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자연과학대학
생명과학전공
Journal papers
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RANKL-induced schlafen2 is a positive regulator of osteoclastogenesis
Title
RANKL-induced schlafen2 is a positive regulator of osteoclastogenesis
Authors
Lee N.K.
;
Choi H.K.
;
Yoo H.J.
;
Shin J.
;
Lee S.Y.
Ewha Authors
이수영
SCOPUS Author ID
이수영
Issue Date
2008
Journal Title
Cellular Signalling
ISSN
0898-6568
Citation
Cellular Signalling vol. 20, no. 12, pp. 2302 - 2308
Indexed
SCI; SCIE; SCOPUS
Document Type
Article
Abstract
Osteoclasts are hematopoietic lineage derived-multinucleated cells that resorb bone. Their activity in balance with that of osteoblast is essential for bone homeostasis. Receptor activator of NF-κB ligand (RANKL) is known as an essential cytokine for the osteoclastogenesis, and c-Jun signaling in cooperation with NFAT family is crucial for RANKL-regulated osteoclastogenesis. We show here that schlafen2 (Slfn2), a member of a new family of growth regulatory genes involved in thymocyte development, is critical for osteoclastogenesis. RANKL selectively induces Slfn2 expression in osteoclast precursors via Rac1 signaling pathway. Targeted inhibition of Slfn2 by small interfering RNAs (siRNAs) markedly inhibits the formation of osteoclasts by diminishing the activation of c-Jun and the expression of c-Jun and NFATc1. In contrast, the overexpression of Slfn2 markedly increased phosphorylation and transactivation of c-Jun by RANKL. Together, these results indicate that Slfn2 has an essential role in osteoclastogenesis, functioning upstream of c-Jun and NFATc1. © 2008 Elsevier Inc. All rights reserved.
DOI
10.1016/j.cellsig.2008.08.019
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