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Distinct pathways affected by menin versus MLL1/MLL2 in MLL-rearranged acute myeloid leukemia.
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Provide molecular insights into how SETD2 mutations accelerate MLLr leukemogenesis.
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Wild-type MLL1 is a regulator of pre-BCR signaling.
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Targeting PRMT5 using small-molecule inhibitors in the treatment of leukemias harboring MLL rearrangements.
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Kmt2a is also important in memory formation
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Collectively, these data indicated that ATR or ATM inhibition represent potential therapeutic strategies for the treatment of AML, especially MLL-driven leukemias.
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Epigenomic profiling indicates an abnormal H3K79me2 pattern on MLL-fusion targeted genes, but the molecular mechanism underlying this epigenetic dependency is not well understood.
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NUP98-HOXA9 interacts with MLL via the NUP98 second FG repeat domain. In the absence of MLL (in knockout mice), NUP98-HOXA9-induced cell immortalization and leukemogenesis are severely inhibited. MLL is important for the recruitment of NUP98-HOXA9 to the HOXA locus and for NUP98-HOXA9-induced HOXA gene expression. MLL is crucial for NUP98-HOXA9 leukemia initiation.
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Atg5-dependent autophagy contributes to the development of acute myeloid leukemia in an MLL-AF9-driven mouse model.
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These results define an important role for MLL1 in regulating macrophage-mediated inflammation in wound repair and identify a potential target for the treatment of chronic inflammation in diabetic wounds.
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these results implicate an important role for MLL1-dependent epigenetic regulation of macrophage antimicrobial functions
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These results reveal a cooperative transcriptional activation mechanism of AEP and DOT1L and suggest a molecular rationale for the simultaneous inhibition of the MLL fusion-AF4 complex and DOT1L for more effective treatment of MLL-rearranged leukemia.
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This study demonstrated that Kmt2a regulates synaptic plasticity in striatal neurons and provides an epigenetic drug target for anxiety and dopamine-mediated behaviors.
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Inactivation of Kmt2a in Men1-deficient mice accelerated pancreatic islet tumorigenesis and shortened the average life span. Increases in cell proliferation were observed in mouse pancreatic islet tumors upon inactivation of both Kmt2a and Men1.
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Data suggest that RAS-homolog enriched in brain protein (Rheb1) promotes MLL-AF9 fusion protein initiated acute myeloid leukemia (AML) progression through target of rapamycin complex 1 (mTORC1) signaling pathway.
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HoxBlinc RNA Recruits Set1/MLL Complexes to Activate Hox Gene Expression Patterns and Mesoderm Lineage Development.
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MLL1 and DOT1L cooperate with meningioma-1 to induce acute myeloid leukemia.
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Set1 role in cellular reprogramming and its interactions with Dpy30,Myc,Sox2 and Ash2l reprogramming factors
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The present study examined the mechanism underlying the development of KMT2A (MLL)-rearranged infant leukemia in response to in utero exposure to etoposide in a mouse model.
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We have demonstrated that the Mll1 gene is critical to Th1 differentiation in humans and mice
