Figure 3.
Figure 3. ICSBP reverses BCR/ABL-mediated morphology changes and disturbed antigen expression. (A) Wright-Giemsa staining. BCR/ABL expression in 32D cells induces a transformed phenotype characterized by vacuolization, anisocytosis, and irregular cell and chromatin morphology, which is reversed to a major extent by coexpression of ICSBP. Original magnification, × 600. (B) Representative dot plots of 32D and 32D/BA cells permanently (i,iii) or inducible (ii) expressing ICSBP. Cells were stained with anti-Mac-1, anti-CD80, or anti-B220 monoclonal antibodies. The staining intensity is plotted against the forward scatter (FSC) after gating tightly to live cells according to the scatter characteristics. For quantitation of antigen-positive cells identical quadrant gates were used for each of the tested antigens and for stable inducible systems. The percentage of positive cells of the right quadrants is indicated in each plot.

ICSBP reverses BCR/ABL-mediated morphology changes and disturbed antigen expression. (A) Wright-Giemsa staining. BCR/ABL expression in 32D cells induces a transformed phenotype characterized by vacuolization, anisocytosis, and irregular cell and chromatin morphology, which is reversed to a major extent by coexpression of ICSBP. Original magnification, × 600. (B) Representative dot plots of 32D and 32D/BA cells permanently (i,iii) or inducible (ii) expressing ICSBP. Cells were stained with anti-Mac-1, anti-CD80, or anti-B220 monoclonal antibodies. The staining intensity is plotted against the forward scatter (FSC) after gating tightly to live cells according to the scatter characteristics. For quantitation of antigen-positive cells identical quadrant gates were used for each of the tested antigens and for stable inducible systems. The percentage of positive cells of the right quadrants is indicated in each plot.

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