Figure 6
Figure 6. Effect of blocking the MEK-ERK signaling pathway on MTOC polarization induced by the cross-linking of CD3 or ICAM-1 on the surface of Jurkat cells transiently transfected with Tax or CD4+ cells naturally infected with HTLV-1. The graphs represent the percentage of Jurkat cells expressing GFP-Tax protein or GFP protein alone (A), and naturally infected T cells (B) whose MTOC was oriented to the cell-bead contact region. Six hours after transfection with the respective plasmid, the cells were treated for 1 hour at 37°C either with cycloheximide (20 μM) or PD98059 (20 μM) or U0126 (100 μM), and then MTOC polarization was induced by cross-linking CD3 or ICAM-1 at the cell surface using latex beads coated with monoclonal antibodies directed against either CD3 or ICAM-1. Between 50 and 200 events were counted per condition, per experiment. The bars represent the mean ± SE of 3 independent experiments.

Effect of blocking the MEK-ERK signaling pathway on MTOC polarization induced by the cross-linking of CD3 or ICAM-1 on the surface of Jurkat cells transiently transfected with Tax or CD4+ cells naturally infected with HTLV-1. The graphs represent the percentage of Jurkat cells expressing GFP-Tax protein or GFP protein alone (A), and naturally infected T cells (B) whose MTOC was oriented to the cell-bead contact region. Six hours after transfection with the respective plasmid, the cells were treated for 1 hour at 37°C either with cycloheximide (20 μM) or PD98059 (20 μM) or U0126 (100 μM), and then MTOC polarization was induced by cross-linking CD3 or ICAM-1 at the cell surface using latex beads coated with monoclonal antibodies directed against either CD3 or ICAM-1. Between 50 and 200 events were counted per condition, per experiment. The bars represent the mean ± SE of 3 independent experiments.

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