ISG15 Regulates RANKL-Induced Osteoclastogenic Differentiation of RAW264 Cells
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- Takeuchi Tomoharu
- Faculty of Pharmaceutical Sciences, Josai University
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- Shimakawa Genki
- Faculty of Pharmaceutical Sciences, Josai University
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- Tamura Mayumi
- Faculty of Pharmaceutical Sciences, Josai University
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- Yokosawa Hideyoshi
- School of Pharmacy, Aichi Gakuin University
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- Arata Yoichiro
- Faculty of Pharmaceutical Sciences, Josai University
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Interferon-stimulated gene 15 kDa (ISG15) is a protein upregulated by interferon-β that negatively regulates osteoclastogenesis. We investigated the role of ISG15 in receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenic differentiation of murine RAW264 cells. RANKL stimulation induced ISG15 expression in RAW264 cells at both the mRNA and protein levels. Overexpression of ISG15 in RAW264 cells resulted in suppression of cell fusion in RANKL-stimulated cells as well as the reduced expression of ATP6v0d2, a gene essential for cell fusion in osteoclastogenic differentiation. These results suggest that ISG15 suppresses RANKL-induced osteoclastogenesis, at least in part, through inhibition of ATP6v0d2 expression.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 38 (3), 482-486, 2015
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390282679608042240
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- NII論文ID
- 130004872278
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- NII書誌ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 026193365
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- PubMed
- 25757932
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 使用不可