Fig. 3.
Fig. 3. Adaphostin and STI571 alter p210bcr/abl-induced signaling in K562 cells in different ways. / K562 cells were treated with 10 μM adaphostin (A) or 20 μM STI571 (B) for the indicated length of time. Lysates containing 50 μg total cellular protein were subjected to SDS-PAGE followed by blotting with antiphosphotyrosine (top panel), anti-abl (middle panel), or anti-histone H1 (bottom panel) as a loading control. Percentages of cells that were apoptotic at each time point of this experiment are indicated in Figure 1B. (C) After K562 cells were treated with diluent (lane 1), 10 μM adaphostin (lane 2), or 20 μM STI571 (lane 3) for 3 hours, cell lysates were subjected to immunoprecipitation with anti-Stat5 monoclonal antibody and probed with anti-phosphoStat5 antiserum (top panel) or anti-Stat5 antibody (bottom panel). Results shown in each panel are representative of at least 3 independent experiments.

Adaphostin and STI571 alter p210bcr/abl-induced signaling in K562 cells in different ways.

K562 cells were treated with 10 μM adaphostin (A) or 20 μM STI571 (B) for the indicated length of time. Lysates containing 50 μg total cellular protein were subjected to SDS-PAGE followed by blotting with antiphosphotyrosine (top panel), anti-abl (middle panel), or anti-histone H1 (bottom panel) as a loading control. Percentages of cells that were apoptotic at each time point of this experiment are indicated in Figure 1B. (C) After K562 cells were treated with diluent (lane 1), 10 μM adaphostin (lane 2), or 20 μM STI571 (lane 3) for 3 hours, cell lysates were subjected to immunoprecipitation with anti-Stat5 monoclonal antibody and probed with anti-phosphoStat5 antiserum (top panel) or anti-Stat5 antibody (bottom panel). Results shown in each panel are representative of at least 3 independent experiments.

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