chip-seq histone methylation data  (Epigenomics ag)

Journal: Molecular Oncology

Article Title: Widespread overexpression from the four DNA hypermethylated HOX clusters in aggressive ( IDH wt) glioma is associated with H3K27me3 depletion and alternative promoter usage

doi: 10.1002/1878-0261.12944

Figure Lengend Snippet: A subset of HOX gene TSS escapes DNA hypermethylation in IDH wt glioma samples. (A) DNA methylation changes (compared with control samples) along each HOX cluster and their surrounding genomic regions (±500 kbp) in IDH wt ( n = 55) and IDH mut ( n = 15) glioma samples, detected with the HM450K array. Hyper‐ and hypomethylated probes are in pink and light blue, respectively. (B) Genome Browser view at the HOXA cluster to show H3K4me3 enrichment, DNA methylation, the strand‐oriented RNA‐seq signal, and the correlation between these signatures in glioma samples (Glioma) and controls (Brain). (C) On the right panel, heatmap showing CpG site density and their mean methylation level in a ±5 kb window centered on the TSS of HOX genes enriched (upper) or depleted (lower) for H3K4me3 in IDH wt glioma samples compared with healthy controls (brain). The ChIP‐seq read density for H3K4me3 is shown on the left panel. (D) Genome Browser view at the HOXA5 and HOXD10 loci to show H3K4me3 and DNA methylation enrichment, and the strand‐oriented RNA‐seq signal in glioma samples (Glioma) and controls (Brain). In B to D, publicly available Glioma H3K4me3 data from IDH wt‐derived cell lines.

Article Snippet: ChIP‐seq data for the H3K4me3, H3K27me3, and histone H3 methylated at lysine 36 (H3K36me3) profiles were obtained from the NIH Roadmap Epigenomics project ( http://www.roadmapepigenomics.org/ ) (neural progenitor cells, NPCs, and brain samples) or from the GEO database (glioblastoma and GSC samples), as follows: NPC samples (H3K4me3: GSM818043, GSM772736.

Techniques: DNA Methylation Assay, Control, RNA Sequencing, Methylation, ChIP-sequencing, Derivative Assay

Journal: Molecular Oncology

Article Title: Widespread overexpression from the four DNA hypermethylated HOX clusters in aggressive ( IDH wt) glioma is associated with H3K27me3 depletion and alternative promoter usage

doi: 10.1002/1878-0261.12944

Figure Lengend Snippet: HOX clusters are depleted for H3K27me3 in IDH wt glioma and GSC lines. (A) Data mining‐derived ChIP‐seq signal at the HOXA cluster for H3K4me3 (green), H3K27me3 (red), and H3K36me3 (purple) in GSC and IDH wt glioma‐derived cell lines (upper panels) and healthy neural stem cell (NSC) and brain tissues (lower panels). (B) ChIP analysis of H3K9ac, H3K4me3, and H3K27me3 at selected HOX genes in control brain samples ( n = 5), and in IDH mut ( n = 5) and IDH wt ( n = 7) glioma samples. The precipitation level was normalized to that at the TBP promoter (for H3K4me3 and H3K9ac) and at the SP6 promoter (for H3K27me3); ** P < 0.01, *** P < 0.001 (Mann–Whitney U ‐test). (C) ChIP‐seq signal at the HOXA cluster for H3K4me3 (green) and H3K27me3 (red) in two independent GSC lines and in two independent NSC lines.

Article Snippet: ChIP‐seq data for the H3K4me3, H3K27me3, and histone H3 methylated at lysine 36 (H3K36me3) profiles were obtained from the NIH Roadmap Epigenomics project ( http://www.roadmapepigenomics.org/ ) (neural progenitor cells, NPCs, and brain samples) or from the GEO database (glioblastoma and GSC samples), as follows: NPC samples (H3K4me3: GSM818043, GSM772736.

Techniques: Derivative Assay, ChIP-sequencing, Control, MANN-WHITNEY

Journal: Molecular Oncology

Article Title: Widespread overexpression from the four DNA hypermethylated HOX clusters in aggressive ( IDH wt) glioma is associated with H3K27me3 depletion and alternative promoter usage

doi: 10.1002/1878-0261.12944

Figure Lengend Snippet: H3K27me3 status recapitulates the transcriptional activity at the HOXA cluster in GSC lines. (A) Genome Browser view at the HOXA cluster to show the strand‐oriented RNA‐seq signal, H3K4me3, H3K27me3, and H3K27ac enrichment, and the DNA methylation signal (only for the GSC‐11 line) in two independent GSC lines. (B) Genome Browser view at the HOXD1 locus to show an integrative view of H3K4me3, H3K27ac, H3K27me3 enrichment, and the strand‐oriented RNA‐seq signal in the two GSC lines. (C) Genome Browser view at the HOXC4‐C6 locus to show H3K4me3, H3K27ac, H3K27me3 enrichment, DNA methylation (only in the GSC‐11 line), and the strand‐oriented RNA‐seq signal in the two GSC lines.

Article Snippet: ChIP‐seq data for the H3K4me3, H3K27me3, and histone H3 methylated at lysine 36 (H3K36me3) profiles were obtained from the NIH Roadmap Epigenomics project ( http://www.roadmapepigenomics.org/ ) (neural progenitor cells, NPCs, and brain samples) or from the GEO database (glioblastoma and GSC samples), as follows: NPC samples (H3K4me3: GSM818043, GSM772736.

Techniques: Activity Assay, RNA Sequencing, DNA Methylation Assay