Figure 6
Figure 6. CK2 inhibition restores Ikaros-mediated transcriptional regulation in primary high-risk B-ALL with deletion of 1 IKZF1 allele. Primary high-risk ALL cells were cultured on stromal cells with or without CK2 inhibitor CX-4945 (20 μM) for 24 hours. (A-B) Expression (measured by qRT-PCR) of Ikaros target genes involved in cell cycle progression (left) and the PI3K pathway (right) in primary high-risk B-ALL following CK2 inhibitor (CX-4945) treatment compared with untreated cells. (C-D) qChIP analysis of Ikaros occupancy of target genes involved in cell cycle progression (left) and the PI3K pathway (right) in wild-type (white and blue bars) and CX-4945–treated primary high-risk B-ALL (yellow and orange bars).

CK2 inhibition restores Ikaros-mediated transcriptional regulation in primary high-risk B-ALL with deletion of 1 IKZF1 allele. Primary high-risk ALL cells were cultured on stromal cells with or without CK2 inhibitor CX-4945 (20 μM) for 24 hours. (A-B) Expression (measured by qRT-PCR) of Ikaros target genes involved in cell cycle progression (left) and the PI3K pathway (right) in primary high-risk B-ALL following CK2 inhibitor (CX-4945) treatment compared with untreated cells. (C-D) qChIP analysis of Ikaros occupancy of target genes involved in cell cycle progression (left) and the PI3K pathway (right) in wild-type (white and blue bars) and CX-4945–treated primary high-risk B-ALL (yellow and orange bars).

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