RANKL


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RANKL

(rank'ĕl),
Abbreviation for receptor activator of nuclear factor-κB.

RANKL

, RANK ligand
Thereceptor activator of nuclear factor kappa B ligand, a chemical produced by osteoblasts that causes osteoclasts to proliferate and break down both the cortex and the trabecula of bone.

Excessive activity of this chemical produces pathological bone loss, e.g., in some forms of inflammatory arthritis and in some diseases in which cancers metastasize to bone.

References in periodicals archive ?
To explore the role of risperidone in preosteoblast development, gene expression of BGP, collagen 1, OPG, RANKL, and TNF-[alpha] were detected by qPCR method.
To further characterize the phenotype of POLCs, we investigate the expression of the main markers of osteoblasts, RUNX2, RANKL, and VDR.
Goh et al., "Roles of the TRAF6 and Pellino E3 ligases in MyD88 and RANKL signaling," Proceedings of the National Academy of Sciences of the United States of America, vol.
For RANK, RANKL, and OPG immunostaining, only the number of positive cells located at the cystic lining epithelium and stromal cells were counted and added, obtaining finally a total mean of positive cells, both in the epithelium and the stroma of each lesions.
Interestingly, a knockout study in mice found that factors that stimulate or suppress bone resorption through osteoclast lineage also influence OPG and RANKL expression at the mRNA and protein levels [69].
Continuous secretion of PTH is associated with increased bone turnover in favor of bone resorption through upregulation of RANKL and downregulation of OPG [37, 38].
However, some studies demonstrated that B cells and plasma cells in the bone microenvironment are significant sources of OPG [50-52], which is a neutralizing soluble decoy receptor that competes with RANKL, thus blocking the binding of RANKL and RANK, which eliminates the effect of RANKL on osteoclasts [53].
In vivo studies have demonstrated that continuous infusion of PTH triggers a decrease of OPG and an increase of RANKL capable of inducing osteoclast differentiation and promoting bone resorption (Ma et al.).
Anti-human Bcl-2, procaspase-3, caspase-3, poly(ADP-ribose) polymerase (PARP), and RANKL antibodies were obtained from Cell Signaling Technology (Beverly, MA).
Carboxyterminal type I collagen cross links (CTX-I) for bone degradation products, human type I procollagen amino terminal propeptide (P1NP, Sunred Biological Technology) for bone formation, sclerostin (SOST), osteoprotegerin (OPG), Dickkopf-related protein-1 (DKK1), and soluble RANKL (ampli-sRANKL, Biomedica Gruppe) were analyzed with enzyme-linked immunosorbent assay [14] in serum samples according to the manufacturer's instructions.
These effects are mediated via redirecting signaling from Signal Transducer and Activator of Transcription (Stat) 3 to Statl in bone cells and reducing receptor activator of nuclear factor kappa-B ligand (RANKL) expression in osteoclasts.