Anti-VEGFR2 / KDR Antibody (Rabbit Polyclonal antibody) General Information
Anti-VEGFR2 / KDR Antibody
Reacts with: Human
Human VEGFR2 / KDR
A synthetic peptide corresponding to the C-terminus of the Human VEGFR2/KDR/Flk-1/CD309
Produced in rabbits immunized with a synthetic peptide corresponding to the C-terminus of the Human VEGFR2/KDR/Flk-1/CD309, and purified by antigen affinity chromatography.
Polyclonal Rabbit IgG
Protein A & Antigen Affinity
0.2 μm filtered solution in PBS
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 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.
Immunochemical staining of human KDR in human breast carcinoma with rabbit polyclonal antibody (1:500, formalin-fixed paraffin embedded sections).
Immunofluorescence staining of KDR in Hela cells. Cells were fixed with 4% PFA, permeabilzed with 0.3% Triton X-100 in PBS,blocked with 10% serum, and incubated with rabbit anti-Human KDR polyclonal antibody (dilution ratio 1:1000) at 4℃ overnight. Then cells were stained with the Alexa Fluor$488-conjugated Goat Anti-rabbit IgG secondary antibody (green). Positive staining was localized to cytoplasm and nucleus.
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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