Steven L. Teitelbaum
J Clin Invest.
2004;
114(4):463–465
doi:10.1172/JCI22644
This article Copyright © 2004, The American Society for Clinical Investigation
Abstract
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P
athological 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 JCI 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 .
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