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 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 .
MeSH terms
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Animals
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Carrier Proteins / metabolism*
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DNA-Binding Proteins / metabolism
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Humans
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Membrane Glycoproteins / metabolism*
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Models, Biological
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NF-kappa B / metabolism*
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NFATC Transcription Factors
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Nuclear Proteins*
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Osteoclasts / metabolism*
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Proteins / metabolism
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Proto-Oncogene Proteins c-fos / metabolism
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Proto-Oncogene Proteins c-jun / metabolism*
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RANK Ligand
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Receptor Activator of Nuclear Factor-kappa B
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Signal Transduction
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TNF Receptor-Associated Factor 6
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Transcription Factor AP-1 / metabolism
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Transcription Factors / metabolism
Substances
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Carrier Proteins
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DNA-Binding Proteins
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Membrane Glycoproteins
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NF-kappa B
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NFATC Transcription Factors
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Nuclear Proteins
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Proteins
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Proto-Oncogene Proteins c-fos
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Proto-Oncogene Proteins c-jun
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RANK Ligand
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Receptor Activator of Nuclear Factor-kappa B
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TNF Receptor-Associated Factor 6
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TNFRSF11A protein, human
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TNFSF11 protein, human
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Transcription Factor AP-1
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Transcription Factors