破骨细胞发育过程中c-Jun的排名
RANKing c-Jun in osteoclast development.
作者信息
Teitelbaum Steven L
机构信息
Department of Pathology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA.
出版信息
J Clin Invest. 2004 Aug;114(4):463-5. doi: 10.1172/JCI22644.
Abstract
Pathological bone loss always reflects enhanced net osteoclastic activity. Recognition and binding of the receptor activator of NF-κB (RANK) by RANK ligand (RANKL) is the key osteoclastogenic event, and the signaling cascades induced by this reaction therefore contain potential anti-osteoporosis therapeutic targets. A study reported in this issue of the documents that a pivotal component of RANKL/RANK-mediated osteoclast recruitment involves sequential induction of the transcription factors c-Jun and nuclear factor of activated T cells 2 .
摘要
病理性骨质流失总是反映出破骨细胞净活性增强。核因子κB受体激活剂（RANK）与RANK配体（RANKL）的识别和结合是关键的破骨细胞生成事件，因此该反应诱导的信号级联包含潜在的抗骨质疏松治疗靶点。本期报道的一项研究表明，RANKL/RANK介导的破骨细胞募集的一个关键组成部分涉及转录因子c-Jun和活化T细胞核因子2的顺序诱导。
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本文引用的文献
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Critical roles of c-Jun signaling in regulation of NFAT family and RANKL-regulated osteoclast differentiation.c-Jun信号在NFAT家族调控及RANKL调节破骨细胞分化中的关键作用。
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