RANK ligand

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RANK ligand

[¦raŋk ′līg·ənd]
(biochemistry)
A local paracrine factor that originates from osteoblasts and mediates the effects of most, if not all, agents that are known to impact osteoclast development in bone. Also known as osteoprotegerin ligand.
McGraw-Hill Dictionary of Scientific & Technical Terms, 6E, Copyright © 2003 by The McGraw-Hill Companies, Inc.
References in periodicals archive ?
BGP, collagen 1, OPG, RANKL, and TNF-[alpha] primer sequences for PCR are shown in Table 1.
This system did not require exogenous MCSF and RANKL. Moreover, this co-culture ratio optimization ensured a good interaction between the bone cells, thus providing us with a reliable bone cell co-culture system capable of mimicking the bone-remodeling process in humans.
Analysis of RANKL showed a significant difference between the presence of RANKL-positive prostate cells between Micro+ and Micro- (Micro+ 283.70 [+ or -] 24.23 vs Micro- 216.60 [+ or -] 18.07; p = 0.0252) (Figure 4(d)).
As an endopeptidase, RPN11 functions to cleave polyubiquitin chains from substrates [126] While CSN5/Jab1 hydrolyzes the ubiquitinlike modifier Nedd8 [127], POH1 enhances osteoclast differentiation and RANKL signaling via regulating Mitf, an important regulator of osteoclast differentiation which required gene expression [128].
For CD138, it was considered as positive immunostain when all those cystic lining epithelium cells exhibited stain at cell membrane, while for RANK, RANKL, and OPG, it was considered as positive immunostain when the cystic lining epithelium cells and the stroma cells exhibited cytoplasm stain.
Smokers have lower, but not statistically significant, levels of RANKL and higher, but not statistically significant, levels of RANKL/OPG ratio [25].
Mechanical unloading of the bone stimulates the production of Wnt inhibitors such as sclerostin by osteocytes and RANKL by osteoblasts in the "unloaded" region, resulting in decreased activation of the Wnt/[beta]catenin pathway in neighboring cells and increased bone resorption [6, 33].
Th17 cells play an important role in the pathogenesis of osteoporosis and directly produce high levels of IL-17, RANKL, and TNF to promote the formation and activation of osteoclasts [38, 45, 46].
One of the key factors for the development of functional osteoclasts is the induction of cytokines, especially the receptor activator of nuclear factor kappa B ligant (RANKL) and its soluble decoy receptor osteoprotegerin (OPG) (Nakashima & de Crombrugghe, 2003).
Breast cancer-induced factors stimulate osteoblastic/stromal cells to produce macrophage-colony-stimulating factor (M-CSF) for the survival of osteoclast precursors and receptor activator of nuclear factor-[kappa]B ligand (RANKL) for osteoclastogenesis [7].
Identification of B- and T-cells and granulocytes in peripheral blood, RANKL surface expression, and immunophenotyping of monocytes in the PBMC samples were performed using matched combinations of anti-human murine mAbs as previously described [12].