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anti-Human VEGFC Antikörper:
anti-Mouse (Murine) VEGFC Antikörper:
anti-Rat (Rattus) VEGFC Antikörper:
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Human Polyclonal VEGFC Primary Antibody für IHC (fro), IHC (p) - ABIN258871
Zampell, Yan, Avraham, Daluvoy, Weitman, Mehrara: HIF-1α coordinates lymphangiogenesis during wound healing and in response to inflammation. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2012
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Human Monoclonal VEGFC Primary Antibody für ICC, IHC (fro) - ABIN438679
Moussai, Mitsui, Pettersen, Pierson, Shah, Suárez-Fariñas, Cardinale, Bluth, Krueger, Carucci: The human cutaneous squamous cell carcinoma microenvironment is characterized by increased lymphatic density and enhanced expression of macrophage-derived VEGF-C. in The Journal of investigative dermatology 2010
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Human Polyclonal VEGFC Primary Antibody für IP, ELISA - ABIN541859
Krishnan, Kirkin, Steffen, Hegen, Weih, Tomarev, Wilting, Sleeman: Differential in vivo and in vitro expression of vascular endothelial growth factor (VEGF)-C and VEGF-D in tumors and its relationship to lymphatic metastasis in immunocompetent rats. in Cancer research 2003
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Human Polyclonal VEGFC Primary Antibody für IHC (p), ELISA - ABIN544825
Su, Shih, Yen, Jeng, Chang, Hsieh, Wei, Yang, Kuo: Cyclooxygenase-2 induces EP1- and HER-2/Neu-dependent vascular endothelial growth factor-C up-regulation: a novel mechanism of lymphangiogenesis in lung adenocarcinoma. in Cancer research 2004
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Human Polyclonal VEGFC Primary Antibody für IF (p), IHC (p) - ABIN731723
Zhuo, Jia, Song, Lu, Ding, Wang, Song, Fu, Luo: The CXCL12-CXCR4 chemokine pathway: a novel axis regulates lymphangiogenesis. in Clinical cancer research : an official journal of the American Association for Cancer Research 2012
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Rat (Rattus) Polyclonal VEGFC Primary Antibody für IP, ELISA - ABIN1589911
Maertens, Erpicum, Detry, Blacher, Lenoir, Carnet, Péqueux, Cataldo, Lecomte, Paupert, Noel: Bone marrow-derived mesenchymal stem cells drive lymphangiogenesis. in PLoS ONE 2014
Human Polyclonal VEGFC Primary Antibody für ELISA, IHC - ABIN6265969
Bai, Wang, Han, Xie, Ji, Yin, Chen, Wang, Jiang, Qi, Jiang: BCL2L10 inhibits growth and metastasis of hepatocellular carcinoma both in vitro and in vivo. in Molecular carcinogenesis 2017
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.
These studies demonstrated the presence of VEGF-C system in porcine endometrium and indicated its possible important role during the time of implantation.
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
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.
This study suggests that the high expression of MMP-9 and VEGF-C could act as markers for the tumor presence in breast cancer. In addition, this study recommends that expression of MMP-9 and VEGF-C was significantly associated with lymph node status and may provide valuable diagnosis of lymph node metastasis in breast cancer patients.
BLACAT2 plays a crucial role in lymphangiogenesis and lymphatic metastasis, and our data highlight a regulatory mechanism for VEGF-C and LN metastasis in bladder cancer
Ambivalent and emerging role of VEGF-C and the lymphatic system in cancer aggressiveness. [review]
Results have shown that CRT is regulated by LPA signaling mediating VEGF-C expression. Clinical evidence also showed the association of CRT with VEGF-C and lymphangiogenesis in human prostate cancer.
Study found an association between VEGFC expression and the adult acute myeloid leukemia patient cytogenetic risk group, with those with a worse prognosis having higher VEGFC expression levels. No correlation was observed between VEGFC expression and survival or complete remission. VEGFC expression strongly correlated with expression of the VEGF receptors FLT1, KDR, and NRP1.
A statistically significant positive correlation of CHI3L1 and Nogo-A expression (r=0.474, p>0.0001) and a positive correlation of Nogo-A and VEGFC expression (r=0.280, p=0.013) were found. CHI3L1 and Nogo-A are important in angiogenesis in invasive ductal breast carcinoma
Blocking CCR8 via a small molecule inhibitor or short hairpin (sh)RNA mitigated the decrease in Ecadherin, and increase in MMP2 and VEGFC, caused by human recombinant (r)CCL18. CCR8 knockdown by shRNA reversed rCCL18induced cancer cell invasion, migration and epithelialmesenchymal transition
These results suggest that VEGF-C-induced MSC migration is mediated via VEGFR2 and VEGFR3, and follows the activation of the ERK and FAK signaling pathway. Thus, VEGF-C may be valuable in tissue regeneration and repair in MSC-based therapy.
MiR-128-3p directly targets VEGFC/VEGFR3 to modulate the proliferation of lymphatic endothelial cells through Ca(2+) signaling
VEGF-C expression is involved in the resistin-induced promotion of lymphatic endothelial cells-associated lymphangiogenesis.
blocking the lectinlike oxLDL1 (LOX1) receptor and the nuclear factor (NF)kappaB signaling pathway following oxLDL (50 microg/ml) treatment in HGC27 cells revealed that oxLDL could activate the NFkappaB signaling pathway mediated by LOX1, with subsequent upregulation of VEGFC expression, and secretion in and from gastric cancer cells, and finally that it could promote the lymphatic metastasis of gastric cancer
These results indicate that AR occurs through the Src/MEK/ERK/STAT-3 pathway, activating VEGF-C expression and contributing to lymphangiogenesis in human chondrosarcoma. Thus, AR could be a therapeutic target in metastasis and lymphangiogenesis of chondrosarcoma.
NCOA1 interacts with NF-kappaB to increase VEGFC levels in human thyroid cancer.
VEGF-C is highly expressed in rectal cancer tissues, and the positive expression of VEGF-C is positively correlated with tumor invasion depth, lymph node metastasis and Dukes stage
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.
miR-210 promoted neovascularization and neural progenitor cell migration via the SOCS1-STAT3-VEGF-C pathway in middle cerebral artery stroke model.
The data suggested that VEGFC/VEGFR3 signaling promotes the proliferation of spermatogonial cells via the AKT /MAPK and cyclin D1 pathway.
High VEGF-C expression promotes the development of lymphatics in bone and bone loss.
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.
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