Fig. 6.
Fig. 6. The effects of AML1-ETO expression on bone marrow–derived hematopoietic progenitors. (A and B) Replating efficiencies in two independent experiments. The open circles with red line depict the results of cell infected with MSCVneo, whereas the solid squares with blue line represent the results from cell infected with MSCV/AML1-ETOneo. (C) Flow cytometric analysis of surface antigen expression on MSCV/AML1-ETOneo–infected hematopoietic progenitors derived from the 13th replating. These cells were carried in liquid cultures for 3 weeks before immunophenotypic analysis. The solid line represents the staining obtained with the antibody specific for the indicated antigen. The dashed line represents the signal obtained with an isotype matched control antibody. (D) Wright-Giemsa–stained cytocentrifuge preparation of cells obtained from the 13th replating. (E) Western blot analysis of cell lysates prepared from MSCV/AML1-ETOneo–infected hematopoietic cells using affinity purified antibodies raised against an AML1–N-terminal peptide.

The effects of AML1-ETO expression on bone marrow–derived hematopoietic progenitors. (A and B) Replating efficiencies in two independent experiments. The open circles with red line depict the results of cell infected with MSCVneo, whereas the solid squares with blue line represent the results from cell infected with MSCV/AML1-ETOneo. (C) Flow cytometric analysis of surface antigen expression on MSCV/AML1-ETOneo–infected hematopoietic progenitors derived from the 13th replating. These cells were carried in liquid cultures for 3 weeks before immunophenotypic analysis. The solid line represents the staining obtained with the antibody specific for the indicated antigen. The dashed line represents the signal obtained with an isotype matched control antibody. (D) Wright-Giemsa–stained cytocentrifuge preparation of cells obtained from the 13th replating. (E) Western blot analysis of cell lysates prepared from MSCV/AML1-ETOneo–infected hematopoietic cells using affinity purified antibodies raised against an AML1–N-terminal peptide.

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