Recombinant Human GITR protein (Fc Chimera)
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Recombinant Human GITR protein (Fc Chimera) is a Human Fragment protein, in the 26 to 161 aa range, expressed in HEK 293 cells, with >90%, < 1 EU/µg endotoxin level, suitable for SDS-PAGE.
View Alternative Names
CD357, AITR, GITR, UNQ319/PRO364, TNFRSF18, Tumor necrosis factor receptor superfamily member 18, Activation-inducible TNFR family receptor, Glucocorticoid-induced TNFR-related protein
- SDS-PAGE
Supplier Data
SDS-PAGE - Recombinant Human GITR protein (Fc Chimera) (AB198670)
4-20% SDS-PAGE analysis of ab198670 (3 μg) with Coomassie staining.
Note : This protein runs at a higher MW by SDS-PAGE due to glycosylation.
Reactivity data
Product details
Sequence info
Properties and storage information
Shipped at conditions
Appropriate short-term storage conditions
Appropriate long-term storage conditions
Storage information
Supplementary information
This supplementary information is collated from multiple sources and compiled automatically.
Biological function summary
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.
Pathways
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.
Specifications
Form
Liquid
General info
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.
Target data
Product promise
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