Recombinant Cynomolgus DcR3/TNFRSF6B Fc Chimera Protein, CF Summary
|Cynomolgus Monkey DcR3/TNFRSF6B |
Accession # EHH65162
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 MES and NaCl.|
|Reconstitution||Reconstitute at 500 μg/mL in water.|
|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.
Recombinant Cynomolgus Monkey DcR3/TNFRSF6B Fc Chimera (Catalog # 9297-DC) inhibits Recombinant Human Fas Ligand/TNFSF6 (Catalog # 126-FL) induced apoptosis of Jurkat human acute T cell leukemia cells. The ED50 for this effect is 15-75 ng/mL.
DcR3 (Decoy Receptor 3), also known as TR6 and TNFRSF6B is a 35-40 kDa secreted member of the TNF Receptor superfamily (1). Mature cynomolgus DcR3 contains four tandem TNFR cysteine-rich domains and shares 92% amino acid sequence identity with human DcR3. It binds to the TNF superfamily ligands Fas Ligand, TL1A, and LIGHT (2-5) and interferes with their respective interactions with Fas, DR3, or HVEM and Lymphotoxin beta R (2-4). It blocks apoptosis triggered through either Fas Ligand, TL1A, or LIGHT (2, 3, 5, 6). DcR3 is up-regulated in a variety of cancers and enhances tumor cell immune evasion (2, 3, 7). It also promotes immune suppression by inducing dendritic cell apoptosis (8), inhibiting NK cell and CD8+ T cell activity (2, 4), and inhibiting the production of inflammatory cytokines during viral infection or autoimmunity (9, 10). In humans, proteolytic removal of the C-terminal 53 amino acids generates a shortened DcR3 that retains the ability to block LIGHT but not Fas Ligand induced apoptosis (11). DcR3 can also induce osteoclast formation from monocytes (12).
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