Rat Monoclonal GITR antibody. Suitable for Flow Cyt, FuncS and reacts with Mouse samples. Cited in 1 publication.
pH: 7.2
Constituents: 0.87% Sodium chloride, 0.12% Sodium dihydrogen phosphate
Flow Cyt | FuncS | |
---|---|---|
Mouse | Expected | Expected |
Species | Dilution info | Notes |
---|---|---|
Species Mouse | Dilution info Use at an assay dependent concentration. | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Mouse | Dilution info Use at an assay dependent concentration. | Notes - |
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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).
CD357, Gitr, Tnfrsf18, Tumor necrosis factor receptor superfamily member 18, Glucocorticoid-induced TNFR-related protein
Rat Monoclonal GITR antibody. Suitable for Flow Cyt, FuncS and reacts with Mouse samples. Cited in 1 publication.
pH: 7.2
Constituents: 0.87% Sodium chloride, 0.12% Sodium dihydrogen phosphate
Endotoxin Level: Less than or equal to 0.01 EU/ug, as determined by the LaL assay. >90% pure as determined by SDS-PAGE analysis.
GITR also known as TNFRSF18 is a 241 amino acid protein with a mass of approximately 27 kDa. It belongs to the tumor necrosis factor receptor superfamily. GITR is highly expressed on activated T cells and regulatory T cells (Tregs). The gene encoding GITR is located on chromosome 1 in humans. High surface expression is also observed in immune tissues such as the thymus spleen and lymph nodes playing an important role in immune responses.
GITR acts as a costimulatory molecule that enhances T cell activation and proliferation. It does not function as part of a complex but interacts directly with ligand GITRL triggering downstream signaling cascades. This interaction is key in the modulation of immune responses notably in enhancing the activity of effector T cells and regulating Treg functions. Activation of GITR can reduce Treg-mediated suppression leading to enhanced immune responses.
The mechanistic role of GITR involves NF-kB and MAPK signaling pathways. Through these GITR impacts immune responses by stimulating the production of cytokines and promoting cell survival and proliferation. GITR signaling intersects with pathways involving proteins such as NF-kB further integrating with the immune system's regulation crescendo.
GITR appears to play a role in autoimmune conditions like rheumatoid arthritis and potential cancer immunotherapy. In autoimmune diseases GITR modulates immune activity influencing the balance between inhibition and activation of T cells. In oncology GITR targeting aims to enhance immune responses against tumors. Through these conditions GITR shows connections to proteins such as CTLA-4 which also contributes to immune regulatory processes.
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This species and application combination has not been tested, but we predict it will work based on strong homology. However, this combination is not covered by our product promise.
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