Fig. 3.
Fig. 3. A short exposure of SKT6 cells to osmotic or heat shock induces transient activation of JNK/SAPK and p38, but suppresses activity of ERK. SKT6 cells were treated with osmotic shock (0.1 mol/L NaCl) (A, C, E) or heat shock (42°C) (B, D, F) for 0, 15, or 60 minutes, and cultured for a further 0, 30, 60, or 180 minutes under normal conditions. (A and B) The JNK1 (left panels) and JNK2 (right panels) activity in the immunoprecipitates at the indicated time points after stress treatment was assayed with GST-c-Jun as a substrate. Arrows indicate the phosphorylated GST-c-Jun. (C and D) The p38 activity in the immunoprecipitates at the indicated time points after stress treatment was assayed with GST-ATF-2 as a substrate. Arrows indicate the phosphorylated GST-ATF-2. (E and F) The ERK1 (left panels) or ERK2 (right panels) activity in the immunoprecipitates at the indicated time points after stress treatment was assayed with major basic protein (MBP) as a substrate. Arrows indicate the phosphorylated MBP.

A short exposure of SKT6 cells to osmotic or heat shock induces transient activation of JNK/SAPK and p38, but suppresses activity of ERK. SKT6 cells were treated with osmotic shock (0.1 mol/L NaCl) (A, C, E) or heat shock (42°C) (B, D, F) for 0, 15, or 60 minutes, and cultured for a further 0, 30, 60, or 180 minutes under normal conditions. (A and B) The JNK1 (left panels) and JNK2 (right panels) activity in the immunoprecipitates at the indicated time points after stress treatment was assayed with GST-c-Jun as a substrate. Arrows indicate the phosphorylated GST-c-Jun. (C and D) The p38 activity in the immunoprecipitates at the indicated time points after stress treatment was assayed with GST-ATF-2 as a substrate. Arrows indicate the phosphorylated GST-ATF-2. (E and F) The ERK1 (left panels) or ERK2 (right panels) activity in the immunoprecipitates at the indicated time points after stress treatment was assayed with major basic protein (MBP) as a substrate. Arrows indicate the phosphorylated MBP.

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