RANKing c-Jun in osteoclast development

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 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 .

Publication types

  • Comment

MeSH terms

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

Substances

  • Carrier Proteins
  • DNA-Binding Proteins
  • Membrane Glycoproteins
  • NF-kappa B
  • NFATC Transcription Factors
  • Nuclear Proteins
  • Proteins
  • Proto-Oncogene Proteins c-fos
  • Proto-Oncogene Proteins c-jun
  • RANK Ligand
  • Receptor Activator of Nuclear Factor-kappa B
  • TNF Receptor-Associated Factor 6
  • TNFRSF11A protein, human
  • TNFSF11 protein, human
  • Transcription Factor AP-1
  • Transcription Factors