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Histone H3 Lysine 79 Methyltransferase Dot1 Is Required for Immortalization by MLL Oncogenes

14 Dec 2010

Abstract excerpt

Chimeric oncoproteins resulting from fusion of MLL to a wide variety of partnering proteins cause biologically distinctive and clinically aggressive acute leukemias. However, the mechanism of MLL-mediated leukemic transformation is not fully understood. Dot1, the only known histone H3 lysine 79 (H3K79) methyltransferase, has been shown to interact with multiple MLL fusion partners including AF9, ENL, AF10, and...

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PMID: 21159644
DOI: 10.1158/0008-5472.can-10-3294

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Histone H3 Lysine 79 Methyltransferase Dot1 Is Required for Immortalization by MLL OncogenesPMID 21159644Read ↗

hDOT1L Links Histone Methylation to LeukemogenesisSemantic proximity Read ↗

MLL-fusion-driven leukemia requires SETD2 to safeguard genomic integritySemantic proximity Read ↗

Targeting Recruitment of Disruptor of Telomeric Silencing 1-like (DOT1L)Semantic proximity Read ↗

Leukemic transformation by the MLL-AF6 fusion oncogene requires the H3K79 methyltransferase Dot1lSemantic proximity Read ↗

Requirement for Dot1l in murine postnatal hematopoiesis and leukemogenesis by MLL translocationSemantic proximity Read ↗

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DOT1L as a therapeutic target for the treatment of DNMT3A-mutant acute myeloid leukemia.Semantic proximity Read ↗

DOT1L inhibits SIRT1-mediated epigenetic silencing to maintain leukemic gene expression in MLL-rearranged leukemia.Semantic proximity Read ↗

Histone H2B ubiquitin ligase RNF20 is required for <i>MLL</i> -rearranged leukemiaSemantic proximity Read ↗

MLL fusion proteins preferentially regulate a subset of wild-type MLL target genes in the leukemic genomeSemantic proximity Read ↗

The histone H3K79 methyltransferase Dot1L is essential for mammalian development and heterochromatin structure.Semantic proximity Read ↗

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