RANKing c-Jun in osteoclast development
AUTOR(ES)
Teitelbaum, Steven L.
FONTE
American Society for Clinical Investigation
RESUMO
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 .
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=503777Documentos Relacionados
- Critical roles of c-Jun signaling in regulation of NFAT family and RANKL-regulated osteoclast differentiation
- TAK1 Participates in c-Jun N-Terminal Kinase Signaling during Drosophila Development
- Estrogens suppress RANK ligand-induced osteoclast differentiation via a stromal cell independent mechanism involving c-Jun repression
- Nucleotide sequence of rat c-jun protooncogene.
- Activation of c-Jun N-Terminal Kinase 1 by UV Irradiation Is Inhibited by Wortmannin without Affecting c-jun Expression
