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• W2023149772 abstract "The lens epithelium-derived growth factor (LEDGF/p75) tethers the mixed-lineage leukemia (MLL1) protein complex to chromatin. Likewise, LEDGF/p75 tethers the HIV-1 pre-integration complex to chromatin. We previously demonstrated that expression of the C-terminal fragment fused to enhanced green fluorescent protein (eGFP) (eGFP-LEDGF325–530) impaired HIV-1 replication. Here, we explored this strategy to selectively interfere with the leukemogenic activity of MLL-fusion proteins. We found that expression of LEDGF325–530 impaired the clonogenic growth of MLL-fusion gene transformed human and mouse hematopoietic cells, without affecting the growth of control cells immortalized by the FLT3-ITD mutant or normal lineage-marker-depleted murine bone marrow cells. Expression of LEDGF325–530 was associated with downregulation of the MLL target Hoxa9 and impaired cell cycle progression. Structure-function analysis revealed two small eGFP-fused LEDGF/p75 peptides, LEDGF424–435 and LEDGF375–386 phenocopying these effects. Both LEDGF325–530 and the smaller active peptides were able to disrupt the LEDGF/p75–MLL interaction. Expression of LEDGF325–530 or LEDGF375–386 fragments increased the latency period to disease development in vivo in a mouse bone marrow transplant model of MLL–AF9-induced AML. We conclude that small peptides disrupting the LEDGF/p75–MLL interface have selective anti-leukemic activity providing a direct rationale for the design of small molecule inhibitors targeting this interaction." @default.
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• W2023149772 date "2013-01-15" @default.
• W2023149772 modified "2023-10-16" @default.
• W2023149772 title "Impairing MLL-fusion gene-mediated transformation by dissecting critical interactions with the lens epithelium-derived growth factor (LEDGF/p75)" @default.
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• W2023149772 doi "https://doi.org/10.1038/leu.2013.10" @default.
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