Chromatin signatures of pluripotent cell lines

By V. Azuara, P. Perry, S. Sauer, M. Spivakov, H. Jørgensen, R. John, Mina Gouti, Miguel Casanova, G. Warnes, Matthias Merkenschlager and 1 more. Nature Cell Biology, 2006

1,441 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/2d3de99652bdd1faa4dbb17ebbf0c36e71440ab7

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Citations in the corpus

Ring1-mediated ubiquitination of H2A restrains poised RNA polymerase II at bivalent genes in mouse ES cells (2007, neutral): “Recent studies have demonstrated that silent developmental regulator genes have an unusual histone modification profile in ES cells, being simultaneously marked with Polycomb repressor-mediated histone H3K27 methylation, and marks normally associated with gene activit”
Histone Marks in the 'Driver's Seat': Functional Roles in Steering the Transcription Cycle. (2017, background): “In embryonic stem cells, both H3K4me3 and H3K27me3 occur at the same gene, which poises the gene for transcription activation once the repressive H3K27me3 mark is removed in response to differentiation cues [30,31].”
Whole-genome mapping of histone H3 Lys4 and 27 trimethylations reveals distinct genomic compartments in human embryonic stem cells. (2007, result): “The types of genes and their enrichment status found here are consistent with studies reported previously ( Azuara et al., 2006; Lee et al., 2006).”
Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “modification marks are often found together in promoters of developmental genes constituting domains of “bivalent chromatin” (Azuara et al., 2006; Bernstein et al., 2006).”
Mechanisms of stem cell self-renewal. (2009, background): “It appears that such domains repress the expression of genes involved in fate determination and differentiation, while poising such genes for activation upon exit from the pluripotent state (Azuara et al. 2006, Bernstein et al. 2006, Boyer et al. 2006, Lee et al. 2006b).”
Polycomb silencing mechanisms and the management of genomic programmes (2007, background): “In these cells, PcG target genes simultaneously bear the 'repressive' trimethylated H3K27 chromatin mark and the 'activating' trimethylated H3K4 mar”
Epigenetics in cancer. (2010, background): “For example, embryonic stem (ES) cells possess “bivalent domains” which contain coexisting active (H3K4me3) and repressive (H3K27me3) marks at promoters of developmentally important genes [35,36].”
A stem cell–like chromatin pattern may predispose tumor suppressor genes to DNA hypermethylation and heritable silencing (2007, background): “This 'bivalent' state has been recently described in mouse ES cell”
Polycomb silencers control cell fate, development and cancer (2006, neutral): “Studies using DNA replication timing as a read-out for transcriptional potential in pluripotent ES cells, multipotent haematopoietic cell lines and unipotent T lymphocytes indicate that lineage-specific genes are primed for expression in ES cells, but are kept in a repressed state by opposing chroma”
Control of Embryonic Stem Cell State (2011, background): “PcG protein complexes catalyze ubiquitylation of histone H2A lysine 119 (H2AK119u) and trimethylation of histone H3 lysine 27 (H3K27me3) and function in ESCs to help silence genes encoding key regulators of development yet allow them to remain in a state that is ‘‘poised’’ for activation during diff”
Aberrant epigenetic landscape in cancer: how cellular identity goes awry. (2010, background): “, 2007) also possess bivalent domains, marked with both H3K27me3 and H3K4me3, similar to those described for embryonic stem cells (ESCs) (Bernstein et al., 2006; Azuara et al., 2006).”
Genomewide Analysis of PRC1 and PRC2 Occupancy Identifies Two Classes of Bivalent Domains (2008, background): “As shown previously, many bivalent mouse promoters correspond to homeobox TFs or other developmental regulators [14,15].”
CpG islands and the regulation of transcription. (2011, neutral): “In ES cells, CGIs silenced by polycomb possess the ‘‘active’’ mark H3K4me3 as well as H3K27me3 (Azuara et al. 2006; Bernstein et al. 2006; Mikkelsen et al. 2007).”
Distinct Epigenomic Landscapes of Pluripotent and Lineage-committed Human Cells (2010, background): “H3K4me3, H3K4me2, H3K4me1, H3K9ac, H3K9me3, H3K27ac, H3K27me3, H3K36me3, H3K18ac and H4K5ac were tested.”