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J Clin Invest. 2009 Oct;119(10):2879-81. doi: 10.1172/JCI40629. Epub 2009 Sep 21.

NF-kappaB2 (p100) limits TNF-alpha-induced osteoclastogenesis.

Author information

1
Department of Orthopaedic Surgery, Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo, Japan. tanakas-ort@h.u-tokyo.ac.jp

Abstract

Bone undergoes a continuous cycle of renewal, and osteoclasts--the cells responsible for bone resorption--play a pivotal role in bone homeostasis. This resorption is largely mediated by inflammatory cytokines such as TNF-alpha. In this issue of the JCI, Yao et al. demonstrate that the NF-kappaB precursor protein NF-kappaB2 (p100) acts as a negative regulator of osteoclastogenesis (see the related article beginning on page 3024). TNF-alpha induced a sustained accumulation of p100 in osteoclast precursors, and TNF-alpha-induced osteoclast formation was markedly increased in Nfkb2-/- mice. They also found that TNF receptor-associated factor 3 (TRAF3) is involved in the posttranslational regulation of p100 expression. These results suggest that blockade of the processing of p100 is a novel strategy to treat TNF-alpha-related bone diseases such as RA.

PMID:
19770519
PMCID:
PMC2752088
DOI:
10.1172/JCI40629
[Indexed for MEDLINE]
Free PMC Article

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