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GITR / Tnfrsf18 (mouse) Antibody - With BSA and Azide
Rat Monoclonal Antibody [Clone DTA-1 ]
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| IF, FC |
|---|---|
| Primary Accession | O35714 |
| Other Accession | 21936 (Mouse), 3180 (Mouse), 482508 (Mouse) |
| Reactivity | Mouse |
| Host | Rat |
| Clonality | Monoclonal |
| Isotype | Rat / IgG2b, lambda |
| Clone Names | DTA-1 |
| Calculated MW | 66-70kDa (Homodimer) |
| Gene ID | 21936 |
|---|---|
| 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 - With BSA and Azide is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | Tnfrsf18 |
|---|---|
| Synonyms | Gitr |
| 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.
Background
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.
References
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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