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Showing 1–12 of 12 results
Advanced filters: Author: Omer Gilan Clear advanced filters

  • Here the authors develop CRISPR–ChIP to enable the identification of factors required for chromatin regulation. Using this new method, they unveil a functional partitioning of H3K79 methylation into two distinct regulatory units, with important implications in MLL leukemia.

    • Omer Gilan
    • Laure Talarmain
    • Mark A. Dawson
    Research
    Nature Structural & Molecular Biology
    Volume: 30, P: 1592-1606

  • The histone methyltransferase DOT1L and the chromatin reader BRD4 together facilitate transcription of genes critical to the molecular pathogenesis of MLL leukemia.

    • Omer Gilan
    • Enid Y N Lam
    • Mark A Dawson
    Research
    Nature Structural & Molecular Biology
    Volume: 23, P: 673-681

  • Systematic assessment of cofactor dependencies of nine transcription factors (TFs) and promoters finds that TFs use unique cofactor combinations to modulate distinct steps in transcription, whereas promoter elements fit into discrete groups where their rate-limiting step for activation influences cofactor compatibility.

    • Charles C. Bell
    • Jesse J. Balic
    • Mark A. Dawson
    Research
    Nature Genetics
    Volume: 56, P: 1181-1192

  • There is increasing evidence that epigenetic mechanisms contribute to therapeutic resistance in cancer. Here the authors study AML patient samples and a mouse model of non-genetic resistance and find that transcriptional plasticity drives stable epigenetic resistance, and identify regulators of enhancer function as important modulators of resistance.

    • Charles C. Bell
    • Katie A. Fennell
    • Mark A. Dawson
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-15

  • B cell development is tightly regulated in a stepwise manner to ensure proper generation of repertoire diversity via somatic gene rearrangements. Here, the authors show that a transcription factor, Erg, functions at the earliest stage to critically control two downstream factors, Ebf1 and Pax5, for modulating this gene rearrangement process.

    • Ashley P. Ng
    • Hannah D. Coughlan
    • Warren S. Alexander
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-14

  • Through three-dimensional CRISPR screening, He et al. report that functional inhibition of BET family of proteins BRD2/3/4 shows mitigating effects on blood endothelial cell (EC) survival and/or proliferation upon VEGFA blockade. An interaction between epigenetic regulation and anti-angiogenesis, which may affect chromosomal structure and activity in ECs through CDC25B phosphatase, is potentially involved with EC resistance to anti-angiogenic therapy.

    • Michael Y. He
    • Michael M. Halford
    • Steven A. Stacker
    ResearchOpen Access
    Communications Biology
    Volume: 4, P: 1-15

  • BET inhibitors that target bromodomain chromatin readers such as BRD4 are being explored as potential therapeutics in cancer; here, in a MLL–AF9 mouse leukaemia model, resistance to BET inhibitors is shown to emerge from leukaemia stem cells, and be partly due to increased Wnt/β-catenin signalling.

    • Chun Yew Fong
    • Omer Gilan
    • Mark A. Dawson
    Research
    Nature
    Volume: 525, P: 538-542