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Current Understanding of RANK Signaling in Osteoclast Differentiation and Maturation

Title
Current Understanding of RANK Signaling in Osteoclast Differentiation and Maturation
Authors
Park, Jin HeeLee, Na KyungLee, Soo Young
Ewha Authors
이수영
SCOPUS Author ID
이수영scopus
Issue Date
2017
Journal Title
MOLECULES AND CELLS
ISSN
1016-8478JCR Link0219-1032JCR Link
Citation
vol. 40, no. 10, pp. 706 - 713
Keywords
nuclear factor-kappa Bnuclear factor of activated Tcells cytoplasmic 1osteoclastsreceptor activator of nuclear factor-kappa Btumor necrosis factor receptor-associated factors
Publisher
KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
Indexed
SCI; SCIE; SCOPUS; KCI WOS
Abstract
Osteoclasts are bone-resorbing cells that are derived from hematopoietic precursor cells and require macrophage-colony stimulating factor and receptor activator of nuclear factor-kappa B ligand (RANKL) for their survival, proliferation, differentiation, and activation. The binding of RANKL to its receptor RANK triggers osteoclast precursors to differentiate into osteoclasts. This process depends on RANKL-RANK signaling, which is temporally regulated by various adaptor proteins and kinases. Here we summarize the current understanding of the mechanisms that regulate RANK signaling during osteoclastogenesis. In the early stage, RANK signaling is mediated by recruiting adaptor molecules such as tumor necrosis factor receptor-associated factor 6 (TRAF6), which leads to the activation of mitogen-activated protein kinases (MAPKs), and the transcription factors nuclear factor-kappa B (NF-kappa B) and activator protein-1 (AP-1). Activated NF-kappa B induces the nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), which is the key osteoclastogenesis regulator. In the intermediate stage of signaling, the co-stimulatory signal induces Ca2+ oscillation via activated phospholipase C gamma 2 (PLC gamma 2) together with c-Fos/AP1, wherein Ca2+ signaling facilitates the robust production of NFATc1. In the late stage of osteoclastogenesis, NFATc1 translocates into the nucleus where it induces numerous osteoclast-specific target genes that are responsible for cell fusion and function.
DOI
10.14348/molcells.2017.0225
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자연과학대학 > 생명과학전공 > Journal papers
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