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Transmembrane protein 173 inhibits RANKL‐induced osteoclast differentiation
Author(s) -
Choe Chung-Hyeon,
Park In Sun,
Park Jisang,
Yu Kang-Yeol,
Jang Hyonseok,
Kim Ju,
Jang Yong-Suk
Publication year - 2015
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2015.02.018
Subject(s) - rankl , osteoclast , microbiology and biotechnology , cathepsin k , chemistry , acid phosphatase , tartrate resistant acid phosphatase , cathepsin , mapk/erk pathway , cancer research , signal transduction , biology , biochemistry , receptor , activator (genetics) , enzyme
Tmem173 was identified as a growth inhibitor associated with major histocompatibility complex (MHC) class II and a potential stimulator for IFN‐β, an innate immune inducer and a negative feedback controller for RANKL‐induced osteoclast differentiation of monocytic macrophage cells. In this study, we confirmed that transmembrane protein 173 (Tmem173) overexpression inhibited the expression of osteoclast‐specific genes, tartrate‐resistant acid phosphatase (TRAP), cathepsin K, and matrix metalloproteinase‐9 (MMP‐9), as well as bone resorption pit formation in RANKL‐treated RAW 264.7 cells. Activation of osteoclast‐specific transcription factors, c‐Fos and nuclear factor of activated T cells cytoplasmic‐1 (NFATc1), and RANKL‐induced activation of ERK were also down‐regulated by Tmem173 overexpression. Collectively, these results suggest that Tmem173 plays a regulatory role in RANKL–RANK‐mediated signaling in osteoclastogenesis.