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Nikolaj Dietrich

Researcher at University of Copenhagen

Publications -  15
Citations -  4085

Nikolaj Dietrich is an academic researcher from University of Copenhagen. The author has contributed to research in topics: PRC2 & Polycomb-group proteins. The author has an hindex of 14, co-authored 15 publications receiving 3862 citations.

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Genome-wide mapping of Polycomb target genes unravels their roles in cell fate transitions

TL;DR: The Polycomb group (PcG) proteins form chromatin-modifying complexes that are essential for embryonic development and stem cell renewal and are commonly deregulated in cancer are identified using genome-wide location analysis in human embryonic fibroblasts.
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The Polycomb group proteins bind throughout the INK4A-ARF locus and are disassociated in senescent cells

TL;DR: The ability of the oncogene BMI1 to repress the INK4A-ARF locus requires its direct association and is dependent on the continued presence of the EZH2-containing Polycomb-Repressive Complex 2 (PRC2) complex.
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A model for transmission of the H3K27me3 epigenetic mark

TL;DR: This model provides a model to explain how trimethylated Lys 27 of histone 3 (H3K27me3), which is catalysed by the EZH2-containing Polycomb Repressive Complex 2 (PRC2), is maintained in proliferating cells, and suggests that once the H3K 27me3 is established, it recruits the PRC2 complex to maintain the mark at sites of DNA replication, thereby preserving chromatin structure and transcriptional programs.
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Bypass of senescence by the polycomb group protein CBX8 through direct binding to the INK4A-ARF locus.

TL;DR: It is demonstrated that the chromodomain‐containing protein, CBX8, which is part of one of the PRC1 complexes, regulates proliferation of diploid human and mouse fibroblasts through direct binding to the INK4A‐ARF locus.
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Polycomb group protein displacement and gene activation through MSK-dependent H3K27me3S28 phosphorylation.

TL;DR: It is proposed that MSK-mediated H3K27me3S28 phosphorylation serves as a mechanism to activate a subset of PcG target genes determined by the biological stimuli and thereby modulate the gene expression program determining cell fate.