Follistatin-like 1 promotes osteoclast formation via RANKL-mediated NF-κB activation and M-CSF-induced precursor proliferation
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- 作者：Hyun-Ju Kima ; b ; biohjk@knu.ac.kr" class="auth_mail" title="E-mail the corresponding author ; Woo Youl Kanga ; Sook Jin Seonga ; Shin-Yoon Kimb ; Mi-Sun Limc ; Young-Ran Yoona ; yry@knu.ac.kr" class="auth_mail" title="E-mail the corresponding author
- 关键词：BMM ; bone marrow-derived macrophage ; FSTL1 ; follistatin-like 1 ; M-CSF ; macrophage colony-stimulating factor ; NFATc1 ; nuclear factor of activated T cells c1 ; RANKL ; receptor activator of NF-κB ligand ; TRAP ; tartrate-resistant acid phosphatase.
- 刊名：Cellular Signalling
- 出版年：2016
- 出版时间：September 2016
- 年：2016
- 卷：28
- 期：9
- 页码：1137-1144
- 全文大小：1320 K
文摘
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Overexpression of FSTL1 enhances osteoclast formation induced by M-CSF and RANKL.
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Knockdown of FSTL1 suppresses osteoclast formation.
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FSTL1 accelerates RANKL-mediated activation of NF-κB, JNK, and ERK pathways.
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FSTL1 promotes precursor proliferation by increasing MCF-induced ERK activation.