Biotinylated Human GITR, His,Avitag (GIR-H82E4) is expressed from human 293 cells (HEK293). It contains AA Gln 26 - Glu 161 (Accession # Q9Y5U5-1).
Predicted N-terminus: Gln 26
This protein carries a polyhistidine tag at the C-terminus, followed by an Avi tag.
The protein has a calculated MW of 18.1 kDa. The protein migrates as 22-26 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.
Biotinylation of this product is performed using Avitag™ technology. Briefly, the single lysine residue in the Avitag is enzymatically labeled with biotin.
The biotin to protein ratio is 0.5-1 as determined by the HABA assay.
Less than 1.0 EU per μg by the LAL method.
>90% as determined by SDS-PAGE.
Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. Normally trehalose is added as protectant before lyophilization.
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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.
Biotinylated Human GITR, His,Avitag on SDS-PAGE under reducing (R) condition. The gel was stained overnight with Coomassie Blue. The purity of the protein is greater than 90%.
Immobilized Human GITR Ligand, Fc Tag (Cat. No. GIL-H5261) at 10 μg/mL (100 μL/well) can bind Biotinylated Human GITR, His,Avitag (Cat. No. GIR-H82E4) with a linear range of 1-78 ng/mL (QC tested).
Glucocorticoid-induced TNFR-related protein (GITR) is also known as Tumor necrosis factor receptor superfamily member 18 (TNFRSF18), activation-inducible TNFR family receptor (AITR), CD antigen CD357, which is a member of the tumor necrosis factor receptor (TNF-R) superfamily. GITR is receptor for TNFSF18, which seems to be involved in interactions between activated T-lymphocytes and endothelial cells and in the regulation of T-cell receptor-mediated cell death. GITR also mediated NF-kappa-B activation via the TRAF2/NIK pathway.