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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
FGF9-induced ovarian cancer cell invasion involves VEGFA/VEGFR2 augmentation by virtue of ETS1 upregulation and metabolic reprogramming.
results disclose unexpected novel roles of VEGFR2 and VEGF-C in the process of EMT of retinal pigment epithelial (RPE) cells and in the Hippo pathway. The data shown here demonstrated that VEGFR2 and VEGF-C are important to maintain the normal physiological state of RPE cells.
"CAGT" haplotype of the KDR gene alters high-grade glioma aggressiveness and risk of grade IV tumors.
Our results demonstrated that simultaneous blockade of VEGFR1/VEGFR2 is an effective strategy to fight solid tumors by targeting a wider range of mediators involved in tumor angiogenesis, growth, and metastasis.
These results provide mechanistic insights into the critical role played by Galphai1/3 proteins in VEGF-induced VEGFR2 endocytosis, signaling and angiogenesis.
Our findings suggest that ACE2, as a potential resister to breast cancer, might inhibit breast cancer angiogenesis through the VEGFa/VEGFR2/ERK pathway.
Rising circulating VEGFA levels in patients with ABC, treated with CisGem, are associated with worse PFS and OS, not seen in patients receiving cediranib. Rising levels of markers of tumour burden (CK18) and potential resistance (VEGFR2) are associated with worse outcomes and warrant validation.
VEGF can impair the migration capacity and immune function of mDCs through the RhoA-cofilin1 pathway mediated by the VEGF receptor 2.
The genetic evaluation revealed two novel variants in KDR and KRIT1 genes causing cystic hygroma.
Our finding shows that elevation of serum level of IL-33, IL-37, and sVEGFR2 in patients with MS is correlated to disease severity.
Loss-of-function variants in FLT4 and KDR contribute substantially to the genetic basis of tetralogy of Fallot (TOF). The findings support dysregulated VEGF signaling as a novel mechanism contributing to the pathogenesis of TOF.
Authors demonstrate the presence of homo-interactions between NRP1 molecules, as well as hetero-interactions between NRP1 and VEGFR2 molecules, in the plasma membrane. Our results underscore the complex nature of the interactions between self-associating receptors, co-receptors, and their ligands in the plasma membrane.
VEGFR-2 (KDR) polymorphism does not influence recurrent pregnancy loss susceptibility.
the findings of this study suggested that d2HG induced angiogenic activity via VEGFR2 signaling and increased MMP2 activity.
Sox7 promotes tumor growth via vessel abnormalization, and its level determines the therapeutic outcome of VEGFR2 inhibition in High-grade glioma.
R11-3 was truncated in size, and its potential in endothelial targeted therapeutics was established using VEGFR2 targeting long interfering RNA (liRNA) aptamer chimera.
ARF6 is pivotal in VEGFR2 trafficking and that targeting ARF6-mediated VEGFR2 trafficking has potential as a therapeutic approach for retinal vascular diseases such as diabetic retinopathy.
high VEGFR-1 and low VEGFR-2 expression in endothelial cells appear to be involved in the progression of colorectal cancer.
these findings indicate potential angiogenic templates and their binding levels with VEGFR-2; sorted viewpoints could be useful as a promising way to describe potential angiogenesis inhibitors with related molecular targets
Survivin in the signal downstream of VEGFR2 played an important role in esophageal cancer cell survival.
Endogenous acetylcholine plays an up-regulatory role for VEGFR2 expression in neurons and astrocytes via different mechanisms.
Taken together, data demonstrated that MG induced angiogenic impairment in endothelial progenitor cells via alterations in the AGE/RAGE-VEGFR-2 pathway which may be utilized in the development of potential therapeutic and preventive targets for diabetic vascular complications.
FAK regulated the expression of VEGFR2, a central mediator of various EC functions and angiogenesis, which requires both FAK kinase activity and its translocation into the nucleus.
VEGF accelerates compensatory lung growth in mice by increasing the alveolar units in a process medicated by VEGFR2 and EGF
VEGFR-2 is expressed on the hair follicles of the dorsum of the mouse and varies in expression on the mouse hair follicles during hair cycling
These results implicate RABEP2 as a key modulator of VEGFR2 endosomal trafficking, and demonstrate the importance of RABEP2 and Rab4 for VEGFR2 signaling in endothelial cells.
Dimethyloxalylglycine protective effect on the neonatal intestinal mucosa may be mediated via VEGFR2 dependent improvement of the intestinal microvasculature
uPARAP controlVEGFR-2/VEGFR-3 heterodimerisation during pathological lymphangiogenesis.
endoglin promoted VEGF-induced tip cell formation. Mechanistically, endoglin interacted with VEGF receptor (VEGFR)-2 in a VEGF-dependent manner, which sustained VEGFR2 on the cell surface and prevented its degradation. Endoglin mutants deficient in the ability to interact with VEGFR2 failed to sustain VEGFR2 on the cell surface and to promote VEGF-induced tip cell formation.
VEGFR2 has a key role in the proangiogenic effects of rHDL in hypoxia/ischemia.
Studied expression of vascular endothelial growth factor receptor 2 (VEGFR2) in nulliparous and parous mice.
Oleanolic acid was verified as a VEGFR-2 binding chemical from anticancer herbs with similar binding affinity as a reference drug in the Protein Data Bank (PDB) entry 3CJG of model A coordination.
VEGFR2 is regulated by deSUMOylation during pathological angiogenesis.
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 is a proangiogenic molecule that acts downstream of VEGF-Flk-1 and restores angiogenesis and enhances skin flap 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 complete knockout and FLK1-specific deletion of Sox7 lead to widespread vascular defects. In contrast, while SOX7 is expressed in the earliest specified blood progenitors, the VAV-specific deletion of Sox7 does not affect the hematopoietic system. Together, our data reveal the unique role of SOX7 in vasculogenesis and angiogenesis during embryonic development.
JAM-C plays an important role in maintaining VEGR2 expression to promote retinal pigment epithelial cell survival under oxidative stress.
Here we demonstrate that VEGF-165 mediates MSC differentiation into ECs via VEGFR-2-dependent induction of Sox18, which ultimately coordinates the transcriptional upregulation of specific markers of the EC phenotype
NOS stimulation via PI3K, calpain proteases, and SIRT1-dependent deacetylation downstream from VEGFR2 activation contributes to these vasodilator responses.
we analyzed the expression and cellular distribution of Flt-1(VEGFR-1) and Flk-1 (KDR/VEGFR-2)in newborn piglet brain
expression of FLK1, CD146 and microvessel density of angiogenesis at the first week of reperfused acute myocardial infarction.
VEGF supplementation at the late embryonic developmental stage might improve the developmental potential of both IVF 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 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/Flk-1/Flt-1 system is activated during myocardial ischemia reperfusion injury.
Hemodialysis graft placement leads to early increases in wall shear stress, VEGF-A, pro-MMP-9, MMP-2, VEGFR-1, VEGFR-2, and TIMP-1, which may contribute to the development of venous stenosis.
binding of Neuropilin-1 to VEGFR-2 requires the PDZ-binding domain of neuropilin-1
in experimental intervertebral disc degeneration, VEGF receptors were expressed in the damaged disc and paradiscal tissues
the inhibitory effect of PEDF appears to be mediated via the processing of VEGF-R2 by gamma-secretase
This mechanism may permit differential control of flow and ligand activation of flk-1 receptor in the presence of ligands.
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 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 and VEGFR-2 are expressed at mid-luteal stages in luteal cells of corpus luteum; galectin-1 binds directly to asparagine-linked glycans (N-glycans) on VEGFR-2 in luteal cells.
MMP-1 promotes VEGFR2 expression and proliferation of endothelial cells through stimulation of PAR-1 and activation of NF-kappaB
The changes of sVEGFR-1 and sVEGFR-2 with the age of the bovine dominant follicle indicate a physiological role in its growth and atresia.
Vascular endothelial growth factor receptor-2 activates ADP-ribosylation factor 1 to promote endothelial nitric-oxide synthase 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 and bFGF 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 and endothelial nitric-oxide synthase (eNOS)
Placenta growth factor expression is regulated by both VEGF and hyperglycaemia via VEGFR-2.
ROS induce expression not only of VEGF but also of VEGFR2. VEGFR2 increase by ROS is mainly driven through a NF-kappaB-dependent pathway.
By regulating VEGFR2 expression and activation, PKC-epsilon expression is critical for activation of Akt and eNOS by VEGF and contributes to VEGF-stimulated Erk activation, whereas PKC-alpha has opposite effects.
These results indicate that VEGF-C-induced MSC osteogenesis is mediated through VEGFR2 and VEGFR3, and followed the activation of the ERK/RUNX2 signaling pathway.
High expression of VEGF-A/VEGFR-2 and FGF-2/FGFR-1 but not of PDGF-BB/PDGFR-beta may contribute to immature and inflammatory intraplaque angiogenesis and plaque instability in a rabbit model of atherosclerosis.
High VEGFR2 expression is associated with retinal neovascularization.
ghrelin can inhibit intraplaque angiogenesis and promote plaque stability by down-regulating VEGF and VEGFR2 expression, inhibiting the plaque content of macrophages, and reducing MCP-1 expression at an advanced stage of atherosclerosis in rabbits
Antenatal intratracheal VEGF administration was associated with an increase in Flk-1 immunoreactivity.
Intronic Flk1 genetic enhancer element directs arterial-specific expression via RBPJ-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