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</script>The Polycomb complex PRC2 and its mark in life
The Polycomb complex PRC2 and its mark in life
Polycomb group proteins maintain the gene-expression pattern of different cells that is set during early development by regulating chromatin structure. In mammals, two main Polycomb group complexes exist - Polycomb repressive complex 1 (PRC1) and 2 (PRC2). PRC1 compacts chromatin and catalyses the monoubiquitylation of histone H2A. PRC2 also contributes to chromatin compaction, and catalyses the methylation of histone H3 at lysine 27. PRC2 is involved in various biological processes, including differentiation, maintaining cell identity and proliferation, and stem-cell plasticity. Recent studies of PRC2 have expanded our perspectives on its function and regulation, and uncovered a role for non-coding RNA in the recruitment of PRC2 to target genes.
- New York University United States
- University of Chicago United States
- Institute Curie France
- Howard Hughes Medical Institute United States
Genome, Polycomb-Group Proteins, Cell Differentiation, Histone-Lysine N-Methyltransferase, Methylation, Chromatin, Evolution, Molecular, Histones, Repressor Proteins, Neoplasms, Animals, Humans
Genome, Polycomb-Group Proteins, Cell Differentiation, Histone-Lysine N-Methyltransferase, Methylation, Chromatin, Evolution, Molecular, Histones, Repressor Proteins, Neoplasms, Animals, Humans
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citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).3K popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.Top 0.01% influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).Top 0.1% impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.Top 0.01%
