Recombinant Human GITR/TNFRSF18 Fc Chimera Protein, CF
Recombinant Human GITR/TNFRSF18 Fc Chimera Protein, CF Summary
Product Specifications
Human GITR (Gln26-Glu161) (Thr45Ala) Accession # Q9Y5U5 | IEGRMD | Human IgG1 (Pro100-Lys330) |
N-terminus | C-terminus | |
Analysis
Product Datasheets
Carrier Free
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.
689-GR
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.
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Reconstitution Calculator
Background: GITR/TNFRSF18
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 human GITR consists of a 137 amino acid (aa) extracellular domain (ECD) with three tandem TNFR cysteine-rich repeats, a 21 aa transmembrane segment, and a 58 aa cytoplasmic domain (3, 4). 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 (4-6), and it is upregulated on antigen-activated conventional CD4+ and CD8+ T cells (3, 4, 6, 7). GITR binding by GITR Ligand/TNFSF18 costimulates the proliferation and activation of CD4+ or CD8+ conventional T cells (3, 7-9). It also induces the proliferation of Treg (8, 10) but inhibits the ability of Treg to suppress immune responses (5, 8, 11-13). This can result in the development of autoimmunity, increased tumor cell killing by effector T cells (5, 11), and increased inflammation in arthritis, allergic asthma, and inflammatory bowel disease (10, 14). GITR is also expressed on sympathetic neurons where it enhances NGF-induced neurite outgrowth and branching (15).
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- O'Keeffe, G.W. et al. (2008) Nat. Neurosci. 11:135.
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