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Publication : Regulatory mechanism of NFATc1 in RANKL-induced osteoclast activation.

First Author  Song I Year  2009
Journal  FEBS Lett Volume  583
Issue  14 Pages  2435-40
PubMed ID  19576893 Mgi Jnum  J:150795
Mgi Id  MGI:3851839 Doi  10.1016/j.febslet.2009.06.047
Citation  Song I, et al. (2009) Regulatory mechanism of NFATc1 in RANKL-induced osteoclast activation. FEBS Lett 583(14):2435-40
abstractText  NFATc1 is a master regulator of RANKL-induced osteoclast differentiation and herein we investigate the regulatory mechanism of NFATc1 in osteoclast activation. Inactivation of NFATc1 strongly attenuates RANKL-induced bone resorption and overexpression of a constitutively active form of NFATc1 in osteoclasts induces formation of actin rings and resorption pits on dentin slices. We demonstrate that NFATc1 binds directly to the promoter regions of its target genes and induces expression of various genes, including LTBP3, ClC7, cathepsin K, MMP9, and c-Src, which are key players in bone resorption. Thus, NFATc1 is essential for RANKL-induced osteoclast activation via up-regulation of osteoclast-activating genes.
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