sRANKL total ELISA kit Assays and Kits

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sRANKL total ELISA kit

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Product Name	sRANKL total ELISA kit	Cat. No.#	K1016
Price	£695	Size	96 wells
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Receptor Activator for Nuclear Factor κ B Ligand (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 Receptor Activator for Nuclear Factor κ B Ligand (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. Overproduction of Receptor Activator for Nuclear Factor κ B Ligand (RANKL) is implicated in a variety of degenerative bone diseases, such as rheumatoid arthritis and osteomyelitis.

It has been shown, that Receptor Activator for Nuclear Factor κ B Ligand (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 Receptor Activator for Nuclear Factor κ B Ligand (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 Receptor Activator for Nuclear Factor κ B Ligand (RANKL) and stimulated OPG expression.

The effects of Receptor Activator for Nuclear Factor κ B Ligand (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.

Receptor Activator for Nuclear Factor κ B Ligand (RANKL) also has a function in the immune system, where it is expressed by T helper cells and is thought to be involved in dendritic cell maturation. 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 the Receptor Activator for Nuclear Factor κ B Ligand (RANKL) 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 lymphocytes, and failed to form lobulo-alveolar mammary structures during pregnancy. Two alternatively spliced transcript variants have been found.