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Human VEGFC Protein expressed in Escherichia coli (E. coli) - ABIN413872
Werchau, Toberer, Enk, Dammann, Helmbold: Merkel cell carcinoma induces lymphatic microvessel formation. in Journal of the American Academy of Dermatology 2011
Show all 6 Pubmed References
Overall, the data show that HHEX controls blood vessel and lymphatic vessel formation by regulating the VEGFC/FLT4/PROX1 signaling axis.
These findings thus underscore a role for posterior cardinal vein and VegfC in patterning the head kidney prior to organ assembly and function.
Vegfc acts through ERK to induce sprouting and differentiation of trunk lymphatic progenitors.
data not only reveal a non-canonical function of Mt2 in angiogenesis, but also propose Mt2 as a novel regulator of vegfc expression.
Vegfc signaling increases mafba expression to control downstream transcription
Vegfc is dispensable for facial lymphatic sprouting but not for the complete development of the facial lymphatic network.
In the embryo, phenotypes driven by increased Vegfc are suppressed in the absence of Ccbe1, and Vegfc-driven sprouting is enhanced by local Ccbe1 overexpression. Moreover, Vegfc- and Vegfr3-dependent Erk signaling is impaired in the absence of Ccbe1.
Vegfc has an essential role in lymphangiogenesis [review]
The parallel growth of motoneuron axons with the dorsal aorta depends on Vegfc/Vegfr3 signaling in zebrafish.
Vegfc acts in two distinct modes during development: as a paracrine factor secreted from arteries to guide closely associated lymphatic vasculature and as an autocrine factor to drive migratory persistence during angiogenesis.
Rspo1-Wnt-VegfC-Vegfr3 signaling plays a crucial role as an endothelial-autonomous permissive cue for developmental angiogenesis.
Here, we show that vascular endothelial growth factor C (Vegfc), an angiogenic as well as a lymphangiogenic factor, is unexpectedly involved in this process in zebrafish.
The development of lymphatic vessels in zebrafish embyros depends on Vegfc signaling.
vegfc signalling is suppressed by Dll4 in developing zebrafish intersegmental arteries.
VEGF-C and VEGF-C156S genes have roles in the pro-lymphangiogenic growth factor therapy of lymphedema
Transcription of the vascular endothelial growth factor C gene (VEGF-C) and translation of the corresponding protein were significantly up-regulated in swine umbilical vein endothelial cells with classical swine fever virus acute infection.
No difference in bioactivity was detected between porcine relaxin-1 and recombinant human relaxin-2 in either mice or rats.
During progressive ischemia, functional and metabolic benefits of intramyocardial VEGF-C gene transfer were apparent. VEGF-C-induced collateral formation occurred at the site of gene transfer
Efficient activation of the lymphangiogenic growth factor VEGF-C requires the C-terminal domain of VEGF-C and the N-terminal domain of CCBE1.
A possible mechanism has been proposed of the TGF-beta-VEGF-C pathway in which TGF-beta promotes VEGF-C production in tubular epithelial cells, macrophages, and mesothelial cells, leading to lymphangiogenesis in renal and peritoneal fibrosis. (Review)
The mutation induced skipping of exon 2 of VEGFC resulting in a frameshift and the introduction of a premature stop codon (p.Ala50ValfsTer18). The mutation leads to a loss of the entire VEGF-homology domain and the C-terminus.
VEGFR-3 and CAV3 expression demonstrated immunohistochemically in SMCs of the tunica media of SV grafts predicted their early restenosis in triple-vessel CAD patients. CAV2 protein expression in SMCs of ITA grafts indicated the risk of early graft failure both in double-vessel and triple-vessel CAD subjects.
VEGF-C expression and secretion in gastric cancer is downregulated by kallistatin.
Concomitant high expression of survivin and VEGF-C is closely associated with LNM status of PTC patients, which suggests their cooperation in the metastatic process.
TNFSF15, a cytokine mainly produced by blood endothelial cells, facilitates tumor lymphangiogenesis by upregulating VEGFC expression in A549 cells.
serum levels not elevated in patients with erythrodermic mycosis fungoides/Sezary syndrome
SPARC expression was inversely associated with the degree of malignancy and it had a negative correlation with VEGF-C and VEGF-D expression. Results suggest SPARC might function as a tumor suppressor inhibiting angiogenesis and lymphangiogenesis in ovarian cancer by reducing the expression of VEGF-C and VEGF-D.
VEGF-A/VEGF-C analysis showed higher positivity in metastatic nodes and higher positivity in the surrounding negative nodes from positive cases in comparison with nonmetastatic patients.
this study shows that decidual NK cells facilitate the interaction between trophoblastic and endothelial cells via VEGF-C and HGF
Lymphangiogenesis during tubulointerstitial fibrosis to be associated with increased expression of CTGF and VEGF-C in human obstructed nephropathy as well as in diabetic kidney disease. vitro, CTGF induced VEGF-C production in HK-2 cells, while CTGF siRNA suppressed transforming growth factor beta1-induced VEGF-C upregulation.
Smad4 expression negatively correlated with VEGF-A and VEGF-C in colon cancer
study is the first to describe the mechanism of leptin-promoted lymphangiogenesis by upregulating VEGF-C expression in chondrosarcomas.
Retroperitoneal tumour progression in EOC patients is associated with high VEGF-C expression.
Mechanistic investigations indicated that BDNF facilitated VEGF-C-dependent lymphangiogenesis through the MEK/ERK/mTOR signaling pathway.
no difference in the levels of VEGF-A, VEGF-C, and VEGF-D in pre-eclampsia compared to normotensive pregnant women stratified by HIV status
Results has shown that VEGF-C was highly expressed in non-small cell lung cancer (NSCLC) tissues and metastatic lymph nodes. VEGF-C expression levels was significantly correlated with lymph node metastasis in NSCLC. Along with CXCR4, VEGF-C might synergically promote lymphatic metastasis in lung cancer and might be a clinical predictor of lymph node metastasis in NSCLC patients.
CXCR4, CCR7, VEGF-C and VEGF-D expression might have synergistic effects on the lymph node metastasis in patients with cervical cancer.
prolactin induction of VEGF-C and Runx2 was inhibited partly by Carboxypeptidase-D inhibitors, implicating nitric oxide , produced by PRL-regulated Carboxypeptidase-D, in breast cancer progression
As shown in mouse model of kidney fibrosis CTGF is significantly involved in fibrosis-associated renal lymphangiogenesis through regulation of, and direct interaction with, VEGF-C.
Fluid shear stress regulates vascular remodeling via VEGFR-3 activation, independently of its ligand, VEGF-C, in the uterus during pregnancy.
A novel heparin conjugate (LHbisD4) is shown to prevent lymphangiogenesis by blocking the vascular endothelial growth factor C (VEGF-C) induced signaling pathway.
lymphangiogenesis is regulated by two distinct proteolytic mechanisms of ligand activation: one in which VEGFC activation by ADAMTS3 and CCBE1 spatially and temporally patterns developing lymphatics, and one in which VEGFD activation by a distinct proteolytic mechanism may be stimulated during inflammatory lymphatic growth
These results reveal an unexpected role for VEGF-C, a major lymphangiogenic growth factor, in the transition to fetal liver erythropoiesis.
Results suggest that interleukin-6 (IL-6) increases VEGF-C induction and lymphangiogenesis may involve, at least in part, Src-FAK-STAT3 cascade in lymphatic endothelial cells (LECs).
Data show that heparanase-1 (HPA-1) induced shedding of heparan sulfate chain from syndecan-1 (SDC-1) facilitated the release of vascular endothelial growth factor C (VEGF-C) from SDC-1/VEGF-C complex into the medium of hepatocarcinoma cell.
Data show that in the MCF-7 breast cancer cell line, only MT1X metallothioneins (MTs) positively correlated with vascular endothelial growth factor C (VEGFC).
The findings in this study strongly suggest the following: i) that VEGF-C promotes the proliferative activity and migratory ability of mesenchymal stem cell ; and ii) VEGF-C and Tgfb reciprocally regulate mesenchymal stem cell commitment to differentiation into lymphatic endothelial or osteoblastic phenotypes, respectively.
The authors show that VEGF-C is necessary for perinatal lymphangiogenesis, but required for adult lymphatic vessel maintenance only in the intestine.
MT1-MMP directly cleaves LYVE-1 on lymphatic endothelial cells to inhibit LYVE-1-mediated lymphangiogenic responses and restrains the production of VEGF-C.
HA increases lymphangiogenesis in renal fibrosis model and also stimulates vascular endothelial cell growth factor-C production from macrophages through Toll-like receptor 4-dependent signal pathway
Results showed that the VEGF-C/VEGFR-3 system underlies the protective effect of ischemic preconditioning against forebrain ischemia in the mouse hippocampus
Vascular endothelial growth factor C/VEGFR-3 signaling modifies HS and CCL21 gradients around lymphatics, regulating lymphocyte migration.
Coronary artery stem development first requires VEGF-C to stimulate vessel growth around the outflow tract.
Data show that the expression of lymphatic vessel endothelial hyaluronan receptor 1 (LYVE 1) was similar with vascular endothelial growth factor C (VEGF-C), but its peak appeared 1-2 d later than that of VEGF-C.
reveal the evolutionary conservation of the lymphatic-like phenotype of the Schlemm's canal (SC), implicate VEGF-C and VEGFR-3 as critical regulators of SC lymphangiogenesis
Sinus venosus-derived and endocardial-derived migratory routes unite to form the coronary vasculature, with the former requiring VEGFC - a tissue-specific mediator of blood endothelial development.
suggest that correction of defective lymphatic function with VEGF-C has potential as a therapeutic strategy for inflammatory bowel disease.
The protein encoded by this gene is a member of the platelet-derived growth factor/vascular endothelial growth factor (PDGF/VEGF) family, is active in angiogenesis and endothelial cell growth, and can also affect the permeability of blood vessels. This secreted protein undergoes a complex proteolytic maturation, generating multiple processed forms which bind and activate VEGFR-3 receptors. Only the fully processed form can bind and activate VEGFR-2 receptors. This protein is structurally and functionally similar to vascular endothelial growth factor D.
vascular endothelial growth factor C
, vascular endothelial growth factor c
, FLT4 ligand DHM
, vascular endothelial growth factor-related protein
, flt4 ligand
, vascular endothelial growth factor C isoform 129
, vascular endothelial growth factor C isoform 184