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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
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 37 Pubmed References
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
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
Human Monoclonal VEGFR2 Primary Antibody for FACS - ABIN4896282
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 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
Hamster Polyclonal VEGFR2 Primary Antibody for ICC, IF - ABIN250774
Gluzman-Poltorak, Cohen, Shibuya, Neufeld: Vascular endothelial growth factor receptor-1 and neuropilin-2 form complexes. in The Journal of biological chemistry 2001
Show all 7 Pubmed References
Mouse (Murine) Monoclonal VEGFR2 Primary Antibody for IHC (f), IHC (fro) - ABIN2689505
Hanahan: Signaling vascular morphogenesis and maintenance. in Science (New York, N.Y.) 1997
Show all 5 Pubmed References
Human Monoclonal VEGFR2 Primary Antibody for FACS - ABIN4896286
De Biasi, Cerri, Bianchini, Gibellini, Persiani, Montanari, Luppi, Carbonelli, Zucchi, Bocchino, Zamparelli, Vancheri, Sgalla, Richeldi, Cossarizza: Levels of circulating endothelial cells are low in idiopathic pulmonary fibrosis and are further reduced by anti-fibrotic treatments. in BMC medicine 2015
Show all 5 Pubmed References
Human Polyclonal VEGFR2 Primary Antibody for CyTOF, FACS - ABIN4900629
Pfister, Pfrommer, Tatagiba, Roser: Vascular endothelial growth factor signals through platelet-derived growth factor receptor β in meningiomas in vitro. in British journal of cancer 2012
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Authors demonstrated that when VEGFR2 was inhibited, NRP-1 (show NELL1 Antibodies) appeared to regulate RAD51 (show RAD51 Antibodies) expression through the VEGFR2-independent ABL-1 (show ABL1 Antibodies) pathway, consequently regulating radiation sensitivity. In addition, the combined inhibition of VEGFR2 and NRP-1 (show NELL1 Antibodies) appears to sensitize cancer cells to radiation.
We found that depletion of FGD5 (show FGD5 Antibodies) in microvascular cells inhibited their migration towards a stable VEGFA (show VEGFA Antibodies) gradient. Furthermore, depletion of FGD5 (show FGD5 Antibodies) resulted in accelerated VEGFR2 degradation, which was reverted by lactacystin-mediated proteasomal inhibition. Our results thus suggest a mechanism whereby FGD5 (show FGD5 Antibodies) sustains VEGFA (show VEGFA Antibodies) signaling and endothelial cell chemotaxis via inhibition of proteasome-dependent VEGFR2 degradation.
ATG5 (show ATG5 Antibodies) and phospho-KDR expression was strongly associated with the density of vasculogenic mimicry in tumors and poor clinical outcome.
Increased expression of VEGFR2 correlated with differentiation.
DDA exhibits anti-angiogenic properties through suppressing VEGF-A (show VEGFA Antibodies) and VEGFR2 signaling
RCAN1.4 plays a novel role in regulating endothelial cell migration by establishing endothelial cell polarity in response to VEGF (show VEGFA Antibodies).
Anlotinib occupied the ATP-binding pocket of VEGFR2 tyrosine kinase (show TXK Antibodies).
the difference between the pro- (VEGF165a) and antiangiogenic (VEGF165b) VEGF (show VEGFA Antibodies) isoforms and its soluble receptors for severity of diabetic retinopathy, is reported.
anlotinib inhibits the activation of VEGFR2, PDGFRbeta and FGFR1 (show FGFR1 Antibodies) as well their common downstream ERK (show EPHB2 Antibodies) signaling
upregulation of sVEGFR-1 with concomitant decline of PECAM-1 (show PECAM1 Antibodies) and sVEGFR-2 levels in preeclampsia compared to normotensive pregnancies, Irrespective of the HIV status
Inositol 1,4,5-trisphosphate receptors (IP3Rs) are required for the hematopoietic and cardiac fate divergence of mouse embryonic stem cells. Deletion of IP3Rs (IP3R (show ITPR1 Antibodies)-tKO (show MRPS12 Antibodies)) reduced Flk1+/PDGFRalpha- hematopoietic mesoderm, c-Kit (show KIT Antibodies)+/CD41+ hematopoietic progenitor cell population, and the colony-forming unit activity, but increased cardiac progenitor markers as well as cardiomyocytes.
Peli1 (show PELI1 Antibodies) is a proangiogenic molecule that acts downstream of VEGF (show VEGFA Antibodies)-Flk-1 and restores angiogenesis and enhances skin flap (show ALOX5AP Antibodies) survivability
KDR/Flk-1 expression was revealed in mononuclear cells of the necrotic area (macrophages and fibroblast cells). The distribution of KDR/Flk-1 remained practically unchanged with lengthening of the postinfarction period (more than 7 days).
By E10.5, both Sox7 (show SOX7 Antibodies) complete knockout and FLK1-specific deletion of Sox7 (show SOX7 Antibodies) lead to widespread vascular defects. In contrast, while SOX7 (show SOX7 Antibodies) is expressed in the earliest specified blood progenitors, the VAV (show VAV1 Antibodies)-specific deletion of Sox7 (show SOX7 Antibodies) does not affect the hematopoietic system. Together, our data reveal the unique role of SOX7 (show SOX7 Antibodies) in vasculogenesis and angiogenesis during embryonic development.
JAM-C (show JAM3 Antibodies) plays an important role in maintaining VEGR2 expression to promote retinal pigment epithelial cell survival under oxidative stress.
Genetic depletion experiments revealed that VEGFR2, but not VEGFR3 (show FLT4 Antibodies), is indispensable for maintenance of thyroid vascular integrity. Notably, blockade of VEGF-A (show VEGFA Antibodies) or VEGFR2 not only abrogated vascular remodeling but also inhibited follicular hypertrophy, which led to the reduction of thyroid weights during goitrogenesis.
Eriocalyxin B inhibited breast tumor angiogenesis by suppressing VEGFR-2 signaling.
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.
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 (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/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 (show VEGFA Antibodies) 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.
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.
High VEGFR2 expression is associated with retinal neovascularization.
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.
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.
fetal liver kinase 1
, fetal liver kinase-1
, protein-tyrosine kinase receptor Flk-1
, soluble VEGFR2
, tyrosine kinase growth factor receptor
, vascular endothelial growth factor receptor 2
, VEGF receptor-2
, 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
, flk-1 receptor
, protein-tyrosine kinase
, flk-1 type VEGF receptor
, 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