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抗Mouse (Murine) VEGFR2 抗体:
抗Rat (Rattus) VEGFR2 抗体:
抗Human VEGFR2 抗体:
Mouse (Murine) Polyclonal VEGFR2 Primary Antibody for CyTOF, FACS - ABIN4899536
Hou, Nilchi, Li, Gangaraju, Jiang, Aylsworth, Monette, Slinn: Semaphorin3A elevates vascular permeability and contributes to cerebral ischemia-induced brain damage. in Scientific reports 2015
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Human Monoclonal VEGFR2 Primary Antibody for FACS - ABIN4896290
den Dekker, Houtgraaf, Rowland, Ligtenberg, de Boer, de Jong, de Winter, den Heijer, Zijlstra, Serruys, Cheng, Duckers: Efficiency of statin treatment on EPC recruitment depends on baseline EPC titer and does not improve angiographic outcome in coronary artery disease patients treated with the Genous stent. in Cell transplantation 2015
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Human Monoclonal VEGFR2 Primary Antibody for FACS - ABIN4896289
Chan, Simpson, Yong, Dunn, Chawantanpipat, Hsu, Yu, Keech, Celermajer, Ng: The relationship between endothelial progenitor cell populations and epicardial and microvascular coronary disease-a cellular, angiographic and physiologic study. in PLoS ONE 2014
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Human Monoclonal VEGFR2 Primary Antibody for CyTOF, FACS - ABIN4899538
Riccioni, Diverio, Mariani, Buffolino, Riti, Saulle, Petrucci, Cedrone, Lo-Coco, Foà, Peschle, Testa: Expression of Tie-2 and other receptors for endothelial growth factors in acute myeloid leukemias is associated with monocytic features of leukemic blasts. in Stem cells (Dayton, Ohio) 2007
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Human Monoclonal VEGFR2 Primary Antibody for CyTOF, FACS - ABIN4899539
Riccioni, Senese, Diverio, Riti, Mariani, Boe, LoCoco, Foà, Peschle, Sporn, Testa: Resistance of acute myeloid leukemic cells to the triterpenoid CDDO-Imidazolide is associated with low caspase-8 and FADD levels. in Leukemia research 2008
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Human Polyclonal VEGFR2 Primary Antibody for IHC (p), IP - ABIN152058
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
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Mouse (Murine) Monoclonal VEGFR2 Primary Antibody for FACS, IHC - ABIN967481
Hanahan: Signaling vascular morphogenesis and maintenance. in Science (New York, N.Y.) 1997
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Human Monoclonal VEGFR2 Primary Antibody for IHC (fro) - ABIN3043643
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 Monoclonal VEGFR2 Primary Antibody for FACS - ABIN4896281
Wang, Tang, Sun, Miao, Lv, Yang, Zhang, Zhang, Liu, Du, Gao, Yin, Ding, Deng: TGFβ inhibition enhances the generation of hematopoietic progenitors from human ES cell-derived hemogenic endothelial cells using a stepwise strategy. in Cell research 2012
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Human Monoclonal VEGFR2 Primary Antibody for FACS - ABIN4896282
Boyer-Di Ponio, El-Ayoubi, Glacial, Ganeshamoorthy, Driancourt, Godet, Perrière, Guillevic, Couraud, Uzan: Instruction of circulating endothelial progenitors in vitro towards specialized blood-brain barrier and arterial phenotypes. in PLoS ONE 2014
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These results indicate that VEGF-C (显示 VEGFC 抗体)-induced MSC (显示 MSC 抗体) osteogenesis is mediated through VEGFR2 and VEGFR3 (显示 FLT4 抗体), and followed the activation of the ERK (显示 MAPK1 抗体)/RUNX2 (显示 RUNX2 抗体) signaling pathway.
VEGFR2-associated alpha(2,6)-linked sialic acid plays an important role in modulating VEGF (显示 VEGFA 抗体)/VEGFR2 interaction, EC pro-angiogenic activation and neovessel formation.
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 (显示 C16orf35 抗体)-GFP/Flk1::myr-mCherry mice are a useful model for studying coordinated hemangiogenic and lymphangiogenic responses
Endoglin (显示 ENG 抗体) prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling
CLEC14A (显示 CLEC14A 抗体) acts in vascular homeostasis by fine-tuning VEGFR-2 and VEGFR-3 (显示 FLT4 抗体) signaling in endothelial cells
The elevated soluble VEGFR-2 that was found in the aortas of apoE (显示 APOE 抗体)(-/-) mice with atherosclerosis binds to and diminishes the activity of VEGF-C (显示 VEGFC 抗体).
Data show that Leishmania major infection initiates enhanced vascular endothelial growth factor-A (显示 VEGFA 抗体)/VEGFR-2 signaling and suggest that VEGFR-2-dependent lymphangiogenesis is a mechanism that restricts tissue inflammation in leishmaniasis.
VEGFR3 (显示 FLT4 抗体) limits VEGFR2 expression and VEGF (显示 VEGFA 抗体)/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 (显示 VEGFA 抗体) stimulation.
FGD5 (显示 FGD5 抗体) regulates VEGFR2 retention in recycling endosomes and coupling to PI3 (显示 PI3 抗体) (phosphoinositide-3) kinase/mTORC2 (显示 CRTC2 抗体)-dependent cytoskeletal remodeling in endothelial cells.
Results indicate that ranibizumab affects the VEGF-A (显示 VEGFA 抗体) metabolism in RPE (显示 RPE 抗体) cells from an extra- as well as intracellular site. The drug is taken up into the cells, with the VEGF receptor 2 (VEGFR-2) being involved, and decreases VEGF-A (显示 VEGFA 抗体) protein levels within the cells as well as extracellularly.
Danggui-Sayuk-Ga-Osuyu-Saenggang-Tang (DSGOST) inhibits angiogenic signaling by blocking VEGF (显示 VEGFA 抗体) binding to VEGFR2.
Data show that anti-VEGFR2 (vascular endothelial growth factor receptor 2) antibody (mAb04) of fusion protein (mAb04-MICA (显示 MICA 抗体)) enhanced immunosurveillance activated by the NKG2D (显示 KLRK1 抗体) pathway.
this study found no difference in VEGFR2 expression in infantile hemangiomas from the study and control group
MiRNA199a-3p suppresses tumor growth, migration, invasion and angiogenesis in hepatocellular carcinoma by targeting VEGFA (显示 VEGFA 抗体), VEGFR1 (显示 FLT1 抗体), VEGFR2, HGF (显示 HGF 抗体) and MMP2 (显示 MMP2 抗体)
Leptin (显示 LEP 抗体)-induced transphosphorylation of vascular endothelial growth factor receptor (显示 RYK 抗体) increases Notch (显示 NOTCH1 抗体) and stimulates endothelial cell angiogenic transformation
The study aimed to assess the usefulness of the determination of cytokines: IL-8 (显示 IL8 抗体), VEGF (显示 VEGFA 抗体) and its soluble receptors: VEGF (显示 VEGFA 抗体)-R1, VEGF (显示 VEGFA 抗体)-R2 in patients with endometrial cancer. The concentrations of IL-8 (显示 IL8 抗体) 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.
Here we demonstrate that VEGF (显示 VEGFA 抗体)-165 mediates MSC (显示 MSC 抗体) differentiation into ECs via VEGFR-2-dependent induction of Sox18 (显示 SOX18 抗体), which ultimately coordinates the transcriptional upregulation of specific markers of the EC phenotype
NOS (显示 NOS 抗体) stimulation via PI3K, calpain proteases, and SIRT1 (显示 SIRT1 抗体)-dependent deacetylation downstream from VEGFR2 activation contributes to these vasodilator responses.
we analyzed the expression and cellular distribution of Flt-1(VEGFR-1 (显示 FLT1 抗体)) and Flk-1 (KDR/VEGFR-2)in newborn piglet brain
expression of FLK1, CD146 (显示 MCAM 抗体) and microvessel density of angiogenesis at the first week of reperfused acute myocardial infarction.
VEGF (显示 VEGFA 抗体) supplementation at the late embryonic developmental stage might improve the developmental potential of both IVF (显示 SCN5A 抗体) 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 (显示 FLT1 抗体) 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 (显示 VEGFA 抗体)/Flk-1/Flt-1 (显示 FLT1 抗体) system is activated during myocardial ischemia reperfusion injury.
Hemodialysis graft placement leads to early increases in wall shear stress, VEGF-A (显示 VEGFA 抗体), pro-MMP-9 (显示 MMP9 抗体), MMP-2 (显示 MMP2 抗体), VEGFR-1 (显示 FLT1 抗体), VEGFR-2, and TIMP-1 (显示 TIMP1 抗体), 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 (显示 TGFB1 抗体) 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 (显示 LGALS1 抗体) and VEGFR-2 are expressed at mid-luteal stages in luteal cells of corpus luteum; galectin-1 (显示 LGALS1 抗体) binds directly to asparagine-linked glycans (N-glycans) on VEGFR-2 in luteal cells.
MMP-1 (显示 MMP1 抗体) promotes VEGFR2 expression and proliferation of endothelial cells through stimulation of PAR-1 (显示 F2R 抗体) and activation of NF-kappaB (显示 NFKB1 抗体)
Vascular endothelial growth factor receptor-2 activates ADP-ribosylation factor 1 (显示 ARF1 抗体) to promote endothelial nitric-oxide synthase (显示 NOS3 抗体) 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 (显示 VEGFA 抗体) and bFGF (显示 FGF2 抗体) 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 (显示 AKT1 抗体) and endothelial nitric-oxide synthase (eNOS (显示 NOS3 抗体))
Placenta growth factor (显示 PGF 抗体) expression is regulated by both VEGF (显示 VEGFA 抗体) and hyperglycaemia via VEGFR-2.
ghrelin (显示 GHRL 抗体) can inhibit intraplaque angiogenesis and promote plaque stability by down-regulating VEGF (显示 VEGFA 抗体) and VEGFR2 expression, inhibiting the plaque content of macrophages, and reducing MCP-1 (显示 CCL2 抗体) expression at an advanced stage of atherosclerosis in rabbits
Antenatal intratracheal VEGF (显示 VEGFA 抗体) administration was associated with an increase in Flk-1 immunoreactivity.
Intronic Flk1 genetic enhancer element directs arterial-specific expression via RBPJ (显示 RBPJ 抗体)-mediated venous repression.
Ca(2 (显示 CA2 抗体)+) oscillations depended upon VEGF receptor-2 (Vegfr2) and Vegfr3 (显示 FLT4 抗体) in endothelial cells budding from the dorsal aorta (DA) and posterior cardinal (显示 CARD8 抗体) vein, respectively.
Methylglyoxal acts on smaller blood vessels in zebrafish via the VEGF receptor (显示 FLT1 抗体) signaling cascade, thereby describing a new mechanism that can explain vascular complications under hyperglycemia and elevated MG concentrations.
methylation of Lys (显示 LYZ 抗体)(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 (显示 HSPA1A 抗体)-HSP90 (显示 HSP90 抗体) heat-shock protein axis stimulates degradation of endothelial VEGFR2.
Data indicate that the increase in FLT1/sFLT1 (显示 FLT1 抗体) protein levels upon miR-10 (显示 LILRB2 抗体) knockdown inhibited the angiogenic behavior of endothelial cells largely by antagonizing vascular endothelial growth factor receptor 2 signaling: [miR10 (显示 LILRB2 抗体)]
Early Flk1 expression may be induced by cooperative interactions between Gata (显示 GATA4 抗体), Tcf (显示 HNF4A 抗体)/Lef, Cdx (显示 CDX1 抗体) and ER71/Etv2 (显示 ETV2 抗体) under the control of Bmp, Wnt (显示 WNT2 抗体) and Fgf signaling.
Using 2 distinct pharmacologic VEGFR2 inhibitors the study shows that rap1b (显示 RAP1A 抗体) 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 (显示 FOXH1 抗体); FoxH1 (显示 FOXH1 抗体) 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