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Cited by 408

The DOI matches its Crossref record; 71 of the 71 references it cites were found in a registry or an index.

NF-κB p50 and p52 Regulate Receptor Activator of NF-κB Ligand (RANKL) and Tumor Necrosis Factor-induced Osteoclast Precursor Differentiation by Activating c-Fos and NFATc1

Open access
Yamashita, Teruhito, Yao, Zhenqiang, Li, Fang, Zhang, Qian, Badell, I. Raul, Schwarz, Edward M., Takeshita, Sunao, Wagner, Erwin F., Noda, Masaki, Matsuo, Koichi, Xing, Lianping, Boyce, Brendan F.·2007·Journal of Biological Chemistry

Abstract

Postmenopausal osteoporosis and rheumatoid joint destruction result from increased osteoclast formation and bone resorption induced by receptor activator of NF-kappaB ligand (RANKL) and tumor necrosis factor (TNF). Osteoclast formation induced by these cytokines requires NF-kappaB p50 and p52, c-Fos, and NFATc1 expression in osteoclast precursors. c-Fos induces NFATc1, but the relationship between NF-kappaB and these other transcription factors in osteoclastogenesis remains poorly understood. We report that RANKL and TNF can induce osteoclast formation directly from NF-kappaB p50/p52 double knockout (dKO) osteoclast precursors when either c-Fos or NFATc1 is expressed. RANKL- or TNF-induced c-Fos up-regulation and activation are abolished in dKO cells and in wild-type cells treated with an NF-kappaB inhibitor. c-Fos expression requires concomitant RANKL or TNF treatment to induce NFATc1 activation in the dKO cells. Furthermore, c-Fos expression increases the number and resorptive capacity of wild-type osteoclasts induced by TNF in vitro. We conclude that NF-kappaB controls early osteoclast differentiation from precursors induced directly by RANKL and TNF, leading to activation of c-Fos followed by NFATc1. Inhibition of NF-kappaB should prevent RANKL- and TNF-induced bone resorption.

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Crossref · 10.1074/jbc.m610701200

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Metadata

Authors
Yamashita, T., Yao, Z., Li, F., Zhang, Q., Badell, I. R., Schwarz, E. M., Takeshita, S., Wagner, E. F., Noda, M., Matsuo, K., Xing, L., & Boyce, B. F.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2007-06
Volume
282
Issue
25
Pages
18245-18253
ISSN
0021-9258 (ISSN-L)
OpenAlex
W2002315265
Cited by
408
References
71
FWCI
6.23
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: NF-κB p50 and p52 Regulate Receptor Activator of NF-κB Ligand (RANKL) and Tumor Necrosis Factor-induced Osteoclast Precursor Differentiation by Activating c-Fos and NFATc1. https://app.cochat.ai/papers/10.1074/jbc.m610701200
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Yamashita, T., Yao, Z., Li, F., Zhang, Q., Badell, I. R., Schwarz, E. M., Takeshita, S., Wagner, E. F., Noda, M., Matsuo, K., Xing, L., & Boyce, B. F. (2007). NF-κB p50 and p52 Regulate Receptor Activator of NF-κB Ligand (RANKL) and Tumor Necrosis Factor-induced Osteoclast Precursor Differentiation by Activating c-Fos and NFATc1. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m610701200

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.