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anti-Mouse (Murine) VEGFR2 Antibodies:
anti-Rat (Rattus) VEGFR2 Antibodies:
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Human Monoclonal VEGFR2 Primary Antibody for FACS - ABIN4896289
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
Show all 49 Pubmed References
Human Monoclonal VEGFR2 Primary Antibody for FACS - ABIN4896290
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
Show all 49 Pubmed References
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
Show all 30 Pubmed References
Human Monoclonal VEGFR2 Primary Antibody for CyTOF, FACS - ABIN4899539
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
Show all 10 Pubmed References
Human Monoclonal VEGFR2 Primary Antibody for CyTOF, FACS - ABIN4899538
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
Show all 10 Pubmed References
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
Show all 8 Pubmed References
Mouse (Murine) Monoclonal VEGFR2 Primary Antibody for FACS, IHC - ABIN967481
Hanahan: Signaling vascular morphogenesis and maintenance. in Science (New York, N.Y.) 1997
Show all 8 Pubmed References
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
Show all 7 Pubmed References
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
Show all 7 Pubmed References
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
Show all 7 Pubmed References
These results indicate that VEGF-C (show VEGFC Antibodies)-induced MSC (show MSC Antibodies) osteogenesis is mediated through VEGFR2 and VEGFR3 (show FLT4 Antibodies), and followed the activation of the ERK (show MAPK1 Antibodies)/RUNX2 (show RUNX2 Antibodies) signaling pathway.
transgenic mice may serve as valid models for the validation of novel therapies blocking the VEGFR-2 signaling pathway in hemangioma-like lesions and other vascular diseases
found that WT1 (show WT1 Antibodies) and KDR are co-expressed in Sertoli cells of the testes and somatic cells of embryonic ovaries. Furthermore, WT1 (show WT1 Antibodies) bound to the Kdr promoter in the chromatin of embryonic testes and ovaries. KDR signaling represses the testis-promoting gene Sox9 (show SOX9 Antibodies) in embryonic XX gonads
This is the first report demonstrating the spatiotemporal expression patterns of Flk1 and Flt1 (show FLT1 Antibodies) 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.
VEGFR2-associated alpha(2,6)-linked sialic acid plays an important role in modulating VEGF (show VEGFA Antibodies)/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 (show C16orf35 Antibodies)-GFP/Flk1::myr-mCherry mice are a useful model for studying coordinated hemangiogenic and lymphangiogenic responses
Endoglin (show ENG Antibodies) prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling
CLEC14A (show CLEC14A Antibodies) acts in vascular homeostasis by fine-tuning VEGFR-2 and VEGFR-3 (show FLT4 Antibodies) signaling in endothelial cells
The elevated soluble VEGFR-2 that was found in the aortas of apoE (show APOE Antibodies)(-/-) mice with atherosclerosis binds to and diminishes the activity of VEGF-C (show VEGFC Antibodies).
Icrucumab and ramucirumab are recombinant human IgG1 monoclonal antibodies that bind vascular endothelial growth factor (VEGF) receptors 1 and 2 (VEGFR-1 and -2), respectively. VEGFR-1 activation on endothelial and tumor cell surfaces increases tumor vascularization and growth and supports tumor growth via multiple mechanisms, including contributions to angiogenesis and direct promotion of cancer cell proliferation.
REVIEW. the interplay among the ETS transcription factor (show FEV Antibodies) ETV2 (show ETV2 Antibodies), vascular endothelial growth factor, and its receptor VEGFR2/FLK1 is essential for hematopoietic and vascular development. Emerging studies also support the role of these three factors and possible interplay in hematopoietic and vascular regeneration.
DOT1L (show DOT1L Antibodies) cooperates with transcription factor ETS (show ETV7 Antibodies)-1 (show ETS1 Antibodies) to stimulate the expression of VEGFR2, thereby activating ERK1/2 (show MAPK1/3 Antibodies) and AKT (show AKT1 Antibodies) signaling pathways and promoting angiogenesis.
This study provides new insights into the mechanism of VEGFR2 dimerization and activation.
Cases with high MDSC infiltration, which was inversely correlated with intratumoral CD8(+) T-cell infiltration, exhibited shorter overall survival. In a mouse model, intratumoral MDSCs expressed both VEGFR1 and VEGFR2. VEGF expression in ovarian cancer induced MDSCs, inhibited local immunity, and contributed to poor prognosis
our results illustrated that CDK5 (show CDK5 Antibodies)-mediated KDR phosphorylation controls prolactin (show PRL Antibodies) pituitary adenoma progression and KDR pSer-229 serves as a potential prognostic biomarker for both noninvasive and invasive pituitary adenomas.
Data indicate that simultaneous targeting of molecules that control distinct phases of angiogenesis, such as ALK1 (show ACVRL1 Antibodies) and VEGFR, is a valid strategy for treatment of metastatic renal cell carcinoma (show MOK Antibodies) (mRCC).
Primary cultures derived from melanomas harboring the KDR variant were more proliferative and invasive than KDR wild type.
this study of cabozantinib (a dual VEGFR2/MET) in metastatic TNBC, while not meeting its prespecified endpoint, showed that treatment is associated with circulating biomarker changes, and is active in a subset of patients.
The efficacy and safety of VEGFR-TKIs after PD-1 (show PDCD1 Antibodies) inhibition were demonstrated in this retrospective study. The response rate was lower and the median progression-free survival was shorter in those patients who received prior PD-1 (show PDCD1 Antibodies) in combination with VEGFR-TKI. PD-1 (show PDCD1 Antibodies) exposure does not seem to significantly influence the safety of subsequent VEGFR-TKI treatment
Here we demonstrate that VEGF (show VEGFA Antibodies)-165 mediates MSC (show MSC Antibodies) differentiation into ECs via VEGFR-2-dependent induction of Sox18 (show SOX18 Antibodies), which ultimately coordinates the transcriptional upregulation of specific markers of the EC phenotype
NOS (show NOS Antibodies) stimulation via PI3K, calpain proteases, and SIRT1 (show SIRT1 Antibodies)-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 Antibodies)) and Flk-1 (KDR/VEGFR-2)in newborn piglet brain
expression of FLK1, CD146 (show MCAM Antibodies) and microvessel density of angiogenesis at the first week of reperfused acute myocardial infarction.
VEGF (show VEGFA Antibodies) supplementation at the late embryonic developmental stage might improve the developmental potential of both IVF (show SCN5A Antibodies) 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 Antibodies) 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 Antibodies)/Flk-1/Flt-1 (show FLT1 Antibodies) 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 (show FLT1 Antibodies), VEGFR-2, and TIMP-1 (show TIMP1 Antibodies), 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 Antibodies) 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 Antibodies) and VEGFR-2 are expressed at mid-luteal stages in luteal cells of corpus luteum; galectin-1 (show LGALS1 Antibodies) binds directly to asparagine-linked glycans (N-glycans) on VEGFR-2 in luteal cells.
MMP-1 (show MMP1 Antibodies) promotes VEGFR2 expression and proliferation of endothelial cells through stimulation of PAR-1 (show F2R Antibodies) and activation of NF-kappaB (show NFKB1 Antibodies)
Vascular endothelial growth factor receptor-2 activates ADP-ribosylation factor 1 (show ARF1 Antibodies) to promote endothelial nitric-oxide synthase (show NOS3 Antibodies) 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 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.
involved in sphingosine 1-phosphate-stimulated phosphorylation of Akt (show AKT1 Antibodies) and endothelial nitric-oxide synthase (eNOS (show NOS3 Antibodies))
Placenta growth factor (show PGF Antibodies) expression is regulated by both VEGF (show VEGFA Antibodies) and hyperglycaemia via VEGFR-2.
ghrelin (show GHRL Antibodies) can inhibit intraplaque angiogenesis and promote plaque stability by down-regulating VEGF (show VEGFA Antibodies) and VEGFR2 expression, inhibiting the plaque content of macrophages, and reducing MCP-1 (show CCL2 Antibodies) expression at an advanced stage of atherosclerosis in rabbits
Antenatal intratracheal VEGF (show VEGFA Antibodies) administration was associated with an increase in Flk-1 immunoreactivity.
Intronic Flk1 genetic enhancer element directs arterial-specific expression via RBPJ (show RBPJ Antibodies)-mediated venous repression.
Ca(2 (show CA2 Antibodies)+) oscillations depended upon VEGF receptor-2 (Vegfr2) and Vegfr3 (show FLT4 Antibodies) in endothelial cells budding from the dorsal aorta (DA) and posterior cardinal (show CARD8 Antibodies) vein, respectively.
Methylglyoxal acts on smaller blood vessels in zebrafish via the VEGF receptor (show FLT1 Antibodies) signaling cascade, thereby describing a new mechanism that can explain vascular complications under hyperglycemia and elevated MG concentrations.
methylation of Lys (show LYZ Antibodies)(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 Antibodies)-HSP90 (show HSP90 Antibodies) heat-shock protein axis stimulates degradation of endothelial VEGFR2.
Data indicate that the increase in FLT1/sFLT1 (show FLT1 Antibodies) 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 signaling: [miR10 (show LILRB2 Antibodies)]
Early Flk1 expression may be induced by cooperative interactions between Gata (show GATA4 Antibodies), Tcf (show HNF4A Antibodies)/Lef, Cdx (show CDX1 Antibodies) and ER71/Etv2 (show ETV2 Antibodies) under the control of Bmp, Wnt (show WNT2 Antibodies) and Fgf signaling.
Using 2 distinct pharmacologic VEGFR2 inhibitors the study shows that rap1b (show RAP1A Antibodies) 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 Antibodies); FoxH1 (show FOXH1 Antibodies) 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