Fig. 5.
Transactivation of the M-CSF receptor promoter by exogenously expressed AML1 proteins in U937 cells. (A) Cells were transfected with a reporter plasmid (8 μg) and indicated AML1 expression constructs (12 μg) by electroporation. Luciferase activities were measured and presented as the fold increase relative to the control transfected with the backbone expression vector. (B) The wild-type AML1 and missense AML1 mutants were coexpressed in varying doses as indicated. Transfection of plasmids was performed with the aid of a nonliposomal transfection reagent, FuGENE6. Luciferase activities are expressed as fold changes relative to the activity observed at the standard dose (0.2 μg) of the wild-type AML1 alone. In both (A) and (B), each value represents the mean of three separate experiments. Standard deviations of the measurements are given either numerically or by thin vertical bars.

Transactivation of the M-CSF receptor promoter by exogenously expressed AML1 proteins in U937 cells. (A) Cells were transfected with a reporter plasmid (8 μg) and indicated AML1 expression constructs (12 μg) by electroporation. Luciferase activities were measured and presented as the fold increase relative to the control transfected with the backbone expression vector. (B) The wild-type AML1 and missense AML1 mutants were coexpressed in varying doses as indicated. Transfection of plasmids was performed with the aid of a nonliposomal transfection reagent, FuGENE6. Luciferase activities are expressed as fold changes relative to the activity observed at the standard dose (0.2 μg) of the wild-type AML1 alone. In both (A) and (B), each value represents the mean of three separate experiments. Standard deviations of the measurements are given either numerically or by thin vertical bars.

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