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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. dans Journal of virology 2013
miR (Montrer MLXIP Protéines)-195 suppresses cell proliferation of ovarian cancer cells through regulation of VEGFR2 and AKT (Montrer AKT1 Protéines) signaling pathways.
Thioredoxin-interacting protein (TXNIP (Montrer TXNIP Protéines)) is highly induced in retinal vascular endothelial cells under diabetic conditions. Data (including data from studies using knockout mice) suggest that TXNIP (Montrer TXNIP Protéines) in retinal vascular endothelial cells plays role in diabetic retinal angiogenesis via VEGF (Montrer VEGFA Protéines)/VEGFR2 and Akt (Montrer AKT1 Protéines)/mTOR (Montrer FRAP1 Protéines) signaling.
Inhibition of FPR1 (Montrer FPR1 Protéines) and/or NADPH oxidase (Montrer NOX1 Protéines) functions prevents VEGFR2 transactivation and the triggering of the downstream signalling cascades.
VEGFA (Montrer VEGFA Protéines) activates VEGFR1 (Montrer FLT1 Protéines) homodimers and AKT (Montrer AKT1 Protéines), leading to a cytoprotective response, whilst abluminal VEGFA (Montrer VEGFA Protéines) induces vascular leakage via VEGFR2 homodimers and p38 (Montrer CRK Protéines)
association of rs519664[T] in TTC39B on 9p22 with endometriosis, is reported.
VEGF (Montrer VEGFA Protéines), VEGFR2 and GSTM1 (Montrer GSTM1 Protéines) 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 (Montrer MUC1 Protéines) levels
The effects of Platelet-rich plasma on vascular endothelial growth factor receptor-2 (VEGFR2) and CD34 (Montrer CD34 Protéines) 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 (Montrer FLT1 Protéines)/R2 leading to activation of cell migration through MMP16 (Montrer MMP16 Protéines) and ROCK1 (Montrer ROCK1 Protéines) upregulation, and inhibition of apoptosis by increase in phospho-ERK1/2 and FABP4 (Montrer FABP4 Protéines), components of VEGF (Montrer VEGFA Protéines) signaling cascades
Single nucleotide polymorphism of VEGFR2 is associated with relapse in gastroenteropancreatic neuroendocrine neoplasms.
significant increase in VEGFR-2 promoter activity after partial hepatectomy
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 (Montrer PELI1 Protéines) is a proangiogenic molecule that acts downstream of VEGF (Montrer VEGFA Protéines)-Flk-1 and restores angiogenesis and enhances skin flap (Montrer ALOX5AP Protéines) 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 (Montrer SOX7 Protéines) complete knockout and FLK1-specific deletion of Sox7 (Montrer SOX7 Protéines) lead to widespread vascular defects. In contrast, while SOX7 (Montrer SOX7 Protéines) is expressed in the earliest specified blood progenitors, the VAV (Montrer VAV1 Protéines)-specific deletion of Sox7 (Montrer SOX7 Protéines) does not affect the hematopoietic system. Together, our data reveal the unique role of SOX7 (Montrer SOX7 Protéines) in vasculogenesis and angiogenesis during embryonic development.
JAM-C (Montrer JAM3 Protéines) 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 (Montrer FLT4 Protéines), is indispensable for maintenance of thyroid vascular integrity. Notably, blockade of VEGF-A (Montrer VEGFA Protéines) 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 (Montrer WT1 Protéines) and KDR are co-expressed in Sertoli cells of the testes and somatic cells of embryonic ovaries. Furthermore, WT1 (Montrer WT1 Protéines) bound to the Kdr promoter in the chromatin of embryonic testes and ovaries. KDR signaling represses the testis-promoting gene Sox9 (Montrer SOX9 Protéines) in embryonic XX gonads
Here we demonstrate that VEGF (Montrer VEGFA Protéines)-165 mediates MSC (Montrer MSC Protéines) differentiation into ECs via VEGFR-2-dependent induction of Sox18 (Montrer SOX18 Protéines), which ultimately coordinates the transcriptional upregulation of specific markers of the EC phenotype
NOS stimulation via PI3K, calpain proteases, and SIRT1 (Montrer SIRT1 Protéines)-dependent deacetylation downstream from VEGFR2 activation contributes to these vasodilator responses.
we analyzed the expression and cellular distribution of Flt-1(VEGFR-1 (Montrer FLT1 Protéines)) and Flk-1 (KDR/VEGFR-2)in newborn piglet brain
expression of FLK1, CD146 (Montrer MCAM Protéines) and microvessel density of angiogenesis at the first week of reperfused acute myocardial infarction.
VEGF (Montrer VEGFA Protéines) supplementation at the late embryonic developmental stage might improve the developmental potential of both IVF (Montrer SCN5A Protéines) 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 (Montrer FLT1 Protéines) system is associated with increased placental vascular density observed with the advancement of gestation in the pig
VEGF (Montrer VEGFA Protéines) ligand-receptor system may play an important role in the development and maintenance of the corpus luteum in pigs.
VEGF (Montrer VEGFA Protéines)/Flk-1/Flt-1 (Montrer FLT1 Protéines) system is activated during myocardial ischemia reperfusion injury.
Hemodialysis graft placement leads to early increases in wall shear stress, VEGF-A (Montrer VEGFA Protéines), pro-MMP-9 (Montrer MMP9 Protéines), MMP-2 (Montrer MMP2 Protéines), VEGFR-1 (Montrer FLT1 Protéines), VEGFR-2, and TIMP-1 (Montrer TIMP1 Protéines), which may contribute to the development of venous stenosis.
VEGFR2 expression in the oviducts.
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 (Montrer TGFB1 Protéines) 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 (Montrer VEGFA Protéines) receptors; but follicular dominance is related to a reduction in the mRNA expression of sVEGFR1 and sVEGFR2.
Data suggest that galectin-1 (Montrer LGALS1 Protéines) and VEGFR-2 are expressed at mid-luteal stages in luteal cells of corpus luteum; galectin-1 (Montrer LGALS1 Protéines) binds directly to asparagine-linked glycans (N-glycans) on VEGFR-2 in luteal cells.
MMP-1 (Montrer MMP1 Protéines) promotes VEGFR2 expression and proliferation of endothelial cells through stimulation of PAR-1 (Montrer F2R Protéines) and activation of NF-kappaB (Montrer NFKB1 Protéines)
Vascular endothelial growth factor receptor-2 activates ADP-ribosylation factor 1 (Montrer ARF1 Protéines) to promote endothelial nitric-oxide synthase (Montrer NOS3 Protéines) 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 (Montrer VEGFA Protéines) and bFGF (Montrer FGF2 Protéines) 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 (Montrer AKT1 Protéines) and endothelial nitric-oxide synthase (eNOS (Montrer NOS3 Protéines))
These results indicate that VEGF-C (Montrer VEGFC Protéines)-induced MSC (Montrer MSC Protéines) osteogenesis is mediated through VEGFR2 and VEGFR3 (Montrer FLT4 Protéines), and followed the activation of the ERK (Montrer MAPK1 Protéines)/RUNX2 (Montrer RUNX2 Protéines) signaling pathway.
High VEGFR2 expression is associated with retinal neovascularization.
ghrelin (Montrer GHRL Protéines) can inhibit intraplaque angiogenesis and promote plaque stability by down-regulating VEGF (Montrer VEGFA Protéines) and VEGFR2 expression, inhibiting the plaque content of macrophages, and reducing MCP-1 (Montrer CCL2 Protéines) expression at an advanced stage of atherosclerosis in rabbits
Antenatal intratracheal VEGF (Montrer VEGFA Protéines) administration was associated with an increase in Flk-1 immunoreactivity.
Intronic Flk1 genetic enhancer element directs arterial-specific expression via RBPJ (Montrer RBPJ Protéines)-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