Inhibition of tumor progression locus 2 protein kinase suppresses receptor activator of nuclear factor-kappaB ligand-induced osteoclastogenesis through down-regulation of the c-Fos and nuclear factor of activated T cells c1 genes.

@article{Hirata2010InhibitionOT,
  title={Inhibition of tumor progression locus 2 protein kinase suppresses receptor activator of nuclear factor-kappaB ligand-induced osteoclastogenesis through down-regulation of the c-Fos and nuclear factor of activated T cells c1 genes.},
  author={Kazuya Hirata and Hirofumi Taki and Kouichiro Shinoda and Hiroyuki Hounoki and Tatsuro Miyahara and Kazuyuki Tobe and Hirofumi Ogawa and Hisashi Mori and Eiji Sugiyama},
  journal={Biological & pharmaceutical bulletin},
  year={2010},
  volume={33 1},
  pages={133-7}
}
Whether tumor progression locus 2 (Tpl2)/cancer Osaka thyroid (Cot) protein kinase participates in osteoclastogenesis from receptor activator of nuclear factor-kappaB ligand (RANKL)-stimulated monocytes/macrophages remains elusive. To clarify this, a selective and potent inhibitor of Tpl2, 1,7-naphtyridine-3-carbonitrile, was used. When RAW264.7 cells were stimulated with RANKL, Tpl2 was found to be activated. Under this condition, the Tpl2 inhibitor suppressed osteoclastogenesis in a dose… CONTINUE READING