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Critical roles of c-Jun signaling in regulation of NFAT family and RANKL-requlated osteoclast differentiation
https://doi.org/10.24517/00027534
https://doi.org/10.24517/000275340cd30228-86ac-48d0-bbe0-f67babef25cf
名前 / ファイル | ライセンス | アクション |
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CA-PR-YOSHIOKA-K-475.pdf (1.0 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-10-05 | |||||
タイトル | ||||||
タイトル | Critical roles of c-Jun signaling in regulation of NFAT family and RANKL-requlated osteoclast differentiation | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
ID登録 | ||||||
ID登録 | 10.24517/00027534 | |||||
ID登録タイプ | JaLC | |||||
著者 |
Ikeda, Fumiyo
× Ikeda, Fumiyo× Nishimura, Riko× Matsubara, Takuma× Tanaka, Sakae× Inoue, Jun-ichiro× Reddy, Sakamuri V.× Hata, Kenji× Yamashita, Kenji× Hiraga, Toru× Watanabe, Toshiyuki× Kukita, Toshio× Yoshioka, Katsuji× Rao, Anjana× Yoneda, Toshiyuki |
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著者別表示 |
善岡, 克次
× 善岡, 克次 |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学がん研究所がん分子細胞制御 | |||||
書誌情報 |
Journal of Clinical Investigation 巻 114, 号 4, p. 475-484, 発行日 2004-08-01 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0021-9738 | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA00695520 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1172/JCI200419657 | |||||
出版者 | ||||||
出版者 | American Society for Clinical Investigation | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Receptor activator of NF-κB ligand (RANKL) plays an essential role in osteoclast formation and bone resorption. Although genetic and biochemical studies indicate that RANKL regulates osteoclast differentiation by activating receptor activator of NF-κB and associated signaling molecules, the molecular mechanisms of RANKL-regulated osteoclast differentiation have not yet been fully established. We investigated the role of the transcription factor c-Jun, which is activated by RANKL, in osteoclastogenesis using transgenic mice expressing dominant-negative c-Jun specifically in the osteoclast lineage. We found that the transgenic mice manifested severe osteopetrosis due to impaired osteoclastogenesis. Blockade of c-Jun signaling also markedly inhibited soluble RANKL-induced osteoclast differentiation in vitro. Overexpression of nuclear factor of activated T cells 1 (NFAT1) (NFATc2/ NFATp) or NFAT2 (NFATc1/NFATc) promoted differentiation of osteoclast precursor cells into tartrate-resistant acid phosphatase-positive (TRAP-positive) multinucleated osteoclast-like cells even in the absence of RANKL. Overexpression of NFAT1 also markedly transactivated the TRAP gene promoter. These osteoclastogenic activities of NFAT were abrogated by overexpression of dominant-negative c-Jun. Importantly, osteoclast differentiation and induction of NFAT2 expression by NFAT1 overexpression or soluble RANKL treatment were profoundly diminished in spleen cells of the transgenic mice. Collectively, these results indicate that c-Jun signaling in cooperation with NFAT is crucial for RANKL-regulated osteoclast differentiation. | |||||
権利 | ||||||
権利情報 | Copyright © 2004, The American Society for Clinical Investigation | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
関連URI | ||||||
識別子タイプ | DOI | |||||
関連識別子 | http://dx.doi.org/10.1172/JCI200419657 | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | http://www.jci.org/articles/view/19657 |