No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human FLT4 Antibodies:
anti-Mouse (Murine) FLT4 Antibodies:
anti-Rat (Rattus) FLT4 Antibodies:
Go to our pre-filtered search.
Mouse (Murine) Polyclonal FLT4 Primary Antibody for CyTOF, FACS - ABIN4899930
Benedito, Rocha, Woeste, Zamykal, Radtke, Casanovas, Duarte, Pytowski, Adams: Notch-dependent VEGFR3 upregulation allows angiogenesis without VEGF-VEGFR2 signalling. in Nature 2012
Show all 54 Pubmed References
Human Monoclonal FLT4 Primary Antibody for FACS - ABIN4896918
Roorda, Ter Elst, Scherpen, Meeuwsen-de Boer, Kamps, de Bont: VEGF-A promotes lymphoma tumour growth by activation of STAT proteins and inhibition of p27(KIP1) via paracrine mechanisms. in European journal of cancer (Oxford, England : 1990) 2010
Show all 7 Pubmed References
Human Monoclonal FLT4 Primary Antibody for FACS - ABIN4896919
Shawber, Funahashi, Francisco, Vorontchikhina, Kitamura, Stowell, Borisenko, Feirt, Podgrabinska, Shiraishi, Chawengsaksophak, Rossant, Accili, Skobe, Kitajewski: Notch alters VEGF responsiveness in human and murine endothelial cells by direct regulation of VEGFR-3 expression. in The Journal of clinical investigation 2007
Show all 7 Pubmed References
Human Monoclonal FLT4 Primary Antibody for ELISA (Detection), FACS - ABIN4899932
Mouawad, Spano, Comperat, Capron, Khayat: Tumoural expression and circulating level of VEGFR-3 (Flt-4) in metastatic melanoma patients: correlation with clinical parameters and outcome. in European journal of cancer (Oxford, England : 1990) 2009
Show all 4 Pubmed References
Human Monoclonal FLT4 Primary Antibody for ELISA, WB - ABIN969147
Goodyear, Kheyfets, Garcia, Stearns: Role of the VEGFR3/VEGFD receptor axis in TGFbeta1 activation of primary prostate cell lines. in The Prostate 2009
Show all 3 Pubmed References
Human Polyclonal FLT4 Primary Antibody for FACS, IF (p) - ABIN678578
Wang, Zhou, Lin, Wang, Lin, Li: RhGH attenuates ischemia injury of intrahepatic bile ducts relating to liver transplantation. in The Journal of surgical research 2011
Show all 3 Pubmed References
Mouse (Murine) Polyclonal FLT4 Primary Antibody for ELISA (Detection), FACS - ABIN4899929
Gale, Prevo, Espinosa, Ferguson, Dominguez, Yancopoulos, Thurston, Jackson: Normal lymphatic development and function in mice deficient for the lymphatic hyaluronan receptor LYVE-1. in Molecular and cellular biology 2007
Show all 3 Pubmed References
Mouse (Murine) Monoclonal FLT4 Primary Antibody for IHC (fro), IHC (p) - ABIN967368
Kubo, Fujiwara, Jussila, Hashi, Ogawa, Shimizu, Awane, Sakai, Takabayashi, Alitalo, Yamaoka, Nishikawa: Involvement of vascular endothelial growth factor receptor-3 in maintenance of integrity of endothelial cell lining during tumor angiogenesis. in Blood 2000
Show all 2 Pubmed References
Human Polyclonal FLT4 Primary Antibody for IHC, WB - ABIN6680309
Yang, Sun, He, Ren, Liu, Liu, Zhang, Zhao: Lymphotoxins Promote the Progression of Human Lymphatic Malformation by Enhancing Lymphatic Endothelial Cell Proliferation. in The American journal of pathology 2017
Human Polyclonal FLT4 Primary Antibody for ELISA, IHC - ABIN5693136
Li, Fan, Song, Zhang, Chen, Li, Mi, Ma, Song, Tao, Li: Expression of angiopoietin-2 and vascular endothelial growth factor receptor-3 correlates with lymphangiogenesis and angiogenesis and affects survival of oral squamous cell carcinoma. in PLoS ONE 2013
study reveals that VEGFR-3 positive expression in tumors represents an independent prognostic factor for both overall and recurrence-free survival in hepatic resected patients with iCCA. VEGFR-3 positive tumors favor lymph node metastasis, tumor recurrence and worse outcomes through tumor-associated lymphangiogenesis.
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.
In this study, a potential link between the FLT4 gene and OHSS has been suggested. Future functional studies are essential to define a more precise involvement of the detected variants in the development of OHSS.
MiR-128-3p directly targets VEGFC/VEGFR3 to modulate the proliferation of lymphatic endothelial cells through Ca(2+) signaling
novel mutation associated with Milroy disease was identified in a Chinese family
activator of G-protein signaling 8 regulated the trafficking of VEGFR-3 to the plasma membrane
Vascular endothelial growth factor receptor 3 is a novel marker differing CD138-positive and CD138-negative multiple myeloma cells.
Results indicated that VEGFR3 levels that were upregulated by HIF1alpha expression promoted human lymphatic endothelial cells colony formation and migration.
VEGFR3 has a role in lymphatic vessel hyperplasia through cell-autonomous and non-cell-autonomous mechanisms
These results suggest functional interactions among ATX, VEGFR-2, and VEGFR-3 in the modulation of hemovascular and lymphovascular cell activation during vascular development.
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.
Single nucleotide polymorphism of VEGFR3 is associated with relapse in gastroenteropancreatic neuroendocrine neoplasms.
VEGFR3 single nucleotide polymorphisms association with lymphedema caused by Wuchereria bancrofti.
The results imply a very good sensitivity of VEGFR-3 in ESCC. VEGFR-3 may be a good diagnostic biomarker for ESCC.
VEGFR-3 expression was associated with depth of invasion and lymph node metastasis in gastric cancer
The finding of rare LAMA5 variants together with FLT4 in Milroy disease suggests that these mutations may be co-responsible for these disorders and most likely interfere with the function of lymphatics.
the difference between the pro- (VEGF165a) and antiangiogenic (VEGF165b) VEGF isoforms and its soluble receptors for severity of diabetic retinopathy, is reported.
Rare inherited and de novo variants in 2,871 congenital heart disease probands identified GDF1, MYH6, and FLT4 as causative genes.
Data show that VEGF-C, VEGF-D, and VEGFR-3 were expressed in a substantial percentage of breast carcinomas.
There was a significant decrease in VEGFR3 expression in pulmonary arterial endothelial cells from pulmonary arterial hypertension patients.
ROS produced in diabetes induced c-Src-dependent but VEGF-C-independent VEGFR3 phosphorylation, and upregulated epsins through the activation of transcription factor AP-1. Augmented epsins bound to and promoted degradation of newly synthesized VEGFR3 in the Golgi, resulting in reduced availability of VEGFR3 at the cell surface.
The data suggested that VEGFC/VEGFR3 signaling promotes the proliferation of spermatogonial cells via the AKT /MAPK and cyclin D1 pathway.
uPARAP controlVEGFR-2/VEGFR-3 heterodimerisation during pathological lymphangiogenesis.
Fluid shear stress regulates vascular remodeling via VEGFR-3 activation, independently of its ligand, VEGF-C, in the uterus during pregnancy.
Genetic depletion experiments revealed that VEGFR2, but not VEGFR3, is indispensable for maintenance of thyroid vascular integrity. Notably, blockade of VEGF-A or VEGFR2 not only abrogated vascular remodeling but also inhibited follicular hypertrophy, which led to the reduction of thyroid weights during goitrogenesis.
Report the generation of a Vegfr3-CreER (T2) knockin mouse by gene targeting in embryonic stem cells. This mouse expresses the tamoxifen-inducible CreER(T2) recombinase under the endogenous transcriptional control of the Vegfr3 gene without altering its physiological expression or regulation in the lymphatic system.
Lymphangiogenic growth in the diaphragm was highly dependent on vascular endothelial growth factor receptor (VEGFR)-3 signaling. During diaphragm development, macrophages appeared first in a linearly arranged pattern, followed by ingrowth of lymphatic vessels along these patterned lines.
CLEC14A acts in vascular homeostasis by fine-tuning VEGFR-2 and VEGFR-3 signaling in endothelial cells
VEGFR3 limits VEGFR2 expression and VEGF/VEGFR2 pathway activity in quiescent and angiogenic blood vascular endothelial cells, thereby preventing excessive vascular permeability.
Blockade of FLT4 suppresses metastasis of melanoma cells by impaired lymphatic vessels.
Vegf-d and its receptor Vegfr-3 were more highly expressed in lungs of hyperoxic, versus normoxic, wild-type mice, indicating that components of the Vegf-d signalling pathway are up-regulated in hyperoxia.
this study uncovers a unique molecular mechanism of lymphangiogenesis in which galectin-8-dependent crosstalk among VEGF-C, podoplanin and integrin pathways plays a key role.
Tnfsf15, a cytokine produced largely by endothelial cells, facilitates lymphangiogenesis by up-regulating Vegfr3 gene expression in LECs, contributing to the maintenance of the homeostasis of the circulatory system.
Results showed that the VEGF-C/VEGFR-3 system underlies the protective effect of ischemic preconditioning against forebrain ischemia in the mouse hippocampus
Experiments in mice and zebrafish demonstrate that changing levels of VEGFR3/Flt4 modulates aortic lumen diameter consistent with flow-dependent remodeling
The VEGF-C/ VEGFR3 pathway is a positive signal that selectively promotes Neural stem cells activation and conversion into progenitor cells in mice.
Lymphangiogenesis is induced by mycobacterial granulomas via vascular endothelial growth factor receptor-3 and supports systemic T-cell responses against mycobacterial antigen.
epsins 1 and 2 have a critical role in the temporal and spatial regulation of VEGFR3 abundance and signaling in collecting lymphatic trunks during lymphatic valve formation
Vascular endothelial growth factor C/VEGFR-3 signaling modifies HS and CCL21 gradients around lymphatics, regulating lymphocyte migration.
FLT4 (VEGFR3) expression in the oviducts.
Overall, the data show that HHEX controls blood vessel and lymphatic vessel formation by regulating the VEGFC/FLT4/PROX1 signaling axis.
miR-126a directs lymphatic endothelial cell sprouting and extension by interacting with Cxcl12a-mediated chemokine signaling and Vegfc-Flt4 signal axis.
Ca(2+) oscillations depended upon VEGF receptor-2 (Vegfr2) and Vegfr3 in endothelial cells budding from the dorsal aorta (DA) and posterior cardinal vein, respectively.
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.
Flt4 plays an essential role in lymphangiogenesis [review]
The parallel growth of motoneuron axons with the dorsal aorta depends on Vegfc/Vegfr3 signaling in zebrafish.
Rspo1-Wnt-VegfC-Vegfr3 signaling plays a crucial role as an endothelial-autonomous permissive cue for developmental angiogenesis.
flt4 signalling is suppressed by Dll4 in developing zebrafish intersegmental arteries.
This gene encodes a tyrosine kinase receptor for vascular endothelial growth factors C and D. The protein is thought to be involved in lymphangiogenesis and maintenance of the lymphatic endothelium. Mutations in this gene cause hereditary lymphedema type IA.
, fms-like tyrosine kinase 4
, soluble VEGFR3 variant 1
, soluble VEGFR3 variant 2
, soluble VEGFR3 variant 3
, tyrosine-protein kinase receptor FLT4
, vascular endothelial growth factor receptor 3
, chylous ascites
, receptor protein tyrosine kinase
, vascular endothelial growth factor receptor-3
, FMS-like tyrosine kinase 4
, tyrosine kinase VEGFR-3
, receptor tyrosine kinase Flt4