Figure 2 | Oncogene

Figure 2

From: Epigenetic therapies by targeting aberrant histone methylome in AML: molecular mechanisms, current preclinical and clinical development

Figure 2

Crosstalk between HMTs and HDMs in MLL-driven transcription. (a) When DOT1L is recruited by MLL fusions, it confers H3K79me2 active mark, which may further expel SUV39H1 and SIRT1, hence leading to a reduction in H3K9me2 repressive mark but an increase in H3K9ac activation mark. (b) After binding to MLL fusions and MOZ-TIF2, PRMT1 and KDM4C cooperate to maintain the activation of MLL-driven transcription by conferring a high level of H4R3me2a, but a low level of H3K9me3 repressive mark.

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