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. 2019 Nov 25;9(66):38438–38446. doi: 10.1039/c9ra07240c

Fig. 6. A proposed scheme of the impacts of CytoZ11 on RANKL-induced osteoclastogenesis. CytoZ11 inhibited c-Fos and NF-κB signaling pathways, resulting in the suppression of NFATc1 activation, as well as the down-regulation of osteoclast-specific genes such as Ctsk, Acp5, and Ctr. Acp5: encoding tartrate-resistant acid phosphatase (TRAcP); CytoZ11: cytochalasin Z11; Ctsk: encoding cathepsin K; Ctr: encoding calcitonin receptor; RANKL: receptor activator of nuclear factor-κB (NF-κB) ligand; NFATc1: nuclear factor of activated T cells 1.

Fig. 6