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 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 (see the related article beginning on page 475).

Original languageEnglish
Pages (from-to)463-465
Number of pages3
JournalJournal of Clinical Investigation
Issue number4
StatePublished - Aug 2004


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