sRANKL Mouse/Rat ELISA

RANKL, receptor activator of nuclear factor (NF)-B ligand (also:
osteoprotegerin ligand, OPGL), its cellular receptor, receptor activator of NF-
B (RANK), and the decoy receptor, osteoprotegerin (OPG) have been
identified as the key molecular regulation system for bone remodelling.
RANKL, a member of the tumor necrosis factor (TNF) family, is the main
stimulatory factor for the formation of mature osteoclasts and is essential for
their survival. Therefore, an increase in RANKL expression leads to bone
resorption and bone loss. RANKL is produced by osteoblastic lineage cells
and activated T lymphocytes. It activates its specific receptor RANK which is
located on osteoclasts and dendritic cells.
The effects of RANKL are counteracted by OPG which is secreted by various
tissues and acts as an endogenous soluble receptor antagonist.
Imbalances of the RANKL/OPG system have been related to the
pathogenesis of Paget’s disease, benign and malignant bone tumors,
postmenopausal osteoporosis, rheumatoid arthritis, bone metastases and
hypercalcemia. It was shown in several studies that in animal models
restoring of the RANKL/OPG balance (e.g. by administering OPG) reduces
the severity of these disorders.
It has been shown that RANKL is produced as a membrane-bound protein
on murine osteoblasts/stromal cells, and cleaved into a soluble form by a
metalloprotease. Stimulators of the osteoclastogenesis such as IL-1beta, IL-6,
IL-11, IL-17, and TNF-alpha, increase the expression of RANKL and decrease
OPG expression in osteoblasts/stromal cells. Cytokines inhibiting the
osteoclastogenesis such as IL-13, INF-gamma, and TGF-beta1, suppress the
expression of RANKL and stimulated OPG expression.