Anti-VEGFR2 / KDR Antibody (PE) (Mouse Monoclonal antibody) General Information
Anti-VEGFR2 / KDR Antibody (PE)
Reacts with: Human
Human VEGFR2 / KDR
Recombinant Human VEGFR2/KDR/Flk-1/CD309 Protein (Catalog#10012-H08H)
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) and conjugated with PE under optimum conditions, the unreacted PE was removed.
Monoclonal Mouse IgG1 Clone #03
Aqueous solution containing 0.5% BSA and 0.09% sodium azide
10 μl/Test, 0.1 mg/ml
This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
This antibody can be stored at 2℃-8℃ for twelve months without detectable loss of activity. Protected from prolonged exposure to light. Do not freeze ! Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.
Flow cytometric analysis of Human VEGFR2(CD309) expression on HUVEC cells. Cells were stained with PE-conjugated anti-Human VEGFR2(CD309). The fluorescence histograms were derived from gated events with the forward and side light-scatter characteristics of intact cells.
Anti-VEGFR2 / KDR Antibody (PE): Alternative Names
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.
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