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

Fig. S1.

Fig. S1.

(A) Tmem178 expression in a gene array comparing WT and PLCγ2−/− BMMs in suspension (Susp) or plated on pRGD for 4 h (Adh). (B) Quantification of osteoblast numbers per bone perimeter [N.Ob./ B.Pm (mm−1) in WT and Tmem178−/− mice]. n = 4 per genotype. n.s., nonsignificant. (C) Quantification of mineral apposition rate (MAR) of 4-wk-old WT and Tmem178−/− mice labeled with calcein and alizarin red. n = 5 per genotype. (D) Quantification of bone formation rate (BFR) of mice in C. (E) Representative images of dynamic histomorphometry quantified in C and D. (F) Q-RT PCR of RANKL mRNA in whole long bones devoid of marrow cells from WT or Tmem178−/− mice. n = 4 per genotype. (G) Q-RT PCR of OPG mRNA from mice in F. (H) Q-RT PCR of Tmem178 mRNA in WT BMMs, OBs, and OCs cultured in vitro. Expression levels were normalized to cyclophilin. (I) Expression of Tmem178 mRNA during RANKL-induced osteoclastogenesis in vitro in control (NFATc1fl/fl) and NFATc1-deficient cells (NFATc1Δ/Δ). *P < 0.05. (J) Q-RT PCR of Tmem178 mRNA in control (p65fl/fl/RANK+/+) or p65-deleted (p65fl/fl/RANKCre/+) BMMs in suspension (Sus) or plated on pRGD for 4 and 8 h. n = 6 per group. ***P < 0.001.