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GITR
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q9Y5U5-1 |
|---|---|
| Species | Human |
| Sequence | Gln26-Glu161 |
| Purity | > 95% as analyzed by SDS-PAGE |
| Endotoxin Level | < 0.1 EU/ µg of protein by gel clotting method |
| Biological Activity | Immobilized GITR, hFc, Human at 5.0 µg/ml (100 µl/well) can bind biotinylated GITR Ligand, hFc, Human (Cat. No.: Z03446) when detected by Streptavidin-HRP. |
| Expression System | HEK 293 |
| Formulation | Lyophilized from a 0.2 µm filtered solution in PBS, 5% trehalose and mannitol. |
| Reconstitution | It is recommended that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Reconstitute the lyophilized powder in ddH₂O or PBS up to 100 µg/ml. |
| Storage & Stability | Upon receiving, this product remains stable for up to 6 months at lower than -70°C. Upon reconstitution, the product should be stable for up to 1 week at 4°C or up to 3 months at -20°C. For long term storage it is recommended that a carrier protein (example 0.1% BSA) be added. Avoid repeated freeze-thaw cycles. |
| Target Background | GITR (glucocorticoid-induced tumor necrosis factor receptor), also known as AITR and TNFRSF18, is a 40 kDa transmembrane glycoprotein that functions in immune regulation. Mature human GITR consists of a 137 amino acid extracellular domain (ECD) with three tandem TNFR cysteine-rich repeats, a 21 aa transmembrane segment, and a 58 aa cytoplasmic domain. Within the ECD, human GITR shares 55% and 60% aa sequence identity with mouse and rat GITR, respectively. Alternative splicing generates an isoform with a short deletion in the cytoplasmic domain and a potentially secreted isoform that is substituted within the third TNFR repeat and lacks the transmembrane and cytoplasmic regions. GITR is expressed on CD4+ CD25+ regulatory T cells (Treg) as well as on subsets of thymocytes, lymph node cells, and splenocytes, and it is upregulated on antigen-activated conventional CD4+ and CD8+ T cells. GITR binding by GITR Ligand/TNFSF18 costimulates the proliferation and activation of CD4+ or CD8+ conventional T cells. It also induces the proliferation of Treg but inhibits the ability of Treg to suppress immune responses. This can result in the development of autoimmunity, increased tumor cell killing by effector T cells, and increased inflammation in arthritis, allergic asthma, and inflammatory bowel disease. GITR is also expressed on sympathetic neurons where it enhances NGF-induced neurite outgrowth and branching. |
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Research Areas
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Cat# PVGS1565
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