VEGFR2/KDR Protein, Human, Recombinant (ECD, His & AVI Tag), Biotinylated: Product Information
> 95 % as determined by SDS-PAGE.
< 1.0 EU per μg protein as determined by the LAL method.
0.5-1 as determined by the HABA assay.
Testing in progress
A DNA sequence encoding the human KDR (NP_002244.1) (Met1-Glu764) was expressed with a c-terminal polyhistidine tagged AVI tag at the C-terminus. The expressed protein was biotinylated in vivo by the Biotin-Protein ligase (BirA enzyme) which is co-expressed.
Predicted N Terminal
The recombinant human KDR consists of 771 amino acids and predicts a molecular mass of 86.5 kDa.
Lyophilized from sterile PBS, pH 7.4. Please contact us for any concerns or special requirements. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization.
Please refer to the specific buffer information in the hard copy of CoA.
In general, recombinant proteins are provided as lyophilized powder which are shipped at ambient temperature. Bulk packages of recombinant proteins are provided as frozen liquid. They are shipped out with blue ice unless customers require otherwise.
Stability & Storage
Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃ Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.
VEGFR2/KDR Protein, Human, Recombinant (ECD, His & AVI Tag), Biotinylated: Images
VEGFR2/KDR Protein, Human, Recombinant (ECD, His & AVI Tag), Biotinylated: 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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