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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 (显示 LAMA5 蛋白) 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 (显示 VEGFA 蛋白) 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 (显示 GDF1 蛋白), MYH6 (显示 MYH6 蛋白), and FLT4 as causative genes.
Data show that VEGF-C (显示 VEGFC 蛋白), VEGF-D (显示 Figf 蛋白), 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.
Fluid shear stress regulates vascular remodeling via VEGFR-3 activation, independently of its ligand, VEGF-C (显示 VEGFC 蛋白), in the uterus during pregnancy.
Genetic depletion experiments revealed that VEGFR2 (显示 KDR 蛋白), but not VEGFR3, is indispensable for maintenance of thyroid vascular integrity. Notably, blockade of VEGF-A (显示 VEGFA 蛋白) or VEGFR2 (显示 KDR 蛋白) 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 (显示 RAG1 蛋白) 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 (显示 VEGF 蛋白) receptor (显示 RYK 蛋白) (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 (显示 CLEC14A 蛋白) acts in vascular homeostasis by fine-tuning VEGFR-2 (显示 KDR 蛋白) and VEGFR-3 signaling in endothelial cells
VEGFR3 limits VEGFR2 (显示 KDR 蛋白) expression and VEGF (显示 VEGFA 蛋白)/VEGFR2 (显示 KDR 蛋白) 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 (显示 Figf 蛋白) 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 (显示 Figf 蛋白) signalling pathway are up-regulated in hyperoxia.
this study uncovers a unique molecular mechanism of lymphangiogenesis in which galectin-8 (显示 LGALS8 蛋白)-dependent crosstalk among VEGF-C (显示 VEGFC 蛋白), podoplanin (显示 PDPN 蛋白) and integrin pathways plays a key role.
Tnfsf15 (显示 TNFSF15 蛋白), 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.
FLT4 (VEGFR3) expression in the oviducts.
miR (显示 MYLIP 蛋白)-126a directs lymphatic endothelial cell sprouting and extension by interacting with Cxcl12a-mediated chemokine (显示 CCL1 蛋白) signaling and Vegfc (显示 VEGFC 蛋白)-Flt4 signal axis.
Ca(2 (显示 CA2 蛋白)+) oscillations depended upon VEGF receptor-2 (Vegfr2) and Vegfr3 in endothelial cells budding from the dorsal aorta (DA) and posterior cardinal (显示 CARD8 蛋白) vein, respectively.
Experiments in mice and zebrafish demonstrate that changing levels of VEGFR3/Flt4 modulates aortic lumen diameter consistent with flow-dependent remodeling
In the embryo, phenotypes driven by increased Vegfc (显示 VEGFC 蛋白) are suppressed in the absence of Ccbe1 (显示 CCBE1 蛋白), and Vegfc (显示 VEGFC 蛋白)-driven sprouting is enhanced by local Ccbe1 (显示 CCBE1 蛋白) overexpression. Moreover, Vegfc (显示 VEGFC 蛋白)- and Vegfr3-dependent Erk (显示 MAPK1 蛋白) signaling is impaired in the absence of Ccbe1 (显示 CCBE1 蛋白).
Flt4 plays an essential role in lymphangiogenesis [review]
The parallel growth of motoneuron axons with the dorsal aorta depends on Vegfc (显示 VEGFC 蛋白)/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 (显示 DLL4 蛋白) 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