Kits
total sRANKL ELISA
Kits
Description
RANKL (receptor activator of nuclear factor (NF)-kB ligand; also: osteoprotegerin ligand,
OPGL), its cellular receptor, receptor activator of NF-kB (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.
OPGL), its cellular receptor, receptor activator of NF-kB (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.