Figure 3
Figure 3. Histone modifications at the MIR155HG promoter in B-CLL. ChIP was performed on crosslinked chromatin from primary B-CLL (N = 9: P250, P254, P255, P143, P130, P161, P162, P164, P179, and P135, black bars) and control B cells (N = 8, gray bars) using the anti-H3K9Ac, H3K4Me3, and control antirabbit IgG antibody, as described in “ChIP.” The levels of H3K9 acetylation and H3K4 trimethylation (y-axis) are expressed relative to control IgG antibody and relative to upstream −4.7 kb locus with consistent low H3K9 acetylation and H3K4 methylation patterns. The x-axes indicate positions of amplicons (in kilobases) relative to TSS (white arrowheads). Gray box represents the position of the CpG; and black box, the exons of human MIR155HG. Error bars represent SEM. *P < .05.

Histone modifications at the MIR155HG promoter in B-CLL. ChIP was performed on crosslinked chromatin from primary B-CLL (N = 9: P250, P254, P255, P143, P130, P161, P162, P164, P179, and P135, black bars) and control B cells (N = 8, gray bars) using the anti-H3K9Ac, H3K4Me3, and control antirabbit IgG antibody, as described in “ChIP.” The levels of H3K9 acetylation and H3K4 trimethylation (y-axis) are expressed relative to control IgG antibody and relative to upstream −4.7 kb locus with consistent low H3K9 acetylation and H3K4 methylation patterns. The x-axes indicate positions of amplicons (in kilobases) relative to TSS (white arrowheads). Gray box represents the position of the CpG; and black box, the exons of human MIR155HG. Error bars represent SEM. *P < .05.

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