Reactive species
Human;Mouse;Rat
Protein name
Tumor necrosis factor ligand superfamily member 11
Immunogen
The antiserum was produced against synthesized peptide derived from the C-terminal region of human TNFSF11. AA range:268-317
Specificity
RANKL Monoclonal Antibody detects endogenous levels of RANKL protein.
Constitute
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Source
Monoclonal, Mouse,IgG
Dilution rate
Western Blot: 1/500 - 1/2000
Purification process
The antibody was affinity-purified from mouse antiserum by affinity-chromatography using epitope-specific immunogen.
Other name
TNFSF11; OPGL; RANKL; TRANCE; Tumor necrosis factor ligand superfamily member 11; Osteoclast differentiation factor; ODF; Osteoprotegerin ligand; OPGLReceptor activator of nuclear factor kappa-B ligand; RANKL; TNF-related activation-induced cytokine; TRANCE; CD254
Background
This gene encodes a member of the tumor necrosis factor (TNF) cytokine family which is a ligand for osteoprotegerin and functions as a key factor for osteoclast differentiation and activation. This protein was shown to be a dentritic cell survival factor and is involved in the regulation of T cell-dependent immune response. T cell activation was reported to induce expression of this gene and lead to an increase of osteoclastogenesis and bone loss. This protein was shown to activate antiapoptotic kinase AKT/PKB through a signaling complex involving SRC kinase and tumor necrosis factor receptor-associated factor (TRAF) 6, which indicated this protein may have a role in the regulation of cell apoptosis. Targeted disruption of the related gene in mice led to severe osteopetrosis and a lack of osteoclasts. The deficient mice exhibited defects in early differentiation of T and B ly
Function
disease:Defects in TNFSF11 are the cause of osteopetrosis autosomal recessive type 2 (OPTB2) [MIM:259710]; also known as osteoclast-poor osteopetrosis. 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. Autosomal recessive osteopetrosis is usually associated with normal or elevated amount of non-functional osteoclasts. OPTB2 is characterized by paucity of osteoclasts, suggesting a molecular defect in osteoclast development.,function:Cytokine that binds to TNFRSF11B/OPG and to TNFRSF11A/RANK. Osteoclast differentiation and activation factor. Augments the ability of dendritic cells to stimulate naive T-cell proliferation. May be an
