Recombinant Mouse GITR/TNFRSF18 Fc Chimera Protein, CF Summary
Accession # Q8C4K3
CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.
In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.
|Formulation||Lyophilized from a 0.2 μm filtered solution in PBS.|
|Reconstitution||Reconstitute at 100 μg/mL in sterile PBS.|
|Shipping||The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.|
|Stability & Storage:||Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
GITR (glucocorticoid-induced tumor necrosis factor receptor), also known as AITR and TNFRSF18, is a 40 kDa transmembrane glycoprotein that functions in immune regulation (1, 2). Mature mouse GITR consists of a 134 amino acid (aa) extracellular domain (ECD) with three tandem TNFR cysteine-rich repeats, a 21 aa transmembrane segment, and a 55 aa cytoplasmic domain (3). Within the ECD, mouse GITR shares 55% and 86% aa sequence identity with human and rat GITR, respectively. Alternative splicing generates additional isoforms with substituted cytoplasmic domains or with a substitution within the third TNFR repeat, transmembrane, and cytoplasmic regions (4). GITR is expressed on CD4+CD25+ regulatory T cells (Treg) as well as on subsets of thymocytes, lymph node cells, and splenocytes (3, 5, 6), and it is upregulated on antigen-activated conventional CD4+ and CD8+ T cells (3, 6-8). GITR binding by GITR Ligand/TNFSF18 costimulates the proliferation and activation of CD4+ or CD8+ conventional T cells (7-10). It also induces the proliferation of Treg (9, 11) but inhibits the ability of Treg to suppress immune responses (5, 9, 12-14). This can result in the development of autoimmunity, increased tumor cell killing by effector T cells (5, 12), and increased inflammation in arthritis, allergic asthma, and inflammatory bowel disease (11, 15). GITR is also expressed on sympathetic neurons where it enhances NGF-induced neurite outgrowth and branching (16).
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