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A bivalent chromatin structure marks key developmental genes in embryonic stem cells, Cell 125
, 2006
"... The most highly conserved noncoding elements (HCNEs) in mammalian genomes cluster within regions enriched for genes encoding developmentally important transcription factors (TFs). This suggests that HCNE-rich regions may contain key regulatory controls involved in development. We explored this by ex ..."
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The most highly conserved noncoding elements (HCNEs) in mammalian genomes cluster within regions enriched for genes encoding developmentally important transcription factors (TFs). This suggests that HCNE-rich regions may contain key regulatory controls involved in development. We explored this by examining histone methylation in mouse embryonic stem (ES) cells across 56 large HCNE-rich loci. We identified a specific modification pattern, termed ‘‘bivalent domains,’ ’ consisting of large regions of H3 lysine 27 methylation harboring smaller regions of H3 lysine 4 methylation. Bivalent domains tend to coincide with TF genes expressed at low levels. We propose that bivalent domains silence developmental genes in ES cells while keeping them poised for activation. We also found striking correspondences between genome sequence and histone methylation in ES cells, which become notably weaker in differentiated cells. These results highlight the importance of DNA sequence in defining the initial epigenetic landscape and suggest a novel chromatin-based mechanism for maintaining pluripotency.
1 Roles for Chromatin Regulators During Differentiation of Embryonic Stem Cells By
, 2012
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Histone H3K27 Modifications and Gene Transcription
, 2011
"... Lysine residues of histone H3 and H4 are covalently modified in the chromatin of eukaryotic cells. Lysine 27 in histone H3 was acetylated (H3K27ac) or methylated at three levels; mono-, di-, and trime-thylation (H3K27me1, H3K27me2, and H3K27me3). These modifications at H3K27 were related with gene t ..."
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Lysine residues of histone H3 and H4 are covalently modified in the chromatin of eukaryotic cells. Lysine 27 in histone H3 was acetylated (H3K27ac) or methylated at three levels; mono-, di-, and trime-thylation (H3K27me1, H3K27me2, and H3K27me3). These modifications at H3K27 were related with gene transcription and/or chromatin structure in distinct patterns. Generally, H3K27ac and H3K27me1 were enriched in active chromatin, such as the locus control region or transcriptionally active genes, while transcriptionally inactive genes were highly marked by H3K27me2 and H3K27me3. These mod-ifications appear to have been catalyzed by distinct histone-modifying enzymes. Recent studies sug-gest that the four kinds of modifications at H3K27 have inter-correlation in gene transcription or chro-matin structure formation.
BRG1-Mediated Chromatin Remodeling Regulates Differentiation and Gene Expression of T Helper Cells†
, 2008
"... All in-text references underlined in blue are linked to publications on ResearchGate, letting you access and read them immediately. ..."
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All in-text references underlined in blue are linked to publications on ResearchGate, letting you access and read them immediately.
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, 2009
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CONTENT ALERTS
, 2006
"... This article cites 55 articles, 27 of which can be accessed free ..."
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CONTENT ALERTS
, 2008
"... This article cites 68 articles, 26 of which can be accessed free ..."
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Review Article Personalized Management in Low-Risk Prostate Cancer: The Role of Biomarkers
"... Copyright © 2012 Siebren Dijkstra et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Current criteria to predict low-risk prostat ..."
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Copyright © 2012 Siebren Dijkstra et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Current criteria to predict low-risk prostate cancer (PCa) are still subject to discussion as a substantial number of PCa patients who progress to a more aggressive disease seem to be missed, using these criteria. The main challenge in PCa diagnosis, therefore, is to distinguish patients with low-risk PCa who will show slow progression of disease from patients at risk for progression to a more aggressive cancer. The current discovered biomarkers could potentially guide in this management and improve detection, staging, and prognosis. This paper provides an overview of the current available serum-, urine-, and tissue-based biomarkers in PCa and evaluates the clinical usefulness of these biomarkers in the detection and management of low-risk PCa. 1.
A tumor suppressive activity of Drosophila Polycomb genes mediated by JAK/STAT signaling
"... A prevailing paradigm posits that Polycomb Group (PcG) proteins maintain stem cell identity by repressing differentiation genes, and abundant evidence points to an oncogenic role for PcG in human cancer 1,2. Here we demonstrate using Drosophila that a conventional PcG complex can also have a potent ..."
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A prevailing paradigm posits that Polycomb Group (PcG) proteins maintain stem cell identity by repressing differentiation genes, and abundant evidence points to an oncogenic role for PcG in human cancer 1,2. Here we demonstrate using Drosophila that a conventional PcG complex can also have a potent tumor suppressive activity. Mutations in all core PRC1 components cause dramatic hyperproliferation of eye imaginal tissue, accompanied by deregulation of epithelial architecture. The mitogenic JAK/STAT pathway is strongly and specifically activated in mutant tissue; activation is driven by transcriptional upregulation of Unpaired (Upd) family ligands. We show that upd genes are direct targets of PcG-mediated repression in imaginal discs. Ectopic JAK/ STAT activity is sufficient to induce overproliferation, while reduction of JAK/STAT activity suppresses the PRC1 mutant tumor phenotype. These findings show that PcG proteins can restrict growth directly by silencing mitogenic signaling pathways, shedding light onto an epigenetic mechanism underlying tumor suppression.
T Helper Cell Differentiatio Regulation by cis Element
"... served regions, including CNS-1 and CNS-2 (Loots clude identification of regulatory sequences, analysis et al., 2000); as it turned out, CNS-1 contained HSS1 and HSS2. To characterize the function of CNS-1, mu-rine CNS-1 was deleted in the endogenous locus (Mohrs et al., 2001) and human CNS-1 was de ..."
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served regions, including CNS-1 and CNS-2 (Loots clude identification of regulatory sequences, analysis et al., 2000); as it turned out, CNS-1 contained HSS1 and HSS2. To characterize the function of CNS-1, mu-rine CNS-1 was deleted in the endogenous locus (Mohrs et al., 2001) and human CNS-1 was deleted in yeast arti-ficial chromosome (YAC) DNA containing the Th2 cyto-kine locus (Loots et al., 2000). In both systems, deletion of CNS-1 resulted in a reduction of cells producing IL-4,
