Biotinylated Human GITR / TNFRSF18 Protein, Fc,Avitag™

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GIR-H82F7-25ug
$360.00
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GIR-H82F7-200ug
$1,565.00
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GIR-H82F7
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Synonyms

AITR, GITR, TNFRSF18, CD357

Source

Biotinylated Human GITR, Fc,Avitag (GIR-H82F7) is expressed from human 293 cells (HEK293). It contains AA Gln 26 - Glu 161 (Accession # Q9Y5U5-1).

Predicted N-terminus: Gln 26

Molecular Characterization

This protein carries a human IgG1 Fc tag at the C-terminus, followed by an Avi tag (Avitag™).

The protein has a calculated MW of 43.3 kDa. The protein migrates as 45-50 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.

Labeling

Biotinylation of this product is performed using Avitag™ technology. Briefly, the single lysine residue in the Avitag is enzymatically labeled with biotin.

Protein Ratio

Passed as determined by the SABA assay / HABA assay / binding ELISA.

Purity

>95% as determined by SDS-PAGE.

Formulation

Lyophilized from 0.22 μm filtered solution in Tris with Glycine, Arginine and NaCl, pH7.5 with trehalose as protectant.

Contact us for customized product form or formulation.

Reconstitution

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

Shipping and Storage

This product is shipped at ambient temperature.

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.

Background Introduction

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.