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Human VEGFR2 Protein expressed in Insect Cells - ABIN809790
Hiley, Chard, Gangeswaran, Tysome, Briat, Lemoine, Wang: Vascular endothelial growth factor A promotes vaccinia virus entry into host cells via activation of the Akt pathway. in Journal of virology 2013
VEGF (show VEGFA Proteins), VEGFR2 and GSTM1 (show GSTM1 Proteins) polymorphisms in outcome of multiple myeloma patients treated with thalidomide-based regimens
In the in vitro tests, JFD-WS effectively inhibited HUVEC proliferation, migration, tube formation and VEGFR2 phosphorylation. Additionally, JFD-WS inhibited the formation of blood vessels in chick chorioallantoic membrane. While inhibiting the xenograft tumor growth in experimental mice, JFD-WS decreased the plasma MUC1 (show MUC1 Proteins) levels
The effects of Platelet-rich plasma on vascular endothelial growth factor receptor-2 (VEGFR2) and CD34 (show CD34 Proteins) expression were evaluated using real-time PCR, flow cytometry, western blot, immunocytochemistry and pathological study, as were carried out in both human umbilical endothelial cell culture and rat skin
metformin's dual effect in hyperglycemia-chemical hypoxia is mediated by direct effect on VEGFR1 (show FLT1 Proteins)/R2 leading to activation of cell migration through MMP16 (show MMP16 Proteins) and ROCK1 (show ROCK1 Proteins) upregulation, and inhibition of apoptosis by increase in phospho-ERK1/2 and FABP4 (show FABP4 Proteins), components of VEGF (show VEGFA Proteins) signaling cascades
Single nucleotide polymorphism of VEGFR2 is associated with relapse in gastroenteropancreatic neuroendocrine neoplasms.
Our data showed that ampelopsin inhibited angiogenesis with no cytotoxicity by suppressing both VEGFR2 signaling and HIF-1alpha (show HIF1A Proteins) expression. These results suggest that Hovenia dulcis Thunb. and its active compound ampelopsin exhibit potent antiangiogenic activities and therefore could be valuable for the prevention and treatment of angiogenesis-related diseases including cancer.
Authors demonstrated that when VEGFR2 was inhibited, NRP-1 (show NELL1 Proteins) appeared to regulate RAD51 (show RAD51 Proteins) expression through the VEGFR2-independent ABL-1 (show ABL1 Proteins) pathway, consequently regulating radiation sensitivity. In addition, the combined inhibition of VEGFR2 and NRP-1 (show NELL1 Proteins) appears to sensitize cancer cells to radiation.
We found that depletion of FGD5 (show FGD5 Proteins) in microvascular cells inhibited their migration towards a stable VEGFA (show VEGFA Proteins) gradient. Furthermore, depletion of FGD5 (show FGD5 Proteins) resulted in accelerated VEGFR2 degradation, which was reverted by lactacystin-mediated proteasomal inhibition. Our results thus suggest a mechanism whereby FGD5 (show FGD5 Proteins) sustains VEGFA (show VEGFA Proteins) signaling and endothelial cell chemotaxis via inhibition of proteasome-dependent VEGFR2 degradation.
ATG5 (show ATG5 Proteins) 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.
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-tKO) reduced Flk1+/PDGFRalpha- hematopoietic mesoderm, c-Kit+/CD41+ hematopoietic progenitor cell population, and the colony-forming unit activity, but increased cardiac progenitor markers as well as cardiomyocytes.
Peli1 (show PELI1 Proteins) is a proangiogenic molecule that acts downstream of VEGF (show VEGFA Proteins)-Flk-1 and restores angiogenesis and enhances skin flap (show ALOX5AP Proteins) 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 Proteins) complete knockout and FLK1-specific deletion of Sox7 (show SOX7 Proteins) lead to widespread vascular defects. In contrast, while SOX7 (show SOX7 Proteins) is expressed in the earliest specified blood progenitors, the VAV (show VAV1 Proteins)-specific deletion of Sox7 (show SOX7 Proteins) does not affect the hematopoietic system. Together, our data reveal the unique role of SOX7 (show SOX7 Proteins) in vasculogenesis and angiogenesis during embryonic development.
JAM-C (show JAM3 Proteins) 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 Proteins), is indispensable for maintenance of thyroid vascular integrity. Notably, blockade of VEGF-A (show VEGFA Proteins) 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 Proteins) and KDR are co-expressed in Sertoli cells of the testes and somatic cells of embryonic ovaries. Furthermore, WT1 (show WT1 Proteins) bound to the Kdr promoter in the chromatin of embryonic testes and ovaries. KDR signaling represses the testis-promoting gene Sox9 (show SOX9 Proteins) in embryonic XX gonads
This is the first report demonstrating the spatiotemporal expression patterns of Flk1 and Flt1 (show FLT1 Proteins) 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 Proteins)-165 mediates MSC (show MSC Proteins) differentiation into ECs via VEGFR-2-dependent induction of Sox18 (show SOX18 Proteins), which ultimately coordinates the transcriptional upregulation of specific markers of the EC phenotype
NOS stimulation via PI3K, calpain proteases, and SIRT1 (show SIRT1 Proteins)-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 Proteins)) and Flk-1 (KDR/VEGFR-2)in newborn piglet brain
expression of FLK1, CD146 (show MCAM Proteins) and microvessel density of angiogenesis at the first week of reperfused acute myocardial infarction.
VEGF (show VEGFA Proteins) supplementation at the late embryonic developmental stage might improve the developmental potential of both IVF (show SCN5A Proteins) 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 Proteins) system is associated with increased placental vascular density observed with the advancement of gestation in the pig
VEGF (show VEGFA Proteins) ligand-receptor system may play an important role in the development and maintenance of the corpus luteum in pigs.
VEGF (show VEGFA Proteins)/Flk-1/Flt-1 (show FLT1 Proteins) system is activated during myocardial ischemia reperfusion injury.
Hemodialysis graft placement leads to early increases in wall shear stress, VEGF-A (show VEGFA Proteins), pro-MMP-9 (show MMP9 Proteins), MMP-2 (show MMP2 Proteins), VEGFR-1 (show FLT1 Proteins), VEGFR-2, and TIMP-1 (show TIMP1 Proteins), 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 Proteins) 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 Proteins) receptors; but follicular dominance is related to a reduction in the mRNA expression of sVEGFR1 and sVEGFR2.
Data suggest that galectin-1 (show LGALS1 Proteins) and VEGFR-2 are expressed at mid-luteal stages in luteal cells of corpus luteum; galectin-1 (show LGALS1 Proteins) binds directly to asparagine-linked glycans (N-glycans) on VEGFR-2 in luteal cells.
MMP-1 (show MMP1 Proteins) promotes VEGFR2 expression and proliferation of endothelial cells through stimulation of PAR-1 (show F2R Proteins) and activation of NF-kappaB (show NFKB1 Proteins)
Vascular endothelial growth factor receptor-2 activates ADP-ribosylation factor 1 (show ARF1 Proteins) to promote endothelial nitric-oxide synthase (show NOS3 Proteins) 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 Proteins) and bFGF (show FGF2 Proteins) 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 Proteins) and endothelial nitric-oxide synthase (eNOS (show NOS3 Proteins))
Placenta growth factor (show PGF Proteins) expression is regulated by both VEGF (show VEGFA Proteins) and hyperglycaemia via VEGFR-2.
These results indicate that VEGF-C (show VEGFC Proteins)-induced MSC (show MSC Proteins) osteogenesis is mediated through VEGFR2 and VEGFR3 (show FLT4 Proteins), and followed the activation of the ERK (show MAPK1 Proteins)/RUNX2 (show RUNX2 Proteins) signaling pathway.
High VEGFR2 expression is associated with retinal neovascularization.
ghrelin (show GHRL Proteins) can inhibit intraplaque angiogenesis and promote plaque stability by down-regulating VEGF (show VEGFA Proteins) and VEGFR2 expression, inhibiting the plaque content of macrophages, and reducing MCP-1 (show CCL2 Proteins) expression at an advanced stage of atherosclerosis in rabbits
Antenatal intratracheal VEGF (show VEGFA Proteins) administration was associated with an increase in Flk-1 immunoreactivity.
Intronic Flk1 genetic enhancer element directs arterial-specific expression via RBPJ (show RBPJ Proteins)-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