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RANKLReceptor Activator of Nuclear Factor Kappa B Ligand (molecular biology)
RANKLReceptor Activator of NF-B Ligand
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At the same time, we detected the gene and protein levels of bone formation relevant biochemical markers BGP, collagen I, TNF-[alpha], OPG, and RANKL. This study explored the effects of risperidone on bone formation and differentiation.
Under a stimulus, with a local increase of cytokines, T-cells are activated and express RANKL, and subsequently, differentiation and activation of pre-odontontoclasts occur.
Our co-culture system is efficient because no additional inducers such as RANKL and MCSF were required as those key regulators were naturally released by the mature OBs.
Specifically, the production of prostaglandins, parathyroid hormone, parathyroid hormone-related peptide, activated vitamin D, IL-6, and TNF by cancer cells may lead to tumor-induced increases in RANKL expression on osteoblasts and bone marrow stromal cells [7].
RANKL exhibited a significant group effect (p < 0.0001), and in post hoc testing, its expression was significantly higher in BM+ (386.7 [+ or -] 32.26) with respect to both BL (169.6 [+ or -] 25.74) and BM- (278.3 [+ or -] 15.24) (BM+ vs BL p = 0.0011; BM+ vs BM- p = 0.0014) (Figures 2(d)-2(f)).
Bacterial lipopolysaccharides and RANKL induce human peripheral blood mononuclear cells to express A20, which is associated with TRAF6 and NF-kB degradation.
To understand the similarities and differences among them that could be useful for diagnosis and therapeutic purposes, it is important to study the cellular and extracellular elements that take part on the physiopathological mechanisms implicated in their origin and growth; therefore, the aim of this study was to evaluate and compare Ki67, CD138, and the molecular RANK, RANKL, and OPG triad expression on the lining epithelium and stroma of UA, OKC, and DC.
RANKL and OPG are members of the superfamily of tumor necrosis factor (TNF) and TNF receptor, respectively, and their binding to receptor activator of NF-kB (RANK) has a fundamental role regulating osteoclast formation, proliferation, activity, and survival [72].
In addition to its effect on bone formation, studies have shown that activation of the Wnt/[beta]-catenin pathway in osteoblasts was also associated with decreased levels of RANKL and increased levels of OPG, which lead to suppressed bone resorption in mice and lower production of resorption markers in cultured osteoblasts [27, 28].
RANKL is a TNF family cytokine that is primarily expressed by osteoblasts and also secreted by bone marrow stromal cells (BMSCs), preosteoblasts, osteocytes, fibroblasts, and cells of the immune system, including antigen-stimulated T cells and mature dendritic cells.
In bone tissue, PTH increases osteoclast formation and bone resorption by regulating the receptor activator of nuclear factor kappa B ligant (RANKL)/osteoprotegerin (OPG) expressed in osteoblasts.