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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
These findings thus underscore a role for posterior cardinal (show CARD8 Proteins) vein and VegfC in patterning the head kidney prior to organ assembly and function.
Vegfc acts through ERK (show MAPK1 Proteins) to induce sprouting and differentiation of trunk lymphatic progenitors.
data not only reveal a non-canonical function of Mt2 (show MT2 Proteins) in angiogenesis, but also propose Mt2 (show MT2 Proteins) as a novel regulator of vegfc expression.
Vegfc signaling increases mafba (show MAFB Proteins) 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 (show CCBE1 Proteins), and Vegfc-driven sprouting is enhanced by local Ccbe1 (show CCBE1 Proteins) overexpression. Moreover, Vegfc- and Vegfr3 (show FLT4 Proteins)-dependent Erk (show MAPK1 Proteins) signaling is impaired in the absence of Ccbe1 (show CCBE1 Proteins).
Vegfc has an essential role in lymphangiogenesis [review]
The parallel growth of motoneuron axons with the dorsal aorta depends on Vegfc/Vegfr3 (show FLT4 Proteins) 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.
VEGF-C and VEGF (show VEGFA Proteins)-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 (show RLN1 Proteins) and recombinant human relaxin-2 (show RLN1 Proteins) 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
SPARC (show SPARC Proteins) expression was inversely associated with the degree of malignancy and it had a negative correlation with VEGF-C and VEGF-D (show Figf Proteins) expression. Results suggest SPARC (show SPARC Proteins) might function as a tumor suppressor inhibiting angiogenesis and lymphangiogenesis in ovarian cancer by reducing the expression of VEGF-C and VEGF-D (show Figf Proteins).
VEGF-A/VEGF (show VEGFA Proteins)-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 (show HGF Proteins)
Lymphangiogenesis during tubulointerstitial fib (show CTGF Proteins)rosis 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 (show SMAD4 Proteins) expression negatively correlated with VEGF-A (show VEGFA Proteins) and VEGF-C in colon cancer
study is the first to describe the mechanism of leptin (show LEP Proteins)-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 (show BDNF Proteins) facilitated VEGF-C-dependent lymphangiogenesis through the MEK (show MAP2K1 Proteins)/ERK (show EPHB2 Proteins)/mTOR (show FRAP1 Proteins) signaling pathway.
no difference in the levels of VEGF-A (show VEGFA Proteins), VEGF-C, and VEGF-D (show Figf Proteins) 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 (show CXCR4 Proteins), VEGF-C might synergically promote lymphatic metastasis in lung cancer and might be a clinical predictor of lymph node metastasis in NSCLC patients.
As shown in mouse model of kidney fibrosis CTGF (show CTGF Proteins) 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 (show FLT4 Proteins) 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 (show Adamts2 Proteins) and CCBE1 (show CCBE1 Proteins) spatially and temporally patterns developing lymphatics, and one in which VEGFD (show Figf Proteins) 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 (show IL6 Proteins)) increases VEGF-C induction and lymphangiogenesis may involve, at least in part, Src (show SRC Proteins)-FAK (show PTK2 Proteins)-STAT3 (show STAT3 Proteins) cascade in lymphatic endothelial cells (LECs).
Data show that heparanase-1 (HPA-1 (show HPSE Proteins)) induced shedding of heparan sulfate chain from syndecan-1 (SDC-1 (show SDC1 Proteins)) facilitated the release of vascular endothelial growth factor C (VEGF-C) from SDC-1 (show SDC1 Proteins)/VEGF-C complex into the medium of hepatocarcinoma cell.
Data show that in the MCF-7 breast cancer cell line, only MT1X (show MT1X Proteins) metallothioneins (MTs (show NEU2 Proteins)) 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 (show TGFB1 Proteins) 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.
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