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. 2016 Feb 16;113(9):E1226–E1235. doi: 10.1073/pnas.1600813113

Fig. 5.

Fig. 5.

FGF2 activates MEKK2 to stabilize β-catenin in osteoblasts. (A) Primary COBs isolated from Mekk2+/+ and Mekk2−/− mice were stimulated with FGF2 for the indicated times, and lysates were blotted with the indicated antibodies. (B) Primary WT COBs were stimulated with FGF2 (25 ng/mL) or IGF1 (25 ng/mL) for 15 min. Cell lysates were immunoprecipitated with anti–phospho-MEKK2/3 antibody and protein G-conjugated Dynabeads and were immunoblotted with the indicated antibodies. (C) C3H10T1/2 cells were transfected with TOPflash-luciferase and Renilla, and 24 h after transfection cells were stimulated with the indicated ligands for 24 h. Luciferase activity was measured subsequently and normalized to Renilla. P < 0.05 by one-way ANOVA. P values for Bonferroni-corrected Student’s t test: **P < 0.01; ***P < 0.001. (D, Left) C3H10T1/2 cells were transfected with TOPflash-luciferase and Renilla and were stimulated with WNT3a in the absence or presence of DKK1 for 24 h. (Right) C3H10T1/2 cells were transfected with TOPflash-luciferase and Renilla along with a construct encoding MEKK2 or a vector control, and then cells were incubated with 1 μg/mL of DKK1. P = N.S. for comparison of DKK1 versus vehicle-treated cells in either the vector control or MEKK2-transfected groups. (E) A diagram of the FGF2/MEKK2/β-catenin pathway in osteoblasts.