NF-kappaB p50 and p52 regulate receptor activator of NF-kappaB ligand (RANKL) and tumor necrosis factor-induced osteoclast precursor differentiation by activating c-Fos and NFATc1.

@article{Yamashita2007NFkappaBPA,
  title={NF-kappaB p50 and p52 regulate receptor activator of NF-kappaB ligand (RANKL) and tumor necrosis factor-induced osteoclast precursor differentiation by activating c-Fos and NFATc1.},
  author={Teruhito Yamashita and Zhenqiang Yao and Fang Li and Qian Zhang and Idelberto R. Badell and Edward M Schwarz and Sunao Takeshita and Erwin F Wagner and Masaki Noda and Koichi Matsuo and Lianping Xing and BrendanF. Boyce},
  journal={The Journal of biological chemistry},
  year={2007},
  volume={282 25},
  pages={
          18245-53
        }
}
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… CONTINUE READING
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