Fig. 5
From: A kinase-independent role for CDK8 in BCR-ABL1+ leukemia
Kinase inhibition fails to mimic the effects of Cdk8 deletion. a Immunoblotting of pSTAT1S727 of BCR-ABL1p185+ cells after 48 h incubation with increasing concentrations of MSC or Senexin B (SnxB). Induction of phosphorylation was induced by 30 min IFN-β stimulation prior collection. β-Actin served as a loading control. b AnnexinV/PI staining (after 48 h) of BCR-ABL1p185+ Cdk8fl/fl and BCR-ABL1p185+ Cdk8Δ/ΔVav-Cre cell lines in the presence of indicated Senexin B or MSC concentrations. DMSO (0.1%) served as solvent control. Bars represent means ± SD from two independent experiments (n = 2 per genotype, measure in triplicates). Asterisks denote statistical significances as determined by unpaired t-test (**p < 0.01). c Heatmap of 159 differentially expressed genes between BCR-ABL1p185+ Cdk8fl/fl and BCR-ABL1p185+ Cdk8Δ/ΔVav-Cre cell lines (n = 4 per genotype). The black line separates the sets of genes, which are differentially regulated upon loss of the entire CDK8 protein (BCR-ABL1p185+ Cdk8Δ/ΔVav-Cre cell lines vs. BCR-ABL1p185+ Cdk8fl/fl; above the black line) from those whose expressions change upon treatment with 1000 nM Senexin B for 48 h (of BCR-ABL1p185+ Cdk8fl/fl cell lines) (FDR < 0.1). Colors display centered and scaled r-log counts ranging from red to gray (high to low expression). Source data are provided as a Source Data file
