ChIP_Glioma_stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
DISEASE(S): Malignant glioma
SUBMITTER: Atsushi Natsume
PROVIDER: E-TABM-1120 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Left ventricle myocytes from Dahl rats with a normal or failed heart was subjected to mRNA quantitation or ChIP-on-chip experiments with Affymetrix Rat Genome 230 2.0 microarrays. Experiment Overall Design: One left venctricle specimen was used for each mRNA quantitation/ChIP-on-chip experiment with a normal or failed heart.
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Project description:To examine H3K27me3 targets on the CpG promoters in MPM cell lines.
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Project description:Epigenetic silencing in cancer cells is mediated by at least two distinct histone modifications, polycomb based histone H3 lysine 27 trimethylation (H3K27triM) and H3K9 dimethylation.<br><br>Using chromatin immunoprecipitation-microarrays (ChIP-chip) in prostate cancer cells, we found that up to 5% of promoters (16% CpG islands and 84% non-CpG islands) were enriched with H3K27triM. These genes were silenced specifically in prostate cancer, and those CpG islands affected showed low levels of DNA methylation.
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Project description:To examine methylation profile of the CpG promoters in glioma stem cells
2012-02-18 | E-TABM-1122 | biostudies-arrayexpress
Project description:A cardinal property of neural stem cells (NSCs) is their ability to adopt multiple fates upon differentiation. The epigenome is widely seen as a read-out of cellular potential and a manifestation of this can be seen in embryonic stem cells (ESCs), where promoters of many lineage-specific regulators are marked by a bivalent epigenetic signature comprising trimethylation of both lysine 4 and lysine 27 of histone H3 (H3K4me3 and H3K27me3, respectively). Bivalency has subsequently emerged as a powerful epigenetic indicator of stem cell potential. Here, we have interrogated the epigenome during differentiation of ESC-derived NSCs to immature GABAergic interneurons. We show that developmental transitions are accompanied by loss of bivalency at many promoters in line with their increasing developmental restriction from pluripotent ESC through multipotent NSC to committed GABAergic interneuron. At the NSC stage, the promoters of genes encoding many transcriptional regulators required for differentiation of multiple neuronal subtypes and neural crest appear to be bivalent, consistent with the broad developmental potential of NSCs. Upon differentiation to GABAergic neurons, all non-GABAergic promoters resolve to H3K27me3 monovalency, whereas GABAergic promoters resolve to H3K4me3 monovalency or retain bivalency. Importantly, many of these epigenetic changes occur prior to any corresponding changes in gene expression. Intriguingly, another group of gene promoters gain bivalency as NSCs differentiate toward neurons, the majority of which are associated with functions connected with maturation and establishment and maintenance of connectivity. These data show that bivalency provides a dynamic epigenetic signature of developmental potential in both NSCs and in early neurons. Neural stem cells derived from mouse embryonic stem cells were differentiated into neurons and FACS purified based on RedStar fluorescence driven by the Tau promoter. Chromatin was prepared from NSCs and neurons (n=1), sonicated to roughly 300bp and immunoprecipitated with antibodies against H3K4me3, H3K27me3, total Histone H3 and total IgG, alongside a 5% input sample. K4/K27 and corresponding input samples were analysed by ChIPSeq
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Project description:Histone variants complement and integrate histone post-translational modifications in regulating transcription. The histone variant macroH2A1 (mH2A1) is almost three times the size of its canonical H2A counterpart due to the presence of a ~25kDa evolutionarily conserved non-histone macro domain. Strikingly, mH2A1 can mediate both gene repression and activation. However, the molecular determinants conferring these alternative functions remain elusive. Here, we report that mH2A1.2 is required for the activation of the myogenic gene regulatory network and muscle cell differentiation. H3K27 acetylation at prospective enhancers is exquisitely sensitive to mH2A1.2, indicating a role of mH2A1.2 in imparting enhancer activation. Both H3K27 acetylation and recruitment of the transcription factor Pbx1 at prospective enhancers are regulated by mH2A1.2. Overall, our findings indicate a role of mH2A1.2 in marking regulatory regions for activation. To establish the role of the histone variant mH2A1.2 in skeletal muscle differentiation we employed the mouse skeletal muscle C2C12 cell line and examined the genome wide distribution mH2A1.2 in myoblast (MB) and myotube (MT) (two replicates). We intersected the distribution of mH2A1.2 with active (H3K4me3 and H3K4me1 from published dataset, and H3K27ac, two replicates) and repressive (H3K27me3, two replicates) epigenetic marks in MB and MT. To gain insite on how chromatin accessibility is remodelled when muscle cells are induced to differentiate, we performed ATAC-seq in C2C12 MB and MT (2 replicates). We then evaluated whether mH2A1.2 was involved in conferring H3K27 acetylation during skeletal muscle differentiation by performing H3K27ac ChIP-seq (two replicates) upon mH2A1.2i in MB and MT. We also prefomred the ChIP-Seq for transcription factor Pbx1 in control and mH2A1.2i cells in MT to address the potential role of mH2A in recruitment of Pbx1. RNA-seq experiments were performed in control and mH2A1.2i C2C12 cells at the stage of MB and MT (three replicates). When mH2A1.2i C2C12 MB were induced to differentiate, a global effect on transcription was observed.
2016-01-15 | E-GEOD-76010 | biostudies-arrayexpress
Project description:Histone H3 monoaminylations at glutamine(Q) 5 represent an important family of epigenetic markers in neurons that play critical roles in the mediation of permissive gene expression (1, 2). We previously demonstrated that H3Q5 serotonylation(ser) and dopaminylation(dop) are catalyzed by the Transglutaminase 2 (TGM2) enzyme and alter both local and global chromatin states (3, 4). Here, we found that TGM2 additionally functions as an “eraser” of H3 monoaminylations that is capable of “re-writing” these epigenetic marks in cells, including a new class of this modification, H3Q5 histaminylation(his), which displays dynamic diurnal expression in brain and contributes to neural rhythmicity. We found that H3Q5his inhibits binding of the MLL1 complex to the H3 N-terminus and attenuates its methyltransferase activity on H3 lysine(K) 4. We determined that H3Q5 monoaminylation dynamics are dictated by local monoamine concentrations, which are utilized by TGM2. Taken together, we present here a novel mechanism through which a single chromatin regulatory enzyme is capable of sensing chemical microenvironments to affect the epigenetic states of cells.
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Project description:To examine methylation profile of the CpG promoters in clinical sample of GISTs.
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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
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Project description:Chromatin states must be stably maintained during cell proliferation to uphold cellular identity and genome integrity. Inheritance of histone modifications across cell division is thought to be central in this process. However, the histone modification landscape is challenged by the incorporation of new unmodified histones during each cell cycle and the principles that govern heritability remain poorly defined. Here, we take a quantitative approach and develop a reusable computational model that describes propagation of K27 and K36 methylation states. We measure combinatorial K27 and K36 methylation patterns by quantitative mass spectrometry on subsequent generations of histones in the presence and absence of enzymatic inhibition. Our modelling rejects active global demethylation and invoke the existence of 8 domains defined by distinct methylation endpoints. We find that K27me3 on pre- existing histones stimulates the rate of de novo K27me3 establishment, supporting a read-write mechanism in timely chromatin restoration. Finally, we provide a detailed, quantitative picture of the mutual antagonism between K27 and K37 methylation, and propose that this antagonism enhance the stability of epigenetic states across cell division.
2020-01-29 | PXD014807 | Pride