Figure 4.
MLL-ENL upregulates Bahcc1 via promoter binding. (A) RT-qPCR of Bahcc1 in myeloid immortalization assays using wild-type MLL-ENL- (ME) or empty vector- (IN) transduced KSL and MP cells. (B) Overview of the genomic region of the Bahcc1 locus in an adapted UCSC Genome Browser view. ChIP-seq data from mouse thymus, BM, and small intestine (SmInt) are shown in the LICR tracks (H3K4m3 and input control, Pol II, and input control). (C) ChIP-qPCR of MLL-ENL around exons 1 and 2 of Bahcc1 using retrovirally FLAG-tagged-MLL-ENL-immortalized KSL cells. Primer sets (1-5) are shown (top). Hoxa9 and Hbb-b1 were used as controls. Bar graphs show the mean with SD of at least 3 independent experiments. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001; ns, not significant (ANOVA followed by Tukey-Kramer multiple comparisons for panel A and unpaired Welch t tests for panel C). IgG1, IgG subclass 1.

MLL-ENL upregulates Bahcc1 via promoter binding. (A) RT-qPCR of Bahcc1 in myeloid immortalization assays using wild-type MLL-ENL- (ME) or empty vector- (IN) transduced KSL and MP cells. (B) Overview of the genomic region of the Bahcc1 locus in an adapted UCSC Genome Browser view. ChIP-seq data from mouse thymus, BM, and small intestine (SmInt) are shown in the LICR tracks (H3K4m3 and input control, Pol II, and input control). (C) ChIP-qPCR of MLL-ENL around exons 1 and 2 of Bahcc1 using retrovirally FLAG-tagged-MLL-ENL-immortalized KSL cells. Primer sets (1-5) are shown (top). Hoxa9 and Hbb-b1 were used as controls. Bar graphs show the mean with SD of at least 3 independent experiments. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001; ns, not significant (ANOVA followed by Tukey-Kramer multiple comparisons for panel A and unpaired Welch t tests for panel C). IgG1, IgG subclass 1.

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