Fig. 3.

aPKCλ deficiency impairs proliferation, survival and B cell differentiation arrest. a Comparative transcriptome and gene-ontology (GO) pathway analyses of the differential expression of genes in WT and DKO leukemic B-cell progenitors showing the differential regulation of genes involved in proliferation, cell cycle regulation, B cell differentiation network, and histone and chromatin modifications. Pathways shown in Blue - proliferation and cell cycle regulation; in Red - B cell differentiation network; in Green - histone and chromatin modification. b In vivo BrDU uptake by leukemic B-cell progenitors in Scl/P210; WT, aPKCζ^−/−, aPKCλ^Δ/Δ, and DKO chimeric mice. c FACS quantification of annexin V-binding of WT, aPKCζ^−/−, aPKCλ^Δ/Δ and DKO leukemic B-cell progenitors. d Representative example of western blots of p-ERK1/2, ERK1/2, p-MEK1/2, MEK1/2, aPKCλ, and Actin in WT, aPKCζ^−/−, aPKCλ^Δ/Δ, and DKO leukemic B-cell progenitors. Activation of MEK/ERK MAPK pathway is impaired in aPKCλ deficient leukemic B-cell progenitors. Western blots with different exposure time for phospho-Erk1/2 and phospho-Mek1/2 were presented to show minimal expression; Low (15 sec), high (1 min). e Representative example of the analyses of Rac GTPase activation by specific effector pulldown (PAK-PBD agarose) assay in leukemic B-cell progenitors derived from WT, aPKCζ^−/−, aPKCλ^∆/∆ and DKO chimeric mice. f FACS-quantification of proB, preB and immature/mature B cells in the BM of WT, aPKCζ^−/−, aPKCλ^Δ/Δ and DKO chimeric mice. Data are presented as mean ± SD of a minimum of three independent experiments. *p < 0.05; **p < 0.01; ***p < 0.001, t-test