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Your Position: Home > Immune Checkpoint Proteins > GITR > Mouse GITR / TNFRSF18 Protein, Fc Tag

Mouse GITR / TNFRSF18 Protein, Fc Tag

  • Synonym
    AITR,GITR,TNFRSF18,CD357
  • Source
    Mouse GITR, Fc Tag (GIR-M5251) is expressed from human 293 cells (HEK293). It contains AA Ser 22 - His 153 (Accession # Q8C4K3).
    Predicted N-terminus: Ser 22
  • Molecular Characterization
    GITR(Ser 22 - His 153) Q8C4K3

    This protein carries a human IgG1 Fc tag at the C-terminus.

    The protein has a calculated MW of 40.3 kDa. The protein migrates as 55 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.

  • Endotoxin
    Less than 1.0 EU per μg by the LAL method.
  • Purity

    >95% as determined by SDS-PAGE.

  • Formulation

    Lyophilized from 0.22 μm filtered solution in 50 mM Tris, 100 mM Glycine, pH7.5. Normally trehalose is added as protectant before lyophilization.

    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.

  • Storage

    For long term storage, the product should be stored at lyophilized state at -20°C or lower.

    Please avoid repeated freeze-thaw cycles.

    No activity loss is observed after storage at:

    1. 4-8°C for 12 months in lyophilized state;
    2. -70°C for 3 months under sterile conditions after reconstitution.
SDS-PAGE
Mouse GITR, Fc Tag (Cat. No. GIR-M5251) SDS-PAGE gel

Mouse GITR, Fc Tag on SDS-PAGE under reducing (R) condition. The gel was stained overnight with Coomassie Blue. The purity of the protein is greater than 95%.

  • Background
    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.
  • References
  • Please contact us via TechSupport@acrobiosystems.com if you have any question on this product.

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