Project description:Genome-wide mapping of H3K4me1, H3K4me3 and H3K27ac in KP and DK ChIP-seq for H3K4me1, H3K4me3 and H3K27ac in KP and DK p63 profiling of DK through ChIP-seq
Project description:We analyzed ChIP-seq profiles for H3K4me3, H3K27ac, BRG1, ARID1A, PPAR? and JMJD1A and FAIRE-seq open chromatin profile in immortalized brown adipocytes (iBATs) treated with 1 ?M isporoterenol (ISO) or vehicle for 2 hr ChIP-seq profiles for H3K4me3, H3K27ac, BRG1, ARID1A, PPAR? and JMJD1A and FAIRE-seq open chromatin profile in iBATs at Day 8 of differentiation treated with 1 ?M isporoterenol (ISO) or vehicle for 2 hr
Project description:We generated maps of H3K4me1, H3K27ac (enhancers), H3K4me3, Pol II (promoters) and H3K27me3 (repressed chromatin) in the genome of human iPSC-derived cardiomyocytes Differentiation of cardiomyocytes from iPSC followed by ChIP-seq of H3K27ac, H34me1, H327me3, H3K4me3 and PolII
Project description:ChIP-seq was performed using Drosophila Kc167 cells using antibodies against H3K4me3 to identify active promoters and H3K4me1 to identify active enhancers. H3K27ac ChIPseq was performed to identify active promoters and enhancers. Once enhancers and promoters were identified, JIL-1 and histone phosphorylation, H3K9acS10ph and H3K27acS28ph, ChIP-seq was performed to look at binding trends. JIL-1 and phosphoacetlation is found at low levels at inactive enhancers and shows increase at active enhancers and promoters. Here we examine histone phosphorylation by JIL-1 and acetylation of H3K27ac by CBP at transcriptionally active vs. inactive promoters and enhancers. ChIP-seq is performed in Kc167 Drosophila cells using antibodies against JIL-1, H3K27acS28ph, H3K9acS10ph, H3K4me3, H3K4me1, and H3K27ac.
Project description:Genome-wide chromatin H3K27ac, H3K18ac and H3K4me3 occupancy changes in response to CBP inhibitor treatment in Treg cells using ChIP sequencing (ChIP-seq). Expression profiling by ChIP-seq of Treg cells treated with DMSO or CBP inhibitor
Project description:Enhancers are fundamental to gene regulation. Post-translational modifications by the small ubiquitin-like modifiers (SUMO) modify chromatin regulation enzymes, including histone acetylases and deacetylases. However, it remains unclear whether SUMOylation regulates enhancer marks, acetylation at the 27th lysine residue of the histone H3 protein (H3K27Ac). We hypothesize that SUMOylation regulates H3K27Ac. To test this hypothesis, we performed genome-wide ChIP-seq analyses. We discovered that knockdown (KD) of the SUMO activating enzyme catalytic subunit UBA2 reduced H3K27Ac at most enhancers. Bioinformatic analysis revealed that TFAP2C-binding sites are enriched in enhancers whose H3K27Ac was reduced by UBA2 KD. ChIP-seq analysis in combination with molecular biological methods showed that TFAP2C binding to enhancers increased upon UBA2 KD or inhibition of SUMOylation by a small molecule SUMOylation inhibitor. However, this is not due to the SUMOylation of TFAP2C itself. Proteomics analysis of TFAP2C interactome on the chromatin identified histone deacetylation (HDAC) machinery. TFAP2C KD reduced HDAC binding to chromatin and increased H3K27Ac marks at enhancer regions, suggesting that TFAP2C is involved in recruiting HDAC. Taken together, our findings provide important insights into regulation of enhancer marks by SUMOylation.
Project description:Here we present the whole genome ChIP-Seq analyses of a wide variety of histone marks, H3K27ac, H3K4me1, H3K4me3, and H3K27me3 in the brain, heart, and liver, along with the RNA-seq data of these organs of early human embryos 12 weeks after gestation. In total, brain, heart, and liver of early human post-implantation embryos were used, and four histone modifications were detected, including H3K27ac, H3K4me1, H3K4me3 and H3K27me3. Also, the transcriptomes of these three organs were analyzed.
Project description:We did ChIP-seq with anti- H3K4me3, H3K4me1, H3K4me2, H3K27me3, H3K27ac, and H3K36me3 antibodies in both C2C12 myoblasts and myotubes Examination of 6 different histone modifications in 2 cell types.
