|Application ||IF, FC|
|Other Accession||21936 (Mouse), 3180 (Mouse), 482508 (Mouse)|
|Isotype||Rat / IgG2b, lambda|
|Calculated MW||66-70kDa (Homodimer)|
|Other Names||Tumor necrosis factor receptor superfamily member 18, Glucocorticoid-induced TNFR-related protein, CD357, Tnfrsf18, Gitr|
|Storage||Store at 2 to 8°C.Antibody is stable for 24 months.|
|Precautions||GITR / Tnfrsf18 (mouse) Antibody - Without BSA and Azide is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Receptor for TNFSF18. Seems to be involved in interactions between activated T-lymphocytes and endothelial cells and in the regulation of T-cell receptor-mediated cell death. Mediated NF-kappa-B activation via the TRAF2/NIK pathway (By similarity).|
|Cellular Location||Isoform A: Cell membrane; Single-pass type I membrane protein Isoform C: Cell membrane; Single-pass type I membrane protein|
|Tissue Location||Preferentially expressed in activated T lymphocytes|
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Provided below are standard protocols that you may find useful for product applications.
GITR (glucocorticoid-induced TNFR-related gene) is a member of the TNF-receptor superfamily, also known as TNFRSF18. It is expressed at low levels on resting T lymphocytes and at high levels on CD25+ĀCD4+ĀTregs. The expression of GITR on T cells can be upregulated upon activation. Interaction of GITR with its ligand (GITRL) has been demonstrated to augment T cell activation, proliferation, cytokine production as well as MAPKs and NF-ĪŗB activation, and abrogate the inhibitory function ofĀCD25+ĀCD4+ĀTregs. In vivoĀactivation of GITR causes development of autoimmune diseases and restores the suppressed immune response.
Stephens GL, et al. 2004. J. Immunol. 173:5008. | Tone M, et al. 2003. Proc. Natl. Acad. Sci. USA 100:15059
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