抗Human FLT1 抗体:
抗Rat (Rattus) FLT1 抗体:
抗Mouse (Murine) FLT1 抗体:
Human Polyclonal FLT1 Primary Antibody for BR, CyTOF - ABIN5013028
Giuliani, Colla, Lazzaretti, Sala, Roti, Mancini, Bonomini, Lunghi, Hojden, Genestreti, Svaldi, Coser, Fattori, Sammarelli, Gazzola, Bataille, Almici, Caramatti, Mangoni, Rizzoli: Proangiogenic properties of human myeloma cells: production of angiopoietin-1 and its potential relationship to myeloma-induced angiogenesis. in Blood 2003
Show all 28 Pubmed References
Mouse (Murine) Polyclonal FLT1 Primary Antibody for BR, ELISA (Capture) - ABIN5013029
Matsuno, Kozawa, Yoshimi, Akamatsu, Hara, Mori, Okada, Ueshima, Matsuo, Uematsu: Lack of alpha2-antiplasmin promotes pulmonary heart failure via overrelease of VEGF after acute myocardial infarction. in Blood 2002
Show all 25 Pubmed References
Human Monoclonal FLT1 Primary Antibody for FACS - ABIN4897100
Karrar, Broomé, Uzunel, Qureshi, Sumitran-Holgersson: Human liver sinusoidal endothelial cells induce apoptosis in activated T cells: a role in tolerance induction. in Gut 2007
Show all 20 Pubmed References
Human Monoclonal FLT1 Primary Antibody for CyTOF, FACS - ABIN4900044
Brave, Eberlein, Shibuya, Wedge, Barry: Placental growth factor neutralising antibodies give limited anti-angiogenic effects in an in vitro organotypic angiogenesis model. in Angiogenesis 2010
Show all 8 Pubmed References
Human Monoclonal FLT1 Primary Antibody for FACS - ABIN4897099
de Groot, Piao, Tran, Gilbert, Wu, Liu, Bekele, Cloughesy, Mehta, Robins, Lassman, DeAngelis, Camphausen, Chen, Yung, Prados, Wen, Heymach: Myeloid biomarkers associated with glioblastoma response to anti-VEGF therapy with aflibercept. in Clinical cancer research : an official journal of the American Association for Cancer Research 2011
Show all 6 Pubmed References
Human Polyclonal FLT1 Primary Antibody for ICC, IF - ABIN151960
Rahimi, Dayanir, Lashkari: Receptor chimeras indicate that the vascular endothelial growth factor receptor-1 (VEGFR-1) modulates mitogenic activity of VEGFR-2 in endothelial cells. in The Journal of biological chemistry 2000
Show all 6 Pubmed References
Mouse (Murine) Monoclonal FLT1 Primary Antibody for FACS - ABIN4897107
Reddy, Zhou, Schadler, Jia, Kleinerman: Bone marrow subsets differentiate into endothelial cells and pericytes contributing to Ewing's tumor vessels. in Molecular cancer research : MCR 2008
Show all 5 Pubmed References
Mouse (Murine) Monoclonal FLT1 Primary Antibody for FACS - ABIN4897104
Weston, Zayas, Perez, George, Jurecic: Dynamic equilibrium of heterogeneous and interconvertible multipotent hematopoietic cell subsets. in Scientific reports 2014
Show all 4 Pubmed References
Polyclonal FLT1 Primary Antibody for WB - ABIN540436
Takahashi, Hattori, Iwamatsu, Takizawa, Shibuya: A novel snake venom vascular endothelial growth factor (VEGF) predominantly induces vascular permeability through preferential signaling via VEGF receptor-1. in The Journal of biological chemistry 2004
Show all 3 Pubmed References
Human Polyclonal FLT1 Primary Antibody for IF (p), IHC (p) - ABIN725795
Cheng, Xiang, Yang, Ma, Zhao: Direct Effects of Bevacizumab on Rat Conjunctival Fibroblast. in Cell biochemistry and biophysics 2015
Show all 3 Pubmed References
Genetic predisposition to pre-eclampsia was found to be associated with single nucleotide polymorphisms near the FLT1 gene.
This study performed FLT1 and transcriptome-wide polyadenylation site (PAS) analysis in preeclampsia. Consistent with soluble Flt1 overproduction being a significant driver of clinical symptoms, placental Flt1 mRNA levels strongly correlate with maternal blood pressure.
The inhibition of FLT1 ectodomain cleavage by VEGF-A is dependent neither on receptor activation nor on internalization.
This is the first study to demonstrate that the ratio of sFlt-1/PlGF can both predict and serve as a diagnostic factor for preeclampsia in pregnant women from different populations within the Xinjiang region of China.
Results find the expression of Flt-1 was 48% higher in the frontal cortex and 72% higher in the basal ganglia of congenital heart disease fetuses compared with controls.
Our findings indicate a mechanism by which the VEGF and the sVEGFR-1 production by immune cells regulates local VEGF signalling.
Have high vascular endothelial growth factor (VEGF)-Flt1 pathway activity.
Maternal serum sFLt-1 levels in preeclampsia were higher in early-onset preeclampsia and were associated with a worse perinatal outcome.
high VEGFR-1 and low VEGFR-2 expression in endothelial cells appear to be involved in the progression of colorectal cancer.
Elevated serum VEGFR-1 levels in patients with Behcet's disease.VEGF/sVEGFR-1 ratio could play an important role in the development of trombosis in in patients with Behcet's disease.
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.
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.
Report the physiological functions of VEGFR1 in the modulation of adipose angiogenesis, obesity, and global metabolism. Pharmacological inhibition and genetic deletion of endothelial VEGFR1 augmented adipose angiogenesis and browning of subcutaneous white adipose tissue, leading to elevated thermogenesis.
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
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