Fig. 1

JNK kinases remain abnormally activated upon the treatment of dasatinib in Ph⁺ B-ALL. a Human Ph⁺ B-ALL cell line SUP-B15 cells were treated with dasatinib at various concentrations for 6 hours (h) and subsequently examined by western blot using indicated antibodies against key effectors in BCR-ABL and MAPK signaling pathways: phosphorylated (p) and total BCR/ABL, Stat5, AKT, ERK, p38 and JNK, respectively. Actin was used as a loading control. b SUP-B15 cells were treated with dasatinib at various concentrations as indicated for 24 h and subsequently examined by western blot using indicated antibodies against phosphorylated and total BCR/ABL, Stat5, AKT, ERK, p38, and JNK, respectively. Actin was used as a loading control. c Western blot analysis of lysates of CD19⁺ B lymphocytes isolated from bone marrows of normal and BCR/ABL^p190 bone marrow transduction and transplantation mice using antibodies described in (a) plus western blot analysis using antibodies against phosphorylated and total c-JUN. d CD19⁺ B lymphocytes from BCR/ABL^p190 bone marrow transduction and transplantation mice were treated with 10 nmol/L dasatinib or vehicle for 12 h, followed by western blot analysis with antibodies against phosphorylated and total BCR-ABL and JNK