6 results found
    1. Chromosomes and Gene Expression

    H3.3K27M mutant proteins reprogram epigenome by sequestering the PRC2 complex to poised enhancers

    Dong Fang et al.
    Redistribution of the PRC2 complex in H3.3K27M mutant cells to poised enhancers contributes to the global reduction of H3K27me3 in cells expressing the mutant proteins.
    1. Chromosomes and Gene Expression

    Histone H3G34R mutation causes replication stress, homologous recombination defects and genomic instability in S. pombe

    Rajesh K Yadav et al.
    Mutation of Glycine 34 to Arginine within the N-terminal tail of histone H3 alters post-translational modifications on Lysine 36 and is associated with a delay in replication restart, defective homologous recombination and an increase in genomic instability.
    1. Chromosomes and Gene Expression

    A histone H3K9M mutation traps histone methyltransferase Clr4 to prevent heterochromatin spreading

    Chun-Min Shan et al.
    A lysine-to-methionine mutation in histone H3 dominantly blocks histone H3K9 methylation by trapping its methyltransferase.
    1. Developmental Biology
    2. Chromosomes and Gene Expression

    EED orchestration of heart maturation through interaction with HDACs is H3K27me3-independent

    Shanshan Ai et al.
    During heart maturation, embryonic ectoderm development as a chromatin remodeler triggers transcriptional silencing, while H3K27me3 is a passenger that is not sufficient for gene silencing.
    1. Chromosomes and Gene Expression
    2. Genetics and Genomics

    ASH1-catalyzed H3K36 methylation drives gene repression and marks H3K27me2/3-competent chromatin

    Vincent T Bicocca et al.
    While SET-2 methylates histone H3K36 during transcription, ASH1 methylates this residue in repressed regions, is important for silencing, and can both positively and negatively influence methylation of histone H3K27.
    1. Developmental Biology

    A switch in transcription and cell fate governs the onset of an epigenetically-deregulated tumor in Drosophila

    Joana Torres et al.
    A previously unknown oncogenic feature of an embryonic transcription factor was uncovered from transcriptomic analysis of tumors that lack functional Polycomb silencing.

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