Figure 1.
UBTF-TD/menin/KMT2A co-occupy genomic loci of genes dysregulated in UBTF-TD AML. (A) IGV tracks of HA:UBTF-TD (black), demonstrating features from 3 cbCD34+ donors transduced with UBTF-TD–expressing lentiviral vectors and maintained in culture for 40 days. CUT&RUN for UBTF, H3K4me3, H3K27ac, POLR2A, menin, and KMT2A in blue were performed in donor A. (B) GO-enrichment pathway analysis of significant targets occupied by UBTF-TD in all 3 donors (n = 226). (C) Overlap of genomic regions occupied by UBTF-TD (HA), KMT2A, and menin. Significance of overlap was calculated using hypergeometric distribution. (D) In situ PLA of endogenous UBTF/menin and UBTF/KMT2A in a UBTF-TD patient sample. Single targets (menin, KMT2A, and UBTF) are shown as controls.

UBTF-TD/menin/KMT2A co-occupy genomic loci of genes dysregulated in UBTF-TD AML. (A) IGV tracks of HA:UBTF-TD (black), demonstrating features from 3 cbCD34+ donors transduced with UBTF-TD–expressing lentiviral vectors and maintained in culture for 40 days. CUT&RUN for UBTF, H3K4me3, H3K27ac, POLR2A, menin, and KMT2A in blue were performed in donor A. (B) GO-enrichment pathway analysis of significant targets occupied by UBTF-TD in all 3 donors (n = 226). (C) Overlap of genomic regions occupied by UBTF-TD (HA), KMT2A, and menin. Significance of overlap was calculated using hypergeometric distribution. (D) In situ PLA of endogenous UBTF/menin and UBTF/KMT2A in a UBTF-TD patient sample. Single targets (menin, KMT2A, and UBTF) are shown as controls.

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