PIXUL-ChIP-seq analysis of genome-wide epigenetic marks binding in human HCT116 cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE115822 | GEO | 2018/06/15
REPOSITORIES: GEO
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Project description:PIXUL-ChIP-seq analysis of genome-wide epigenetic marks binding in human HCT116 cells
| PRJNA476139 | ENA
Project description:We performed the newly mapping of genome-wide NFATc1 binding events in VEGF-stimulated primary cultured endothelial cells, by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq). Combined NFATc1 ChIP-seq profile and the epigenetic histone marks revealed that predominant NFATc1-occupied peaks were overlapped with promoter marking but not silencer marking. DNA microarrays with NFATc1 expression or knockdown indicated the predominant NFATc1 binding targets were correlated with induced patterns. Examination of NFATc1 and two different histone marks in HUVEC in the presence/absense of VEGF.
2013-09-01 | E-GEOD-49428 | biostudies-arrayexpress
Project description:High-throughput RNA-IP sequencing was employed to identify the CNBP binding mRNAs and their binding sites in HCT116 cells.
2017-11-16 | GSE106918 | GEO
Project description:We performed the newly mapping of genome-wide NFATc1 binding events in VEGF-stimulated primary cultured endothelial cells, by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq). Combined NFATc1 ChIP-seq profile and the epigenetic histone marks revealed that predominant NFATc1-occupied peaks were overlapped with promoter marking but not silencer marking. DNA microarrays with NFATc1 expression or knockdown indicated the predominant NFATc1 binding targets were correlated with induced patterns.
2013-09-01 | GSE49428 | GEO
Project description:Lysine methylation is part of the posttranscriptional histone code employed to recruit modification specific readers to chromatin. Unbiased, quantitative mass spectrometry approaches combined with peptide pull-downs have been used to study histone methylation-dependent binders in mammalian cells. Here, we extend the study to birds by investigating the interaction partners for H3K4me3, H3K9me3, H3K27me3 and H3K36me3 in chicken (gallus gallus) and zebra finch (taeniopygia guttata) using label free quantitative proteomics. In general, we find very strong overlap in interaction partners for the trimethyl marks in birds compared to mammals, underscoring the known conserved function of these modifications. In agreement with their epigenetic role, we find binding of PHF2 and members of the TFIID, SAGA, SET1 and NURF complex to the activation mark H3K4me3. Our data furthermore supports the existence of a LID complex in vertebrates recruited to the H3K4me3. The repressive marks are bound by the HP1 proteins and the EED subunit of the PRC2 complex as well as by WIZ. Like the screens in mammals, we found ZNF462, ZNF828 and POGZ enriched at H3K9me3. However, we noted some unexpected differences. First, we did not observe the enrichment of CDYL and CDYL2 at the repressive marks. Second N-PAC (also known as GLYR1), an H3K36me3 interactor in mammals, is not binding to this modification in our screen. This suggests that despite strong conservation of the histone tail sequence, species-specific differences in epigenetic readers may have evolved.
2016-01-04 | PXD002282 | Pride
Project description:Analysis of cross talk of epigenetic marks in HBEC by using tilling arrays chr19. In Human Bronchial epithelia cells (HBEC), H3K9me3, H4K20me3, H3K4me3, H3K27me3, H3K36me3 and DNA methylation were profiled. In these cells, DNA methylation status was analyzed by MIRA and UnmethylCollector (UMC). Study of epigenetic changes in HCT116 DNMT1-/- and DNMT3b -/- (HCT116-DKO) in comparison to intact HCT116. In HCT116 and HCT116-DKO, H3K9me3, H3K36me3 and DNA methylation were profiled. In these cells, DNA methylation status was analyzed by MIRA. Analysis of epigenetic changes caused by siRNA for SED2 transcript in HBEC. In HBEC and SETD2 siRNA HBEC, H3K36me3 and DNA methylation were profiled. In these cells, DNA methylation status was analyzed by MIRA. Comapre DNA methylation and other histone modification marks
2011-03-31 | E-GEOD-26040 | biostudies-arrayexpress
Project description:High throughput PIXUL-ChIP-seq genome-wide study allows to map simultaneously Pol II peaks in multiple organs harvested from the same mouse.
2018-06-19 | GSE100348 | GEO
Project description:This is one of expressional parts of the study. These data were correlated to epigenetic changes and CG density of genes in analyzed cells. The whole study has a following summary: To elucidate possible roles of DNA methylation and chromatin marks in transcription, we performed epigenetic profiling of chromosome 19 in human bronchial epithelial cells (HBEC) and in the colorectal cancer cell line HCT116 as well as its counterpart with double knockout of DNMT1 and DNMT3B (HCT116-DKO). We found that H3K9me3 forms intragenic chromatin blocks along genes with low CpG density in the gene body. Analysis of H3K36me3 profiles indicated that this mark associates either with active genes with low CpG density and H3K9me3 in the gene body or with active genes with high CpG density and DNA hypermethylation in the gene body. In HCT116 cells with double knockout of DNMT1 and DNMT3B, transcription of genes with low CpG density in the gene body was highly elevated and associated with promoter DNA demethylation and rearrangement of H3K9me3 and H3K36me3 occupation. Our finding suggests that similar to DNA methylation, H3K9me3 may play a role in intragenic gene regulation. Further, we observed that a combination of low CpG density in gene bodies together with H3K9me3 and H3K36me3 marking is a specific epigenetic feature of zinc finger (ZNF) genes, which comprise 90% of all genes carrying both histone marks on chromosome 19. For high CpG density genes, transcription and H3K36me3 occupancy were not changed in condition of partial or intensive loss of DNA methylation in gene bodies in the HCT116-DKO cell line. siRNA experiments with SETD2 knockdown in both HBEC and HCT116-DKO cell lines failed to reduce DNA methylation in gene bodies under conditions of H3K36me3 depletion. Our study suggests that the H3K36me3 and DNA methylation marks in gene bodies are established independently from each other and points to similar functional roles of intragenic DNA methylation and intragenic H3K9me3 for CpG-rich and CpG-poor genes, respectively. To elucidate how a loss of DNA methylation affects a gene expression and epigenome we studied colon cancer cell line HCT116 and its derivative, HCT116 DNMT1-/- DNMT3b -/- (HCT116-DKO). According to previous studies HCT116-DKO is characterized by 95% of loss of DNA methylation. In HCT116 and HCT116-DKO cells, we profiled diverse epigenetic marks and gene expression. Further a crosstalk between epigenetic changes and transcriptional changes was analyzed. This is the expressional part of study.
2011-03-31 | E-GEOD-26018 | biostudies-arrayexpress
Project description:RFX7 DNA binding landscape in HCT116
| PRJNA680775 | ENA
Project description:Analysis of cross talk of epigenetic marks in HBEC by using tilling arrays chr19. In Human Bronchial epithelia cells (HBEC), H3K9me3, H4K20me3, H3K4me3, H3K27me3, H3K36me3 and DNA methylation were profiled. In these cells, DNA methylation status was analyzed by MIRA and UnmethylCollector (UMC). Study of epigenetic changes in HCT116 DNMT1-/- and DNMT3b -/- (HCT116-DKO) in comparison to intact HCT116. In HCT116 and HCT116-DKO, H3K9me3, H3K36me3 and DNA methylation were profiled. In these cells, DNA methylation status was analyzed by MIRA. Analysis of epigenetic changes caused by siRNA for SED2 transcript in HBEC. In HBEC and SETD2 siRNA HBEC, H3K36me3 and DNA methylation were profiled. In these cells, DNA methylation status was analyzed by MIRA.
2011-03-31 | GSE26040 | GEO