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. 2013 Feb;46(2):107–112. doi: 10.5483/BMBRep.2013.46.2.141

Fig. 4. Silencing of ALK2, ALK3, ALK6, BMPRII, and ActRII attenuated BMP6-induced osteogenic differentiation and Smads signaling of C3H10T1/2 cells. (A) Effective knockdown of ALK2, ALK3, ALK6, BMPRII and ActRII was confirmed by qPCR. **P ＜ 0.01 vs NC (negative control). (B) After achieving effective knockdown of ALK2, ALK3, ALK6, BMPRII and ActRII, ALP activity was assessed at 7 days post BMP6-sitmulation. Data were means ± SD of three experiments. **P ＜ 0.01 vs BMP6 + NC, *P ＜ 0.05 vs BMP6 + NC. (C) After achieving effective knockdown of ALK2, ALK3, ALK6, BMPRII and ActRII, BMP6-induced matrix mineralization was detected at 21 days post BMP6-stimulation. Magnification, 100×. (D) After achieving effective knockdown of ALK2, ALK3, ALK6, BMPRII and ActRII, luciferase activity was assessed at 24 hour post BMP6-stimulation. Data were means ± SD of three experiments. **P ＜ 0.01 vs BMP6 + NC. (E) After achieving effective knockdown of ALK2, ALK3, ALK6, BMPRII, and ActRII, phosphorylation of Smad1/5/8 was detected at 24 hours post infection by western blot.

Fig. 4.