RANKL/TNFSF11/CD254 Protein, Cynomolgus, Recombinant (hFc)

1. Immobilized Cynomolgus S4-Fc3L3-TNFSF11 at 10 μg/ml (100 μl/well) can bind biotinylated human TNFRSF11B-His , The EC50 of biotinylated human TNFRSF11B-His is 7.94-18.52 ng/ml. 2. The bioactivity of RANKL was determined by measuring the ability of RANKL to induce TRAP activity in RAW264.7 cells. The ED50 for this effect is typically 7-35 ng/mL.

RANKL/TNFSF11/CD254 Protein, Cynomolgus, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 48.9 kDa and the accession number is G7PW41.

Cynomolgus

HEK293 Cells

> 85 % as determined by SDS-PAGE

Tumor necrosis factor ligand superfamily member 11, also known as Receptor activator of nuclear factor kappa-B ligand, Osteoprotegerin ligand, TNFSF11, RANKL, TRANCE, OPGL and CD254, is a single-pass type II membrane protein that belongs to the tumor necrosis factor family. The receptor activator of nuclear factor-kappaB ligand (RANKL), its cognate receptor RANK, and its natural decoy receptor osteoprotegerin have been identified as the final effector molecules of osteoclastic bone resorption. RANK and RANKL are key regulators of bone remodeling and regulate T cell/dendritic cell communications, and lymph node formation. Moreover, RANKL and RANK are expressed in mammary gland epithelial cells and control the development of a lactating mammary gland during pregnancy. Genetically, RANKL and RANK are essential for the development and activation of osteoclasts and bone loss in response to virtually all triggers tested. Inhibition of RANKL function via the natural decoy receptor osteoprotegerin (OPG, TNFRSF11B) prevents bone loss in postmenopausal osteoporosis and cancer metastases. Importantly, RANKL appears to be the pathogenetic principle that causes bone and cartilage destruction in arthritis. RANK-RANKL signaling not only activates a variety of downstream signaling pathways required for osteoclast development, but crosstalk with other signaling pathways also fine-tunes bone homeostasis both in normal physiology and disease. In addition, RANKL and RANK have essential roles in lymph node formation, establishment of the thymic microenvironment, and development of a lactating mammary gland during pregnancy.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy