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anti-Human FLT1 Antibodies:
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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 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 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
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
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 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 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
Human Monoclonal FLT1 Primary Antibody for ELISA, WB - ABIN969146
Flick, Sapi, Perrotta, Maher, Halaban, Carter, Kacinski: Recognition of activated CSF-1 receptor in breast carcinomas by a tyrosine 723 phosphospecific antibody. in Oncogene 1997
Show all 2 Pubmed References
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 (show PGF Antibodies) 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 (show PGF Antibodies), and the sFlt-1/PlGF (show PGF Antibodies) ratio in pre-eclamptic women with an onset at < 32 weeks were sig (show PICALM Antibodies)- 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 (show VEGFA Antibodies)/VEGFR1 signaling and provide additional information to clarify the role of EBVLMP1 in nasopharyngeal carcinoma (NPC (show NPC1 Antibodies))pathophysiology
An sFlt-1:PlGF (show PGF Antibodies) 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 (show PGF Antibodies) ratio in women with hypertensive disorders in pregnancy carries prognostic value for the development of preeclampsia.
VEGFA (show VEGFA Antibodies) activates VEGFR1 homodimers and AKT (show AKT1 Antibodies), leading to a cytoprotective response, whilst abluminal VEGFA (show VEGFA Antibodies) induces vascular leakage via VEGFR2 (show KDR Antibodies) homodimers and p38 (show CRK Antibodies)
metformin's dual effect in hyperglycemia-chemical hypoxia is mediated by direct effect on VEGFR1/R2 leading to activation of cell migration through MMP16 (show MMP16 Antibodies) and ROCK1 (show ROCK1 Antibodies) upregulation, and inhibition of apoptosis by increase in phospho-ERK1/2 and FABP4 (show FABP4 Antibodies), components of VEGF (show VEGFA Antibodies) signaling cascades
we determined that radial glia control this process via the Vegf (show VEGFA Antibodies) 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 (show AKT1 Antibodies) pathway.
Elevated Notch (show NOTCH1 Antibodies) signaling downstream of perturbed VEGF (show VEGFA Antibodies) signaling contributes to aberrant flt-1(-/-) blood vessel formation.
Data indicate that the increase in FLT1/sFLT1 protein levels upon miR-10 (show LILRB2 Antibodies) knockdown inhibited the angiogenic behavior of endothelial cells largely by antagonizing vascular endothelial growth factor receptor 2 (show KDR Antibodies) signaling.
Motor neurons control blood vessel patterning by an autocrine mechanism that titrates motor neuron-derived VEGF (show VEGFA Antibodies) via their own expression of sFlt1.
inducible endothelial genetic deletion of Neuropilin1 (Nrp1 (show NRP1 Antibodies)) 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 (show ARG1 Antibodies) 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 (show CAD Antibodies) 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 (show KDR Antibodies) 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 (show PADI4 Antibodies)(-/-) 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
First-in-class selective PET tracers for imaging VEGFR-1 and VEGFR-2 (show KDR Antibodies) were constructed and successfully validated in an orthotopic murine tumor model.
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 (show VEGFA Antibodies) 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.
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 (show VEGFA Antibodies) and bFGF (show FGF2 Antibodies) 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 (show TGFB1 Antibodies) 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 (show KDR Antibodies) heterodimer (VEGFR-1/R-2) is essential for PGI(2 (show PTGIR Antibodies)) synthesis mediated by VEGF-A (show VEGFA Antibodies)(165) and VEGF-A (show VEGFA Antibodies)(121), which cannot be reproduced by the parallel activation of VEGFR-1 and VEGFR-2 (show KDR Antibodies) homodimers with corresponding agonists
PEDF (show SERPINF1 Antibodies) 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 (show KDR Antibodies))in newborn piglet brain
data shows that members of the VEGF (show VEGFA Antibodies)-VEGFR (show KDR Antibodies) 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 (show EGFR Antibodies), VEGFR (show KDR Antibodies) and FGFR (show FGFR2 Antibodies) are expressed in porcine oviduct and endometrium during the time of implantation [review]
VEGF (show VEGFA Antibodies) ligand-receptor system may play an important role in the development and maintenance of the corpus luteum in pigs.
VEGF (show VEGFA Antibodies)/Flk-1 (show KDR Antibodies)/Flt-1 system is activated during myocardial ischemia reperfusion injury.
Hemodialysis graft placement leads to early increases in wall shear stress, VEGF-A (show VEGFA Antibodies), pro-MMP-9 (show MMP9 Antibodies), MMP-2 (show MMP2 Antibodies), VEGFR-1, VEGFR-2 (show KDR Antibodies), and TIMP-1 (show TIMP1 Antibodies), which may contribute to the development of venous stenosis.
in experimental intervertebral disc degeneration, VEGF (show VEGFA Antibodies) receptors were expressed in the damaged disc and paradiscal tissues
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