VGFR3 Antibody
Purified Mouse Monoclonal Antibody (Mab)
- SPECIFICATION
- CITATIONS: 1
- PROTOCOLS
- BACKGROUND
Application
| WB, IHC-P, E |
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Primary Accession | P35916 |
Reactivity | Human |
Host | Mouse |
Clonality | Monoclonal |
Isotype | IgG1 κ |
Clone/Animal Names | 44CT92.4.4 |
Calculated MW | 152757 Da |
Gene ID | 2324 |
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Other Names | Vascular endothelial growth factor receptor 3, VEGFR-3, Fms-like tyrosine kinase 4, FLT-4, Tyrosine-protein kinase receptor FLT4, FLT4, VEGFR3 |
Target/Specificity | Purified His-tagged VGFR3 protein(Fragment) was used to produced this monoclonal antibody. |
Dilution | WB~~1:2000 IHC-P~~1:10~50 |
Format | Purified monoclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein G column, followed by dialysis against PBS. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | VGFR3 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | FLT4 |
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Synonyms | VEGFR3 |
Function | Tyrosine-protein kinase that acts as a cell-surface receptor for VEGFC and VEGFD, and plays an essential role in adult lymphangiogenesis and in the development of the vascular network and the cardiovascular system during embryonic development. Promotes proliferation, survival and migration of endothelial cells, and regulates angiogenic sprouting. Signaling by activated FLT4 leads to enhanced production of VEGFC, and to a lesser degree VEGFA, thereby creating a positive feedback loop that enhances FLT4 signaling. Modulates KDR signaling by forming heterodimers. The secreted isoform 3 may function as a decoy receptor for VEGFC and/or VEGFD and play an important role as a negative regulator of VEGFC-mediated lymphangiogenesis and angiogenesis. Binding of vascular growth factors to isoform 1 or isoform 2 leads to the activation of several signaling cascades; isoform 2 seems to be less efficient in signal transduction, because it has a truncated C-terminus and therefore lacks several phosphorylation sites. Mediates activation of the MAPK1/ERK2, MAPK3/ERK1 signaling pathway, of MAPK8 and the JUN signaling pathway, and of the AKT1 signaling pathway. Phosphorylates SHC1. Mediates phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase. Promotes phosphorylation of MAPK8 at 'Thr-183' and 'Tyr-185', and of AKT1 at 'Ser-473'. |
Cellular Location | Cell membrane; Single-pass type I membrane protein Cytoplasm Nucleus. Note=Ligand-mediated autophosphorylation leads to rapid internalization [Isoform 2]: Cell membrane; Single-pass type I membrane protein |
Tissue Location | Detected in endothelial cells (at protein level). Widely expressed. Detected in fetal spleen, lung and brain. Detected in adult liver, muscle, thymus, placenta, lung, testis, ovary, prostate, heart, and kidney. |
Provided below are standard protocols that you may find useful for product applications.
Background
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.
References
A genetic association study of maternal and fetal candidate genes that predispose to preterm prelabor rupture of membranes (PROM). Romero R, et al. Am J Obstet Gynecol, 2010 Jul 29. PMID 20673868.
Variation at the NFATC2 Locus Increases the Risk of Thiazolinedinedione-Induced Edema in the Diabetes REduction Assessment with ramipril and rosiglitazone Medication (DREAM) Study. Bailey SD, et al. Diabetes Care, 2010 Jul 13. PMID 20628086.
Milroy's primary congenital lymphedema in a male infant and review of the literature. Kitsiou-Tzeli S, et al. In Vivo, 2010 May-Jun. PMID 20555004.
Identification of fetal and maternal single nucleotide polymorphisms in candidate genes that predispose to spontaneous preterm labor with intact membranes. Romero R, et al. Am J Obstet Gynecol, 2010 May. PMID 20452482.
Endothelial cell adhesion to the extracellular matrix induces c-Src-dependent VEGFR-3 phosphorylation without the activation of the receptor intrinsic kinase activity. Galvagni F, et al. Circ Res, 2010 Jun 25. PMID 20431062.
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