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. Author manuscript; available in PMC: 2009 May 1.

Published in final edited form as: Cell Signal. 2008 Jan 11;20(5):892–906. doi: 10.1016/j.cellsig.2008.01.001

(A) MAPKs phosphorylation was examined after transfection of various mutants of Mst1 in which D326, D349, and both D326 and D349 were mutated. Each construct was transfected into Mst1-knockdown selected cell clone (#6), then after 48 h of transfection, phosphorylation of various MAPKs was examined after the cells were treated with TRAIL (200 ng/ml, 4 h). Upper panel: Western blot analysis, C, control; T, TRAIL. Lower panel: The ratio of the phosphorylated MAPKs to corresponding actin in TRAIL-treated cells was set equal to 1 in wild-type, and the ratio of the phosphorylated MAPKs to corresponding actin in TRAIL-treated cells with different Mst1 deletions was compared to this. Data are expressed as mean ± SE of the densitometry data from three independent experiments. (B) After construction of several deletion mutants of Myc-tagged Mst1 (Myc-tagged 1–349 amino acids of Mst1, Myc-tagged 1–349 amino acids with D326N of Mst1, and Myc-tagged 1–326 amino acids of Mst1), each deletion mutant was transfected into Mst1-knockdown selected cell clone (#6). After 48 h of transfection, phosphorylation of various MAPKs was examined after the cells were treated with TRAIL (200 ng/ml, 4 h). Upper panel: Western blot analysis, C, control; T, TRAIL. Lower panel: The ratio of the phosphorylated MAPKs to corresponding actin in TRAIL-treated cells in wild-type was set equal to 1, and the ratio of the phosphorylated MAPKs to corresponding actin in TRAIL-treated cells with different Myc-tagged Mst1 deletions was compared to this. Note the difference in vertical scale of the three sub-panels. Data are expressed as mean ± SE of the densitometry data from three independent experiments.

(A) MAPKs phosphorylation was examined after transfection of various mutants of Mst1 in which D326, D349, and both D326 and D349 were mutated. Each construct was transfected into Mst1-knockdown selected cell clone (#6), then after 48 h of transfection, phosphorylation of various MAPKs was examined after the cells were treated with TRAIL (200 ng/ml, 4 h). Upper panel: Western blot analysis, C, control; T, TRAIL. Lower panel: The ratio of the phosphorylated MAPKs to corresponding actin in TRAIL-treated cells was set equal to 1 in wild-type, and the ratio of the phosphorylated MAPKs to corresponding actin in TRAIL-treated cells with different Mst1 deletions was compared to this. Data are expressed as mean ± SE of the densitometry data from three independent experiments. (B) After construction of several deletion mutants of Myc-tagged Mst1 (Myc-tagged 1–349 amino acids of Mst1, Myc-tagged 1–349 amino acids with D326N of Mst1, and Myc-tagged 1–326 amino acids of Mst1), each deletion mutant was transfected into Mst1-knockdown selected cell clone (#6). After 48 h of transfection, phosphorylation of various MAPKs was examined after the cells were treated with TRAIL (200 ng/ml, 4 h). Upper panel: Western blot analysis, C, control; T, TRAIL. Lower panel: The ratio of the phosphorylated MAPKs to corresponding actin in TRAIL-treated cells in wild-type was set equal to 1, and the ratio of the phosphorylated MAPKs to corresponding actin in TRAIL-treated cells with different Myc-tagged Mst1 deletions was compared to this. Note the difference in vertical scale of the three sub-panels. Data are expressed as mean ± SE of the densitometry data from three independent experiments.