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. 2021 Jul 29;36(1):68–79. doi: 10.1038/s41375-021-01346-7

Fig. 1. MLL-AF4 transcriptionally induces IGF2BP3.

Fig. 1

a GSEA of differentially expressed genes from IGF2BP3 depleted RS4;11 cells shows significant negative enrichment with MLL-AF4 ChIP targets (nominal P value: 0.001, FDR: 0.001, Normalized ES: −1.54)). b Schematic of MLL-AF4 binding site in intron 1 of IGF2BP3 (top). ChIP-qPCR shows fold enrichment for IGF2BP3 and CDKN1B with MLL and AF4 IP in RS4;11. Normalized to UNTR20, an untranscribed region (t test; *P < 0.05, **P < 0.01). c Fold enrichment from ChIP-qPCR of SEM cells show reduced binding of MLL-AF4 to IGF2BP3 with treatment of the DOT1L inhibitor, EPZ5676. Normalized to DMSO. (t test; **P < 0.01, ***P < 0.001, ****P < 0.0001). d Expression of MLL through RT-qPCR of 70Z/3 transduced with either control (Ctrl) or MLL-Af4 vector selected with G418 and MLL expression at the RNA level in the BM of WT recipients transplanted with Ctrl or MLL-Af4 HSPCs. e Induction of Igf2bp3 at the RNA level in selected 70Z/3 with MLL-Af4 and in the BM of WT recipients transplanted with Ctrl or MLL-Af4 HSPCs (bottom) (t test; **P < 0.01). f Induction of IGF2BP3 at the protein level in BM from mice transplanted with MLL-Af4-transduced WT donor HSPCs.