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anti-Human FLT4 Anticorps:
anti-Mouse (Murine) FLT4 Anticorps:
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Mouse (Murine) Polyclonal FLT4 Primary Antibody pour CyTOF, FACS - ABIN4899930
Benedito, Rocha, Woeste, Zamykal, Radtke, Casanovas, Duarte, Pytowski, Adams: Notch-dependent VEGFR3 upregulation allows angiogenesis without VEGF-VEGFR2 signalling. dans Nature 2012
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Human Monoclonal FLT4 Primary Antibody pour 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. dans European journal of cancer (Oxford, England : 1990) 2010
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Human Monoclonal FLT4 Primary Antibody pour 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. dans The Journal of clinical investigation 2007
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Human Monoclonal FLT4 Primary Antibody pour 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. dans European journal of cancer (Oxford, England : 1990) 2009
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Human Monoclonal FLT4 Primary Antibody pour WB - ABIN1882290
Pajusola, Aprelikova, Korhonen, Kaipainen, Pertovaara, Alitalo, Alitalo: FLT4 receptor tyrosine kinase contains seven immunoglobulin-like loops and is expressed in multiple human tissues and cell lines. dans Cancer research 1992
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Human Monoclonal FLT4 Primary Antibody pour ELISA, WB - ABIN969147
Goodyear, Kheyfets, Garcia, Stearns: Role of the VEGFR3/VEGFD receptor axis in TGFbeta1 activation of primary prostate cell lines. dans The Prostate 2009
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Human Polyclonal FLT4 Primary Antibody pour FACS, IF (p) - ABIN678578
Wang, Zhou, Lin, Wang, Lin, Li: RhGH attenuates ischemia injury of intrahepatic bile ducts relating to liver transplantation. dans The Journal of surgical research 2011
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Mouse (Murine) Monoclonal FLT4 Primary Antibody pour 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. dans Blood 2000
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Human Monoclonal FLT4 Primary Antibody pour IHC, ELISA - ABIN1003451
Jussila, Valtola, Partanen, Salven, Heikkilä, Matikainen, Renkonen, Kaipainen, Detmar, Tschachler, Alitalo, Alitalo: Lymphatic endothelium and Kaposi's sarcoma spindle cells detected by antibodies against the vascular endothelial growth factor receptor-3. dans Cancer research 1998
Mouse (Murine) Monoclonal FLT4 Primary Antibody pour WB - ABIN1589862
Tempfer, Kaser-Eichberger, Korntner, Lehner, Kunkel, Traweger, Trost, Strohmaier, Bogner, Runge, Bruckner, Krefft, Heindl, Reitsamer, Schrödl: Presence of lymphatics in a rat tendon lesion model. dans Histochemistry and cell biology 2015
Rare inherited and de novo variants in 2,871 congenital heart disease probands identified GDF1 (Montrer GDF1 Anticorps), MYH6 (Montrer MYH6 Anticorps), and FLT4 as causative genes.
Data show that VEGF-C (Montrer VEGFC Anticorps), VEGF-D (Montrer Figf Anticorps), 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.
By treating LECs with VEGF (Montrer VEGFA Anticorps)-C156S and analyzing subsequent changes in gene expression, we identified several 'immediate early (Montrer JUN Anticorps)' transcription factors that showed a rapid transient upregulation VEGFR-3 stimulation. these results reveal an important and unanticipated role of HOXD10 (Montrer HOXD10 Anticorps) in the regulation of VEGFR-3 signaling in lymphatic endothelial cells, and in the control of lymphangiogenesis and permeability.
The normalized methylation values for the VEGFR1 (Montrer FLT1 Anticorps), VEGFR2 (Montrer KDR Anticorps) and VEGFR3 promoters tended to be higher in the tumour cell lines than in normal tonsil samples, whereas amounts of VEGFR1 (Montrer FLT1 Anticorps), VEGFR2 (Montrer KDR Anticorps) and VEGFR3 messenger RNA were significantly higher
These results indicate that VEGF-C (Montrer VEGFC Anticorps)-induced MSC (Montrer MSC Anticorps) osteogenesis is mediated through VEGFR2 (Montrer KDR Anticorps) and VEGFR3, and followed the activation of the ERK (Montrer EPHB2 Anticorps)/RUNX2 (Montrer RUNX2 Anticorps) signaling pathway.
Assessment of VEGFR-2/VEGFR (Montrer KDR Anticorps)-3 on tumor samples might serve as a putative prognostic factor in renal cell carcinoma (Montrer MOK Anticorps) cases, identifying a subset of patients that may benefit from antiangiogenic treatments targeting VEGFR (Montrer KDR Anticorps) receptors.
This study suggests that NRP1 (Montrer NELL1 Anticorps) expression and LVD are independent factors that are likely to predict the risk of LN metastasis in squamous cell carcinoma (SCC (Montrer CYP11A1 Anticorps))of the tongue, whereas the expression of VEGFC (Montrer VEGFC Anticorps), VEGFR3, CCR7 (Montrer CCR7 Anticorps), and SEMA3E (Montrer SEMA3E Anticorps) are nonindependent predictive factors
Data indicate that vascular endothelial growth factor D (VEGF-D (Montrer Figf Anticorps)) was the best indicator of metastasis and vascular endothelial growth factors and receptor-3 (VEGFR-3) may help to determine the prognosis and management of colorectal cancer (CRC (Montrer CALR Anticorps)).
The summarizes the structure and function features of pathway-related molecules of VEGFC (Montrer VEGFC Anticorps)/D-VEGFR3/NRP2 (Montrer NELL2 Anticorps) axis, stages of various tumors and their molecular mechanisms and significances in tuthe expression changes of these molecules in different anatomic organs or histopathologic types or development lymphatic metastasis.
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 (Montrer RAG1 Anticorps) 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 (Montrer RYK Anticorps) (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 (Montrer CLEC14A Anticorps) acts in vascular homeostasis by fine-tuning VEGFR-2 (Montrer KDR Anticorps) and VEGFR-3 signaling in endothelial cells
VEGFR3 limits VEGFR2 (Montrer KDR Anticorps) expression and VEGF (Montrer VEGFA Anticorps)/VEGFR2 (Montrer KDR Anticorps) 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 (Montrer Figf Anticorps) 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 (Montrer Figf Anticorps) signalling pathway are up-regulated in hyperoxia.
this study uncovers a unique molecular mechanism of lymphangiogenesis in which galectin-8 (Montrer LGALS8 Anticorps)-dependent crosstalk among VEGF-C (Montrer VEGFC Anticorps), podoplanin (Montrer PDPN Anticorps) and integrin pathways plays a key role.
Tnfsf15 (Montrer TNFSF15 Anticorps), 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 (Montrer VEGFC Anticorps)/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
miR (Montrer MYLIP Anticorps)-126a directs lymphatic endothelial cell sprouting and extension by interacting with Cxcl12a-mediated chemokine (Montrer CCL1 Anticorps) signaling and Vegfc (Montrer VEGFC Anticorps)-Flt4 signal axis.
Ca(2 (Montrer CA2 Anticorps)+) oscillations depended upon VEGF receptor-2 (Vegfr2) and Vegfr3 in endothelial cells budding from the dorsal aorta (DA) and posterior cardinal (Montrer CARD8 Anticorps) vein, respectively.
In the embryo, phenotypes driven by increased Vegfc (Montrer VEGFC Anticorps) are suppressed in the absence of Ccbe1 (Montrer CCBE1 Anticorps), and Vegfc (Montrer VEGFC Anticorps)-driven sprouting is enhanced by local Ccbe1 (Montrer CCBE1 Anticorps) overexpression. Moreover, Vegfc (Montrer VEGFC Anticorps)- and Vegfr3-dependent Erk (Montrer MAPK1 Anticorps) signaling is impaired in the absence of Ccbe1 (Montrer CCBE1 Anticorps).
Flt4 plays an essential role in lymphangiogenesis [review]
The parallel growth of motoneuron axons with the dorsal aorta depends on Vegfc (Montrer VEGFC Anticorps)/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 (Montrer DLL4 Anticorps) 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