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. 2011 Apr 7;286(22):19589–19596. doi: 10.1074/jbc.M110.197111

FIGURE 2.

FIGURE 2.

SMO-dependent migration requires Gi and PI3K signaling. A, serum-starved Ptc1+/− MEFs were stimulated for 15 min with 5 μm purmorphamine (PUR) or vehicle (control) in the absence or presence of 0.5 μm KAAD-cyclopamine. Whole cell lysates were separated by SDS-PAGE and blotted for P-Akt (Ser-473) and total Akt. Densitometry values of P-Akt (Ser-473) normalized to total Akt represent the mean ± S.E. of three experiments. *, p < 0.05. B, quantification of wound healing assays of Ptc1+/− MEFs pretreated with 100 ng/ml pertussis toxin or 15 μm LY294002 and stimulated with 5 μm purmorphamine or vehicle (DMSO) (n = 6; *, p < 0.001) C–E, representative experiment of P-Akt (Ser-473) and P-PDK1 (Ser-241) levels in serum-starved Ptc1+/− MEFs (C), SMO−/− MEFs (D), and Ptc1−/− MEFs (E) treated overnight with 100 ng/ml PTX or 0.5 μm KAAD-cyclopamine (KAAD) (n = 3). F, migration of Ptc1−/− MEFs (gray bars) or SMO−/− MEFs (black bars) in scratch-wound healing assays (t = 8 h) preincubated with 0.5 μm KAAD-cyclopamine (KAAD), 100 ng/ml PTX, or 15 μm LY294002 (LY). (n = 4–6; *, p < 0.05; ¶, p < 0.01).