|Recombinant Mouse VEGFR2 / Flk-1 / CD309 / KDR protein (Catalog#50998-M08H)|
|0.2 μm filtered solution in PBS with 5% trehalose|
|This antibody was obtained from a rabbit immunized with purified, recombinant Mouse VEGFR2 / Flk-1 / CD309 / KDR (rM VEGFR2 / Flk-1 / CD309 / KDR; Catalog#50998-M08H; P35918-1; Met1-Glu762).|
|Mouse VEGFR2 / Flk-1 / CD309 / KDR|
No cross-reactivity in ELISA with
ELISA: 0.1-0.2 μg/mL
This antibody can be used at 0.1-0.2 μg/mL with the appropriate secondary reagents to detect Mouse VEGFR2 / Flk-1 / CD309 / KDR. The detection limit for Mouse VEGFR2 / Flk-1 / CD309 / KDR is approximately 0.0049 ng/well.
|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.|
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.
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.