Project description:In this study we have examine the deposition of H3K4me1,H3K4Me3 and H3K27Ac and the Nodal transcription factor, Smad2/3, immediately following zygotic transcription and continuing through gastrulation. We profiled 4 histone modifications (H3K4Me3, H3K27Me3, H3K27AC, H3K4Me1) and one transcription factor smad2/3 (+ chromatin input) using ChIP-Seq, and expression profiles (3' RNA-Seq) for Xenopus tropicalis embryos stage8, stage9 and stage10.5. Furthermore, we have profile two histone modifications (H3K4Me1 and H3K27Ac) in absance of nodal signaling in stage9 Xenopus tropicalis embryos using ChIP-seq and 3-seq
Project description:ChIP-Seq (H3K4me3, H3K4me1, H3K9me3, H3K27ac, H3K27me3, H3K36me3, Input) data for HL60 cell line generated at Centre for Epigenome Mapping Technologies, Genome Sciences Center, B.C. Cancer Agency.
Project description:The dataset contains ChIP-Seq data of the Set3 and Hos2 proteins in Candida albicans, assayed in two morphological phases (yeast and hypha). The Set3 and Hos2 proteins in the respective strains carry 9myc epitopes and ChIP was performed with an anti-myc antibody. Included samples are the following: 1 input and 1 ChIP sample of an untagged wild type strain as negative control assayed in the yeast phase, 1 input and 3 ChIP biological replicates of the Set3-9myc strain in the yeast phase, 1 input and 2 ChIP biological replicates of the Set3-9myc strain in the hypha phase, 1 input and 2 ChIP biological replicates of the Hos2-9myc strain in the yeast phase, 1 input and 2 ChIP biological replicates of the Hos2-9myc strain in the hypha phase, 1 input and 3 ChIP biological replicates of Set3-9myc in a set1delta/delta background in the yeast phase.
Project description:Using the Fucci cell cycle indicator system in hESCs, we evaluated the patterns of bivalent histone marks and enhancer histone marks during the cell cycle by ChIP-seq. We further evaluated how the chromatin architecture changed during the cell cycle. We found that bivalent domains are cell cycle regulated, and H3K4me3 specifically peaks during the late G1 stage of the cell cycle. H3K27me3, however, is largely unchanged during the cell cycle. Cell cycle-regulated bivalent domains interact with enhancers and form cell cycle regulated chromatin interactions. FACS-isolated cell cycle fractions (DN, early G1; KO2, late G1; AzL, S-phase; and AzH, G2/M) from Fucci hESCs were subject to ChIP-seq for H3K4me3, H3K27me3, H3K27ac and H3K4me1, and used for sequencing along with input controls for each of the 4 cell cycle fractions (20 samples total), using Illumina platform, or 4C-seq for each cell cycle fraction using viewpoints neighboring the GATA6 or SOX17 promoters.
Project description:We profiled 16 patient tumour samples by ChIP-seq. H3K27ac and Input are provided for 16 samples and H3K27me3 is provided for 14 samples.
Among the 16 samples, 9 are G34WT and 7 are G34R/V. The raw fastq or bam files are provided.
Project description:Ezh2 and EZH1 are histone H3 lysine 27 (H3K27)-specific methyltransferases. Their hyperactive mutations and overexpression were found in cancer including various hematological malignancies. UNC1999 is a highly selective inhibitor for both enzymes. It suppresses H3K27 tri- and di-methylation globally and inhibits growth of MLL-rearranged acute leukemia. Here we performed ChIP-Seq to profile how UNC1999 affects distribution of H3K27me3 and its antagonizing H3K27ac in MLL-AF9-immortalized leukemia cells. We also performed ChIP-seq of SUZ12, an essential common cofactor of EZH2 and EZH1 following compound treatments. We treated MLL-AF9 transformed murine leukemia cells with DMSO, UNC1999 or UNC2400 (an inactive analog compound of UNC1999). Cells were then collected and used for ChIP-Sequencing of Input, H3K27me3, SUZ12, and H3K27ac.
Project description:The impact of drugs inhibiting DNA methylation (5-aza-2'-deoxycytodine, DAC) and EZH2 (EPZ-6438) on H3K27me3 coverage was analyzed in two neuroblastoma cell lines. Parallel analyses investigated associated changes in RNA expression and DNA methylation. The neuroblastoma cell lines Be(2)-C and IMR5-75 were treated with a combination of DAC and EPZ-6438. Controls were treated with solvent (DMSO). H3K27me3 ChIP seq was done to investigate treatment-related changes of this mark. In addition, H3K4me3 and H3K27ac ChIP seq was done in DMSO treated samples to identify putative regulatory regions.
Project description:This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. It contains ChIP-seq data generated on Solexa Genome Analyzer for 6 Histone modifications (H3K9me3, H3K27me3, H3K4me3, H3K4me1, H3K27Ac, H3K9Ac), PolII and CBP/p300. Each factor has been studied for 12 different time-points of Drosophila development. Keywords: Epigenetics For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf For each combination of time-point and antibody, triplicate ChIP experiments have been performed and hybridized on Agilent 244K arrays. The hybridizations have been verified by sequencing one replicate of IP and one replicate of Input following Solexa sequencing procedure.