AML1-ETO inhibits coactivation of PU.1 by c-Jun.

(A) F9 cells do not express c-Jun. Nuclear extracts (100 μg) of 293T, F9, and Kasumi-1 cells along with in vitro–translated c-Jun were subjected to SDS-PAGE and immunoblotted for c-Jun. (B) AML1-ETO inhibits PU.1/c-Jun transactivation capacity. F9 cells were transfected with p(PU.1)4TK, a minimal TK promoter driven by PU.1 DNA-binding sites only or control vector p(mut.PU.1)4TK along with expression plasmids of PU.1 (100 ng), c-Jun (50 ng), and AML1-ETO (20 ng). (C) AML1-ETO down-regulates the PU.1-regulated M-CSF receptor promoter activity by inhibiting PU.1/c-Jun function. F9 cells were transfected with M-CSF receptor promoter and PU.1 (100 ng), c-Jun (50 ng), and AML1-ETO (20 ng). PU.1, c-Jun, and AML1-ETO had no effects on control vector pXP2 (data not shown).