The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Biological activityInhibits Human rhsRANKL biological functions. Binds to Human and Mouse RANKL.
Endotoxin level< 0.100 Eu/µg
Additional notesAfter reconstitution, prepare aliquots and store at -20°C. Avoid freeze/thaw cycles. PBS containing at least 0.1% BSA should be used for further dilutions.
Inhibits Human rhsRANKL biological functions. Binds to Human and Mouse RANKL.
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Preparation and Storage
Stability and Storage
Shipped at 4°C. Store at 4°C (up to 6 months). Store at -20°C.
ReconstitutionReconstitute with 50µl sterile water to give a final concentration of 1mg/ml.
Loss of heterozygosity 18 chromosomal region 1
Osteoclast differentiation factor receptor
Paget disease of bone 2
Receptor activator of NF KB
Receptor activator of NF-KB
receptor activator of nuclear factor kappa B
Tumor necrosis factor receptor superfamily member 11A
Tumor necrosis factor receptor superfamily member 11a NFKB activator
Tumor necrosis factor receptor superfamily member 11a activator of NFKB
FunctionReceptor for TNFSF11/RANKL/TRANCE/OPGL; essential for RANKL-mediated osteoclastogenesis. Involved in the regulation of interactions between T-cells and dendritic cells.
Tissue specificityUbiquitous expression with high levels in skeletal muscle, thymus, liver, colon, small intestine and adrenal gland.
Involvement in diseaseDefects in TNFRSF11A are the cause of familial expansile osteolysis (FEO) [MIM:174810]. FEO is a rare autosomal dominant bone disorder characterized by focal areas of increased bone remodeling. The osteolytic lesions develop usually in the long bones during early adulthood. FEO is often associated with early onset deafness and loss of dentition. Defects in TNFRSF11A are a cause of Paget disease of bone type 2 (PDB2) [MIM:602080]; also known as familial Paget disease of bone. PDB2 is a bone-remodeling disorder with clinical similarities to FEO. Unlike FEO, however, affected individuals have involvement of the axial skeleton with lesions in the spine, pelvis and skull. Defects in TNFRSF11A are the cause of osteopetrosis autosomal recessive type 7 (OPTB7) [MIM:612301]; also called osteoclast-poor osteopetrosis with hypogammaglobulinemia. Osteopetrosis is a rare genetic disease characterized by abnormally dense bone, due to defective resorption of immature bone. The disorder occurs in two forms: a severe autosomal recessive form occurring in utero, infancy, or childhood, and a benign autosomal dominant form occurring in adolescence or adulthood. OPTB7 is characterized by paucity of osteoclasts, suggesting a molecular defect in osteoclast development. OPTB7 is associated with hypogammaglobulinemia.