FIG. 4.

The ability of c-Abl to stabilize IκBα is not shared by the oncogenic Abl. (A) A vector expressing IκBα was cotransfected with a plasmid encoding Bcr-Abl (lane 1), c-Abl(KD) (lane 2) or c-Abl(KA) (lane 3). The cells were analyzed as described for Fig. 2. (B) A series of deletion mutants of c-Abl were prepared. (C) cDNAs of the indicated c-Abl deletion mutants were subcloned into Flag-tagged pCDNA3 vector and were transfected into 293T cells. The cells were then fractionated into cytoplasmic and nuclear fractions, which then were subjected to anti-Flag (top panels) or anti-actin (second panels) immunoblotting analysis. Anti-histone (nuclear marker) and anti-tubulin (cytoplasmic marker) immunoblotting were included to assess the purity of each fraction. (D) The cytoplasmic and nuclear fractions were also immunoblotted with anti-P-tyr. (E) A plasmid encoding IκBα was cotransfected with the indicated mutants of c-Abl and the IκBα levels were analyzed as described for Fig. 2.