaling-mediated recruitment of circulating monocytes/macrophages
that Flt-1 plays a critical role in cardiac hypertrophy induced by pressure overload via the activation of AKT
Flt-1 appears to play a role in oxidative stress, which promotes apoptosis of trophoblasts
There is a possibility that steatosis can be suppressed by the CC genotype in VEGFR1.
These results suggest that non-dominant follicles maintain a greater concentration of the mRNA expression of both membrane and soluble VEGF receptors; but follicular dominance is related to a reduction in the mRNA expression of sVEGFR1 and sVEGFR2.
VEGFR-1 negatively regulates primary bovine retinal pericytes survival, and its blockade protects the blood-brain barrier integrity.
The changes of sVEGFR-1 and sVEGFR-2 with the age of the bovine dominant follicle indicate a physiological role in its growth and atresia.
gamma-Secretase and presenilin mediate cleavage and phosphorylation of vascular endothelial growth factor receptor-1
VEGFR1 mRNA expression was lower at estrus and at the early I and early II luteal stages than at the other stages, whereas VEGFR1 protein expression did not change significantly throughout the estrous cycle (P<0.05)
Alterations in the expression of VEGF-A and bFGF systems suggest that angiogenic factors are involved in abnormal placental development in cloned gestations, contributing to impaired fetal development and poor survival rates.
inhibition of VEGFR-1 results in decrease in number of capillary connections indicating VEGFR-1 ligands promote branching angiogenesis.
TGF-beta1 induction of VEGFR-1 in endothelial cells explains pericyte protection of vessels and the selective vulnerability of neonatal vessels to oxygen(VEGFR-1)
the activation of VEGFR-1 and VEGFR-2 heterodimer (VEGFR-1/R-2) is essential for PGI(2) synthesis mediated by VEGF-A(165) and VEGF-A(121), which cannot be reproduced by the parallel activation of VEGFR-1 and VEGFR-2 homodimers with corresponding agonists
PEDF and VEGFR-1 have roles in the negative regulation of angiogenesis
FLT-1 differentially methylated region was hypermethylated in parthenogenetic placenta.
we analyzed the expression and cellular distribution of Flt-1(VEGFR-1) and Flk-1 (KDR/VEGFR-2)in newborn piglet brain
data shows that members of the VEGF-VEGFR system are temporally and spatially well localized for playing key roles during umbilical cord formation and its intensive growth observed after day 75 of pregnancy
The VEGFR1 was stably expressed during the whole lifespan of mesonephric glomeruli, and VEGFR1 is important for the maintenance of endothelial fenestrations.
increased placental expression of the VEGF receptor system is associated with increased placental vascular density observed with the advancement of gestation in the pig.
EGFR, VEGFR and FGFR are expressed in porcine oviduct and endometrium during the time of implantation [review]
VEGF ligand-receptor system may play an important role in the development and maintenance of the corpus luteum in pigs.
VEGF/Flk-1/Flt-1 system is activated during myocardial ischemia reperfusion injury.
Hemodialysis graft placement leads to early increases in wall shear stress, VEGF-A, pro-MMP-9, MMP-2, VEGFR-1, VEGFR-2, and TIMP-1, which may contribute to the development of venous stenosis.
in experimental intervertebral disc degeneration, VEGF receptors were expressed in the damaged disc and paradiscal tissues
Luteal sVEGFR-1 may be involved in the maintenance of corpus luteal function whenever pregnancy occurs in pigs.
This gene encodes a member of the vascular endothelial growth factor receptor (VEGFR) family. VEGFR family members are receptor tyrosine kinases (RTKs) which contain an extracellular ligand-binding region with seven immunoglobulin (Ig)-like domains, a transmembrane segment, and a tyrosine kinase (TK) domain within the cytoplasmic domain. This protein binds to VEGFR-A, VEGFR-B and placental growth factor and plays an important role in angiogenesis and vasculogenesis. Expression of this receptor is found in vascular endothelial cells, placental trophoblast cells and peripheral blood monocytes. Multiple transcript variants encoding different isoforms have been found for this gene. Isoforms include a full-length transmembrane receptor isoform and shortened, soluble isoforms. The soluble isoforms are associated with the onset of pre-eclampsia.
fms-like tyrosine kinase 1
, fms-related tyrosine kinase 1 (vascular endothelial growth factor/vascular permeability factor receptor)
, tyrosine-protein kinase FRT
, tyrosine-protein kinase receptor FLT
, vascular endothelial growth factor receptor 1
, vascular permeability factor receptor
, FMS-like tyrosine kinase 1
, Fms-related tyrosine kinase 1 (vascular endothelial growth factor/vascular permeability factor receptor)
, vascular endothelial growth factor receptor-1
, fms-related tyrosine kinase 1
, receptor tyrosine kinase Flt1b
, soluble fms-like tyrosine kinase 1
, embryonic receptor kinase 2
, vascular endothelial growth factor/vascular permeability factor receptor
, ascular endothelial growth factor/vascular permeability factor receptor
, vascular endothelial growth factor 1
, flt-1 type VEGF receptor