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. 2015 Dec 7;112(51):15654–15659. doi: 10.1073/pnas.1511285112

Fig. 4.

Fig. 4.

Tmem178 controls RANKL-induced NFATc1 activation. (A) Q-RT PCR analysis of NFATc1 during osteoclastogenesis. **P < 0.01. (B) Quantification of NFATc1 nuclear localization. Data are pooled from two independent experiments, 3–9 coverslips/condition per experiment. ***P < 0.001. (C) Q-RT PCR analysis of osteoclastogenic markers in WT and Tmem178−/− cells during osteoclastogenesis. Acp5, TRAP; Calcr, Calcitonin receptor; Ctsk K, Cathepsin K. **P < 0.01, ***P < 0.001. (D) Western blot analysis of NFATc1 nuclear translocation in response to RANKL in WT and Tmem178−/− OCs for the indicated days of culture. Histone 3 and actin are shown as nuclear and cytoplasmic loading controls, respectively. Representative of three experiments. (E) Q-RT PCR analysis of NFATc1 mRNA during osteoclastogenesis in WT cells expressing pMX or Tmem178-HA. **P < 0.01, ***P < 0.001. (F) Western blot analysis of NFATc1 as in D in pMX and Tmem178-expressing cells. Representative of three experiments. (G) Representative images of TRAP+ OCs expressing pMX or Tmem178-HA. (H) Quantification of percent area covered by OCs in G. **P < 0.01.