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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 (zeige VEGFA Proteine), VEGFR2 and GSTM1 (zeige GSTM1 Proteine) 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 (zeige MUC1 Proteine) levels
The effects of Platelet-rich plasma on vascular endothelial growth factor receptor-2 (VEGFR2) and CD34 (zeige CD34 Proteine) 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 (zeige FLT1 Proteine)/R2 leading to activation of cell migration through MMP16 (zeige MMP16 Proteine) and ROCK1 (zeige ROCK1 Proteine) upregulation, and inhibition of apoptosis by increase in phospho-ERK1/2 and FABP4 (zeige FABP4 Proteine), components of VEGF (zeige VEGFA Proteine) 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 (zeige HIF1A Proteine) 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 (zeige NELL1 Proteine) appeared to regulate RAD51 (zeige RAD51 Proteine) expression through the VEGFR2-independent ABL-1 (zeige ABL1 Proteine) pathway, consequently regulating radiation sensitivity. In addition, the combined inhibition of VEGFR2 and NRP-1 (zeige NELL1 Proteine) appears to sensitize cancer cells to radiation.
We found that depletion of FGD5 (zeige FGD5 Proteine) in microvascular cells inhibited their migration towards a stable VEGFA (zeige VEGFA Proteine) gradient. Furthermore, depletion of FGD5 (zeige FGD5 Proteine) resulted in accelerated VEGFR2 degradation, which was reverted by lactacystin-mediated proteasomal inhibition. Our results thus suggest a mechanism whereby FGD5 (zeige FGD5 Proteine) sustains VEGFA (zeige VEGFA Proteine) signaling and endothelial cell chemotaxis via inhibition of proteasome-dependent VEGFR2 degradation.
ATG5 (zeige ATG5 Proteine) 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 (zeige PELI1 Proteine) is a proangiogenic molecule that acts downstream of VEGF (zeige VEGFA Proteine)-Flk-1 and restores angiogenesis and enhances skin flap (zeige ALOX5AP Proteine) 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 (zeige SOX7 Proteine) complete knockout and FLK1-specific deletion of Sox7 (zeige SOX7 Proteine) lead to widespread vascular defects. In contrast, while SOX7 (zeige SOX7 Proteine) is expressed in the earliest specified blood progenitors, the VAV (zeige VAV1 Proteine)-specific deletion of Sox7 (zeige SOX7 Proteine) does not affect the hematopoietic system. Together, our data reveal the unique role of SOX7 (zeige SOX7 Proteine) in vasculogenesis and angiogenesis during embryonic development.
JAM-C (zeige JAM3 Proteine) 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 (zeige FLT4 Proteine), is indispensable for maintenance of thyroid vascular integrity. Notably, blockade of VEGF-A (zeige VEGFA Proteine) 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 (zeige WT1 Proteine) and KDR are co-expressed in Sertoli cells of the testes and somatic cells of embryonic ovaries. Furthermore, WT1 (zeige WT1 Proteine) bound to the Kdr promoter in the chromatin of embryonic testes and ovaries. KDR signaling represses the testis-promoting gene Sox9 (zeige SOX9 Proteine) in embryonic XX gonads
This is the first report demonstrating the spatiotemporal expression patterns of Flk1 and Flt1 (zeige FLT1 Proteine) 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 (zeige VEGFA Proteine)-165 mediates MSC (zeige MSC Proteine) differentiation into ECs via VEGFR-2-dependent induction of Sox18 (zeige SOX18 Proteine), which ultimately coordinates the transcriptional upregulation of specific markers of the EC phenotype
NOS stimulation via PI3K, calpain proteases, and SIRT1 (zeige SIRT1 Proteine)-dependent deacetylation downstream from VEGFR2 activation contributes to these vasodilator responses.
we analyzed the expression and cellular distribution of Flt-1(VEGFR-1 (zeige FLT1 Proteine)) and Flk-1 (KDR/VEGFR-2)in newborn piglet brain
expression of FLK1, CD146 (zeige MCAM Proteine) and microvessel density of angiogenesis at the first week of reperfused acute myocardial infarction.
VEGF (zeige VEGFA Proteine) supplementation at the late embryonic developmental stage might improve the developmental potential of both IVF (zeige SCN5A Proteine) 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 (zeige FLT1 Proteine) system is associated with increased placental vascular density observed with the advancement of gestation in the pig
VEGF (zeige VEGFA Proteine) ligand-receptor system may play an important role in the development and maintenance of the corpus luteum in pigs.
VEGF (zeige VEGFA Proteine)/Flk-1/Flt-1 (zeige FLT1 Proteine) system is activated during myocardial ischemia reperfusion injury.
Hemodialysis graft placement leads to early increases in wall shear stress, VEGF-A (zeige VEGFA Proteine), pro-MMP-9 (zeige MMP9 Proteine), MMP-2 (zeige MMP2 Proteine), VEGFR-1 (zeige FLT1 Proteine), VEGFR-2, and TIMP-1 (zeige TIMP1 Proteine), 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 (zeige TGFB1 Proteine) 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 (zeige VEGFA Proteine) receptors; but follicular dominance is related to a reduction in the mRNA expression of sVEGFR1 and sVEGFR2.
Data suggest that galectin-1 (zeige LGALS1 Proteine) and VEGFR-2 are expressed at mid-luteal stages in luteal cells of corpus luteum; galectin-1 (zeige LGALS1 Proteine) binds directly to asparagine-linked glycans (N-glycans) on VEGFR-2 in luteal cells.
MMP-1 (zeige MMP1 Proteine) promotes VEGFR2 expression and proliferation of endothelial cells through stimulation of PAR-1 (zeige F2R Proteine) and activation of NF-kappaB (zeige NFKB1 Proteine)
Vascular endothelial growth factor receptor-2 activates ADP-ribosylation factor 1 (zeige ARF1 Proteine) to promote endothelial nitric-oxide synthase (zeige NOS3 Proteine) 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 (zeige VEGFA Proteine) and bFGF (zeige FGF2 Proteine) 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 (zeige AKT1 Proteine) and endothelial nitric-oxide synthase (eNOS (zeige NOS3 Proteine))
Placenta growth factor (zeige PGF Proteine) expression is regulated by both VEGF (zeige VEGFA Proteine) and hyperglycaemia via VEGFR-2.
These results indicate that VEGF-C (zeige VEGFC Proteine)-induced MSC (zeige MSC Proteine) osteogenesis is mediated through VEGFR2 and VEGFR3 (zeige FLT4 Proteine), and followed the activation of the ERK (zeige MAPK1 Proteine)/RUNX2 (zeige RUNX2 Proteine) signaling pathway.
High VEGFR2 expression is associated with retinal neovascularization.
ghrelin (zeige GHRL Proteine) can inhibit intraplaque angiogenesis and promote plaque stability by down-regulating VEGF (zeige VEGFA Proteine) and VEGFR2 expression, inhibiting the plaque content of macrophages, and reducing MCP-1 (zeige CCL2 Proteine) expression at an advanced stage of atherosclerosis in rabbits
Antenatal intratracheal VEGF (zeige VEGFA Proteine) administration was associated with an increase in Flk-1 immunoreactivity.
Intronic Flk1 genetic enhancer element directs arterial-specific expression via RBPJ (zeige RBPJ Proteine)-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