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Human VEGFR2 ELISA Kit for Sandwich ELISA - ABIN414630
Nassehi, Sørensen, Dyrbye, Thomsen, Juhler, Laursen, Broholm: Peritumoral brain edema in angiomatous supratentorial meningiomas: an investigation of the vascular endothelial growth factor A pathway. in APMIS : acta pathologica, microbiologica, et immunologica Scandinavica 2013
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Human VEGFR2 ELISA Kit for Sandwich ELISA - ABIN625109
Navid, Baker, McCarville, Stewart, Billups, Wu, Davidoff, Spunt, Furman, McGregor, Hu, Panetta, Turner, Fofana, Reddick, Leung, Santana: Phase I and clinical pharmacology study of bevacizumab, sorafenib, and low-dose cyclophosphamide in children and young adults with refractory/recurrent solid tumors. in Clinical cancer research : an official journal of the American Association for Cancer Research 2013
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Human VEGFR2 ELISA Kit for Sandwich ELISA - ABIN1672753
Li, Huang, Chen, Chen, Xiong, Chen, You, Jin, Liang: Oriented immobilization of anti-CD34 antibody on titanium surface for self-endothelialization induction. in Journal of biomedical materials research. Part A 2010
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Human VEGFR2 ELISA Kit for Sandwich ELISA - ABIN365817
Du, Wang, Ren, Lv, He: Revealing multi-binding sites for taspine to VEGFR-2 by cell membrane chromatography zonal elution. in Journal of chromatography. B, Analytical technologies in the biomedical and life sciences 2012
These results indicate that VEGF-C (show VEGFC ELISA Kits)-induced MSC (show MSC ELISA Kits) osteogenesis is mediated through VEGFR2 and VEGFR3 (show FLT4 ELISA Kits), and followed the activation of the ERK (show MAPK1 ELISA Kits)/RUNX2 (show RUNX2 ELISA Kits) signaling pathway.
These results revealed that vascular sprouting and permeability are both controlled through the VEGFR2-TSAd-c-Src signaling pathway in a subset of tissues, which may be useful in developing strategies to control tissue-specific pathological angiogenesis.
Data show that editing of genomic VEGFR2 locus using rAAV1-mediated CRISPR/Cas9 abrogates angiogenesis in the mouse models of oxygen-induced retinopathy and laser-induced choroid neovascularization.
Our study demonstrates that Prox1-GFP/Flk1::myr-mCherry mice are a useful model for studying coordinated hemangiogenic and lymphangiogenic responses
Endoglin (show ENG ELISA Kits) prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling
CLEC14A (show CLEC14A ELISA Kits) acts in vascular homeostasis by fine-tuning VEGFR-2 and VEGFR-3 (show FLT4 ELISA Kits) signaling in endothelial cells
The elevated soluble VEGFR-2 that was found in the aortas of apoE (show APOE ELISA Kits)(-/-) mice with atherosclerosis binds to and diminishes the activity of VEGF-C (show VEGFC ELISA Kits).
Data show that Leishmania major infection initiates enhanced vascular endothelial growth factor-A (show VEGFA ELISA Kits)/VEGFR-2 signaling and suggest that VEGFR-2-dependent lymphangiogenesis is a mechanism that restricts tissue inflammation in leishmaniasis.
VEGFR3 (show FLT4 ELISA Kits) limits VEGFR2 expression and VEGF (show VEGFA ELISA Kits)/VEGFR2 pathway activity in quiescent and angiogenic blood vascular endothelial cells, thereby preventing excessive vascular permeability.
fetal mouse lung mesenchymal cells express Vegfr2 and respond to VEGF-A (show VEGFA ELISA Kits) stimulation.
Deletion of microRNA miR (show MLXIP ELISA Kits)-150 increased the retinal pathological angiogenesis in high-fat-diet (HFD) induced type 2 diabetic mice, which was in part through vascular endothelial growth factor receptor 2 (VEGFR2).
this study found no difference in VEGFR2 expression in infantile hemangiomas from the study and control group
These results indicate that VEGF actively induces the reprogramming of EPCs to become more primitive stem cells that display active cell growth.
MiRNA199a-3p suppresses tumor growth, migration, invasion and angiogenesis in hepatocellular carcinoma by targeting VEGFA (show VEGFA ELISA Kits), VEGFR1 (show FLT1 ELISA Kits), VEGFR2, HGF (show HGF ELISA Kits) and MMP2 (show MMP2 ELISA Kits)
Cigarette-smoke-derived reactive oxygen/nitrogen species react with VEGFR2, rendering VEGFR2 inactive for its downstream signaling.
Leptin (show LEP ELISA Kits)-induced transphosphorylation of vascular endothelial growth factor receptor (show RYK ELISA Kits) increases Notch (show NOTCH1 ELISA Kits) and stimulates endothelial cell angiogenic transformation
The study aimed to assess the usefulness of the determination of cytokines: IL-8 (show IL8 ELISA Kits), VEGF (show VEGFA ELISA Kits) and its soluble receptors: VEGF (show VEGFA ELISA Kits)-R1, VEGF (show VEGFA ELISA Kits)-R2 in patients with endometrial cancer. The concentrations of IL-8 (show IL8 ELISA Kits) were an independent prognostic factor in the assessment of overall survival in patients with type I endometrial cancer, while the concentrations of VEGFR2 in those with type II.
High VEGFR expression is associated with melanoma.
OGN (show OGN ELISA Kits) plays a critical role in negatively regulating ischaemia-induced angiogenesis by inhibiting VEGF (show VEGFA ELISA Kits)-VEGFR2 signalling and thereby attenuating endothelial cells tube formation, proliferation, and migration.
Cryptotanshinone potently inhibits VEGF (show VEGFA ELISA Kits)-induced angiogenesis by suppressing VEGFR2 activation and its downstream Src (show SRC ELISA Kits)/FAK (show PTK2 ELISA Kits) and ERK1/2 (show MAPK1/3 ELISA Kits) signaling pathways in HUVECs.
The model showed agreement at several key nodes, involving scaffolding proteins Gab1, Gab2 (show GAB2 ELISA Kits) and their complexes with Shp2 (show PTPN11 ELISA Kits). VEGFR2 recruitment of Gab1 is greater in magnitude, slower, and more sustained than that of Gab2 (show GAB2 ELISA Kits). As Gab2 (show GAB2 ELISA Kits) binds VEGFR2 complexes more transiently than Gab1, VEGFR2 complexes can recycle and continue to participate in other signaling pathways.
Here we demonstrate that VEGF (show VEGFA ELISA Kits)-165 mediates MSC (show MSC ELISA Kits) differentiation into ECs via VEGFR-2-dependent induction of Sox18 (show SOX18 ELISA Kits), which ultimately coordinates the transcriptional upregulation of specific markers of the EC phenotype
NOS (show NOS ELISA Kits) stimulation via PI3K, calpain proteases, and SIRT1 (show SIRT1 ELISA Kits)-dependent deacetylation downstream from VEGFR2 activation contributes to these vasodilator responses.
we analyzed the expression and cellular distribution of Flt-1(VEGFR-1 (show FLT1 ELISA Kits)) and Flk-1 (KDR/VEGFR-2)in newborn piglet brain
expression of FLK1, CD146 (show MCAM ELISA Kits) and microvessel density of angiogenesis at the first week of reperfused acute myocardial infarction.
VEGF (show VEGFA ELISA Kits) supplementation at the late embryonic developmental stage might improve the developmental potential of both IVF (show SCN5A ELISA Kits) and somatic nuclear transfer preimplantation porcine embryos through its receptors.
The VEGFR2 mRNA was only upregulated in early glomerulogenesis, suggesting that VEGFR2 is important for the vascular growth.
increased placental expression of the VEGF receptor (show FLT1 ELISA Kits) system is associated with increased placental vascular density observed with the advancement of gestation in the pig
VEGF ligand-receptor system may play an important role in the development and maintenance of the corpus luteum in pigs.
VEGF (show VEGFA ELISA Kits)/Flk-1/Flt-1 (show FLT1 ELISA Kits) system is activated during myocardial ischemia reperfusion injury.
Hemodialysis graft placement leads to early increases in wall shear stress, VEGF-A (show VEGFA ELISA Kits), pro-MMP-9 (show MMP9 ELISA Kits), MMP-2 (show MMP2 ELISA Kits), VEGFR-1 (show FLT1 ELISA Kits), VEGFR-2, and TIMP-1 (show TIMP1 ELISA Kits), which may contribute to the development of venous stenosis.
data for the first time demonstrate a calpain/PTP1B/VEGFR2 negative feedback loop in the regulation of VEGF-induced angiogenesis. Modulation of local PTP1B and/or calpain activities may prove beneficial in the treatment of impaired wound healing in diabetes.
endothelial cells exposed to TGF-beta1 (show TGFB1 ELISA Kits) lose both tip and stalk cell identity, possibly mediated by loss of VEGFR2 signaling.
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.
Data suggest that galectin-1 (show LGALS1 ELISA Kits) and VEGFR-2 are expressed at mid-luteal stages in luteal cells of corpus luteum; galectin-1 (show LGALS1 ELISA Kits) binds directly to asparagine-linked glycans (N-glycans) on VEGFR-2 in luteal cells.
MMP-1 (show MMP1 ELISA Kits) promotes VEGFR2 expression and proliferation of endothelial cells through stimulation of PAR-1 (show F2R ELISA Kits) and activation of NF-kappaB (show NFKB1 ELISA Kits)
Vascular endothelial growth factor receptor-2 activates ADP-ribosylation factor 1 (show ARF1 ELISA Kits) to promote endothelial nitric-oxide synthase (show NOS3 ELISA Kits) activation and nitric oxide release from endothelial cells
VEGFR2 mRNA expression was higher at the mid and late luteal stages than at the early I and early II luteal stages, and VEGFR2 protein was higher at the mid and late luteal stages than at estrus (P<0.05)
Alterations in the expression of VEGF-A (show VEGFA ELISA Kits) and bFGF (show FGF2 ELISA Kits) systems suggest that angiogenic factors are involved in abnormal placental development in cloned gestations, contributing to impaired fetal development and poor survival rates.
involved in sphingosine 1-phosphate-stimulated phosphorylation of Akt (show AKT1 ELISA Kits) and endothelial nitric-oxide synthase (eNOS (show NOS3 ELISA Kits))
Placenta growth factor (show PGF ELISA Kits) expression is regulated by both VEGF (show VEGFA ELISA Kits) and hyperglycaemia via VEGFR-2.
Antenatal intratracheal VEGF (show VEGFA ELISA Kits) administration was associated with an increase in Flk-1 immunoreactivity.
Intronic Flk1 genetic enhancer element directs arterial-specific expression via RBPJ (show RBPJ ELISA Kits)-mediated venous repression.
Ca(2 (show CA2 ELISA Kits)+) oscillations depended upon VEGF receptor-2 (Vegfr2) and Vegfr3 (show FLT4 ELISA Kits) in endothelial cells budding from the dorsal aorta (DA) and posterior cardinal (show CARD8 ELISA Kits) vein, respectively.
Methylglyoxal acts on smaller blood vessels in zebrafish via the VEGF receptor (show FLT1 ELISA Kits) signaling cascade, thereby describing a new mechanism that can explain vascular complications under hyperglycemia and elevated MG concentrations.
methylation of Lys (show LYZ ELISA Kits)(1041) promotes the activation of VEGFR-2 and that similar posttranslational modification could also regulate the activity of other receptor tyrosine kinases.
Perturbation of the HSP70 (show HSPA1A ELISA Kits)-HSP90 (show HSP90 ELISA Kits) heat-shock protein axis stimulates degradation of endothelial VEGFR2.
Data indicate that the increase in FLT1/sFLT1 (show FLT1 ELISA Kits) protein levels upon miR-10 (show LILRB2 ELISA Kits) knockdown inhibited the angiogenic behavior of endothelial cells largely by antagonizing vascular endothelial growth factor receptor 2 signaling: [miR10 (show LILRB2 ELISA Kits)]
Early Flk1 expression may be induced by cooperative interactions between Gata (show GATA4 ELISA Kits), Tcf (show HNF4A ELISA Kits)/Lef, Cdx (show CDX1 ELISA Kits) and ER71/Etv2 under the control of Bmp, Wnt (show WNT2 ELISA Kits) and Fgf signaling.
Using 2 distinct pharmacologic VEGFR2 inhibitors the study shows that rap1b (show RAP1A ELISA Kits) and VEGFR2 act additively to control angiogenesis in vivo.
Data show that flk1 is not required for proper vasculogenesis and hematopoiesis in zebrafish embryos; however, the disruption of flk1 impairs the formation or function of vessels generated by sprouting angiogenesis
flk1 is a direct target of FoxH1 (show FOXH1 ELISA Kits); FoxH1 (show FOXH1 ELISA Kits) is involved in vessel formation in zebrafish.
Vascular endothelial growth factor (VEGF) is a major growth factor for endothelial cells. This gene encodes one of the two receptors of the VEGF. This receptor, known as kinase insert domain receptor, is a type III receptor tyrosine kinase. It functions as the main mediator of VEGF-induced endothelial proliferation, survival, migration, tubular morphogenesis and sprouting. The signalling and trafficking of this receptor are regulated by multiple factors, including Rab GTPase, P2Y purine nucleotide receptor, integrin alphaVbeta3, T-cell protein tyrosine phosphatase, etc.. Mutations of this gene are implicated in infantile capillary hemangiomas.
vascular endothelial growth factor receptor 2
, VEGF receptor-2
, fetal liver kinase 1
, kinase NYK
, protein-tyrosine kinase receptor flk-1
, soluble vascular endothelial growth factor receptor 2
, vascular endothelial growth factor receptor- 2
, vascular endothelial growth factor receptor-2
, vascular endothelial growth factor receptor-3
, FLK1 kinase insert domain receptor (VEGF receptor 2)
, FLK1 kinase insert domain receptor (a type III receptor tyrosine kinase) (VEGF receptor 2)
, kinase insert domain protein receptor
, fetal liver kinase-1
, protein-tyrosine kinase receptor Flk-1
, soluble VEGFR2
, tyrosine kinase growth factor receptor
, flk-1 type VEGF receptor
, flk-1 receptor
, protein-tyrosine kinase
, tyrosine kinase receptor
, VEGF receptor-2/Flk-1
, VEGFR-2 homolog B
, fetal liver kinase 1b
, kinase insert domain receptor (a type III receptor tyrosine kinase), b
, kinase insert domain receptor-B
, protein-tyrosine kinase receptor flk-1b
, vascular endothelial growth factor receptor 2 homolog B
, kinase insert domain receptor-A
, kinase insert domain receptor-like
, vascular endothelial growth factor receptor 4
, vascular endothelial growth factor receptor kdr-like
, vascular endothelial growth factor receptor type 2