>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
<0.10 EU per 1 μg of the protein by the LAL method.
Measured by its binding ability in a functional ELISA. When Recombinant Cynomolgus Monkey GITR/TNFRSF18 Fc Chimera
is immobilized at 0.5 μg/mL, 100 μL/well, the concentration of biotinylated recombinant human GITR Ligand/TNFSF18 that produces 50% of the optimal binding
response is 8-40 ng/mL.
When Recombinant Cynomolgus Monkey GITR/TNFRSF18 Fc Chimera (Catalog # 9428‑GR) is immobilized at 0.5 µg/mL, biotinylated recombinant human GITRLigand/TNFSF18 binds with an ED50 of 8-40 ng/mL.
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
TNF R cysteine-rich repeats, a 21 aa transmembrane segment, and a 58 aa
cytoplasmic domain (3, 4). Within the ECD region, cyno GITR shares 89.8% and
53.2% aa sequence identity with human and mouse 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 TNF R
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
up-regulated on antigen-activated conventional CD4+ and CD8+
T cells (3, 4, 6, 7). GITR binding by GITR Ligand/TNFSF18 co-stimulates 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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