Function: Acts as allurement receptor for TNFSF11/RANKL and thereby neutralizes its action in
osteoclastogenesis. Inhibits the activation of osteoclasts and promotes osteoclast apoptosis in vitro.
Cartilage homeostasis seems to depend on the bounded arrangement amid TNFSF11 and TNFRSF11B. May aswell play a
role in preventing arterial calcification. May act as allurement receptor for TNFSF10/TRAIL and assure adjoin
apoptosis. TNFSF10/TRAIL bounden blocks the inhibition of osteoclastogenesis. Ref.12 Ref.16
Subunit structure: Homodimer. Interacts with TNFSF10 and TNFSF11. Ref.13 Ref.16
Subcellular location: Secreted.
Tissue specificity: Highly bidding in developed lung, heart, kidney, liver, spleen, thymus, prostate, ovary,
baby intestine, thyroid, lymph node, trachea, adrenal gland, testis, and cartilage marrow. Detected at actual
low levels in brain, placenta and ashen muscle. Highly bidding in fetal kidney, alarmist and lung.
Induction: Up-regulated by accretion calcium-concentration in the average and estrogens. Down-regulated by
Post-translational modification: N-glycosylated. Contains sialic acerbic residues. Ref.16The N-terminus is
Involvement in disease: Juvenile Paget ache (JPD) [MIM:239000]: Rare autosomal backward osteopathy that
presents in adolescence or aboriginal childhood. The ataxia is characterized by rapidly adjustment alloyed
bone, osteopenia, debilitating fractures, and deformities due to a clearly accelerated amount of cartilage
adjustment throughout the skeleton. Approximately 40 cases of JPD accept been appear worldwide. Unless it is
advised with drugs that block osteoclast-mediated ashen resorption, the ache can be fatal.Note: The ache is
acquired by mutations affecting the gene represented in this entry.