Anti-VEGFR2 / KDR Antibody

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Anti-VEGFR2 / KDR Antibody (Mouse Monoclonal antibody) General Information

Product name
Anti-VEGFR2 / KDR Antibody
Validated applications
FCM
Species reactivity
Reacts with: Human
Specificity
Human VEGFR2 / KDR
Immunogen
Recombinant Human VEGFR2/KDR/Flk-1/CD309 Protein (Catalog#10012-H08H)
Preparation
This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human VEGFR2/KDR/Flk-1/CD309 (rh VEGFR2/KDR/Flk-1/CD309; Catalog#10012-H08H; NP_002244.1; Met1-Glu764). The IgG fraction of the cell culture supernatant was purified by Protein A affinity chromatography.
Source
Monoclonal Mouse IgG1 Clone #03
Purification
Protein A
Formulation
0.2 μm filtered solution in PBS
Conjugate
Unconjugated
Form
Liquid
Shipping
This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
Storage
This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free. Avoid repeated freeze-thaw cycles.

Anti-VEGFR2 / KDR Antibody (Mouse Monoclonal antibody) Validated Applications

Application Dilution
FCM 1:25-1:100
Please Note: Optimal concentrations/dilutions should be determined by the end user.

Anti-VEGFR2 / KDR Antibody (Mouse Monoclonal antibody) Images

Flow cytometric analysis of Human VEGFR2(CD309) expression on HUVEC cells. Cells were stained with purified anti-Human VEGFR2(CD309), then a FITC-conjugated second step antibody. The fluorescence histograms were derived from gated events with the forward and side light-scatter characteristics of intact cells.

Anti-VEGFR2 / KDR Antibody: Alternative Names

Anti-CD309 Antibody; Anti-Flk-1 Antibody; Anti-FLK1 Antibody; Anti-VEGFR Antibody; Anti-VEGFR2 Antibody

VEGFR2 / KDR Background Information

VEGFR2, also called as KDR or Flk-1, is identified as the receptor for VEGF and VEGFC and an early marker for endothelial cell progenitors, whose expression is restricted to endothelial cells in vivo. VEGFR2 was shown to be the primary signal transducer for angiogenesis and the development of pathological conditions such as cancer and diabetic retinopathy. It has been shown that VEGFR2 is expressed mainly in the endothelial cells, and the expression is upregulated in the tumor vasculature. Thus the inhibition of VEGFR2 activity and its downstream signaling are important targets for the treatment of diseases involving angiogenesis. VEGFR2 transduces the major signals for angiogenesis via its strong tyrosine kinase activity. However, unlike other representative tyrosine kinase receptors, VEGFR2 does not use the Ras pathway as a major downstream signaling but rather uses the phospholipase C-protein kinase C pathway to signal mitogen-activated protein (MAP)-kinase activation and DNA synthesis. VEGFR2 is a direct and major signal transducer for pathological angiogenesis, including cancer and diabetic retinopathy, in cooperation with many other signaling partners; thus, VEGFR2 and its downstream signaling appear to be critical targets for the suppression of these diseases. VEGF and VEGFR2-mediated survival signaling is critical to endothelial cell survival, maintenance of the vasculature and alveolar structure and regeneration of lung tissue. Reduced VEGF and VEGFR2 expression in emphysematous lungs has been linked to increased endothelial cell death and vascular regression.
Full Name
kinase insert domain receptor
Research Areas
References
  • Shibuya M. (2006) Vascular endothelial growth factor (VEGF)-Receptor2: its biological functions, major signaling pathway, and specific ligand VEGF-E. Endothelium. 13(2): 63-9.
  • Marwick JA, et al. (2010) Cigarette smoke regulates VEGFR2-mediated survival signaling in rat lungs. J Inflamm (Lond). 7(1): 11.
  • Bruns AF, et al. (2010) Ligand-stimulated VEGFR2 signaling is regulated by co-ordinated trafficking and proteolysis. Traffic. 11(1): 161-74.

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