ActiveMax® Mouse VEGF120, Tag Free (VE0-M4211) is expressed from human 293 cells (HEK293). It contains AA Ala 27 - Arg 146 (Accession # AAB22254.1 ).
Predicted N-terminus: Ala 27
This protein carries no "tag".
The protein has a calculated MW of 14.1 kDa. The protein migrates as 18-22 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.
Less than 1.0 EU per μg by the LAL method.
>95% as determined by SDS-PAGE.
Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. Normally trehalose is added as protectant before lyophilization.
Contact us for customized product form or formulation.
Please see Certificate of Analysis for specific instructions.
For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.
For long term storage, the product should be stored at lyophilized state at -20°C or lower.
Please avoid repeated freeze-thaw cycles.
This product is stable after storage at:
- -20°C to -70°C for 12 months in lyophilized state;
- -70°C for 3 months under sterile conditions after reconstitution.
ActiveMax® Mouse VEGF120, Tag Free on SDS-PAGE under reducing (R) condition. The gel was stained overnight with Coomassie Blue. The purity of the protein is greater than 95%.
Immobilized ActiveMax® Mouse VEGF120, Tag Free (Cat. No. VE0-M4211) at 2 μg/mL (100 μL/well) can bind Human VEGF R1, His Tag (Cat. No. VE1-H5220) with a linear range of 6-100 ng/mL (QC tested).
Vascular endothelial growth factor A (VEGFA) is also known as Vascular permeability factor (VPF). VEGFA belongs to the PDGF/VEGF growth factor family. VEGFA is a glycosylated mitogen that specifically acts on endothelial cells and has various effects, including mediating increased vascular permeability, inducing angiogenesis, vasculogenesis and endothelial cell growth, promoting cell migration, and inhibiting apoptosis. Alternatively spliced transcript variants, encoding either freely secreted or cell-associated isoforms, have been characterized. VEGFA is produced by a group of three major isoforms as a result of alternative splicing and if any three isoforms are produced (VEGFA120, VEGFA164, and VEGFA188) then this will not result in vessel defects and death of the full VEGFA knockout in mice.