Fig. 9.
The SH2 domain of p210 Bcr/Abl is not required for activation of PI 3-kinase in malignant myeloid cells from mice with CML-like disease.
Lysates from spleen cells or peripheral blood leukocytes from mice with CML-like disease induced by wild-type p210 and the p210 ΔSH2 mutant were assayed for PI 3-kinase activity in antiphosphotyrosine immunoprecipitates. Wright-Giemsa staining of cytospin preparations indicated that all populations were more than 90% maturing myeloid cells (neutrophils, macrophages, and erythroid cells for spleen, and neutrophils, metamyelocytes, and myelocytes for peripheral blood) (data not shown). Results represent the mean and standard error of PI 3-kinase activity in cell lysates from several independent animals for each genotype, with the number of samples analyzed indicated. As controls, Ba/F3 parental cells or a population transformed with wild-type p210 BCR/ABL (Ba/F3-210) and untransduced bone marrow from Balb/c mice (more than 70% maturing myeloid and erythroid cells by cytospin analysis) were used. The difference in mean PI 3-kinase activity between p210 WT and p210 ΔSH2 was not significant (P = .41, Student t test).