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ABSTRACT: ChIP-seq with H3K27Ac antibody

PROVIDER: PRJNA723041 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14276378.fastq.gz	Fastqsanger.gz
	SRR14276379.fastq.gz	Fastqsanger.gz
	SRR14276380.fastq.gz	Fastqsanger.gz
	SRR14276381.fastq.gz	Fastqsanger.gz
	SRR14276382.fastq.gz	Fastqsanger.gz

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Regulation of Histone Acetylation by SUMOylation Through TFAP2C Binding to the Chromatin and Recruitment of HDAC Complex

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.

2024-04-13 | PXD045644 | Pride

Genome-wide maps of H3K27ac localization in HUVECs

Project description:H3K27Ac is one of the expressed enhancer markers in endothelial cells, but its genomic localization is unknown. This time, we established a new antibody for H3K27ac, and performed ChIP-seq to identify H3K27ac binding site in whole genome manner under hypoxia. We used chromatin immunoprecipitation with deep sequencing (ChIP-seq) of HUVECs treated with or without hypoxia (1%O2) for 24hours, then H3K27ac binding regions were identified. Normoxia was used as a control condition. HUVECs were used within the first 6 passages.

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Project description:Estrogen Receptor alpha (ERα) is a key driver of most breast cancers, and it is the target of endocrine therapies used in the clinic to treat women with ERα positive (ER+) breast cancer. The two methods ChIP-seq (chromatin immunoprecipitation coupled with deep sequencing) and RIME (Rapid Immunoprecipitation of Endogenous Proteins) have greatly improved our understanding of ERα function during breast cancer progression and in response to anti-estrogens. A critical component of both ChIP-seq and RIME protocols is the antibody that is used to pull down the bait protein. To date, most of the ChIP-seq and RIME experiments for the study of ERα have been performed using the sc-543 antibody from Santa Cruz Biotechnology. However, this antibody has been discontinued, thereby severely impacting the study of ERα in normal physiology as well as diseases such as breast cancer and ovarian cancer. Here, we compare the sc-543 antibody with other commercially available antibodies, and we show that 06-935 (EMD Millipore) and ab3575 (Abcam) antibodies can successfully replace the sc-543 antibody for ChIP-seq and RIME experiments.

2019-03-21 | PXD012930 | Pride

Enhancer profiling using H3K27Ac ChIP-seq signals in Kasumi-7, Kasumi-9, NAGL-1, and NALM-1 cell lines

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Project description:To investigate the function of XAF1 in chromatin openning. Wild-type or XAF1 knockout HT29 cells were infected with VSV for 0 or 3 hours, ChIP-seq was did with H3K27Ac antibody. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for histone modifications H3K27Ac in HT29 cells.

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Project description:H3K27ac ChIP-seq was performed to identify active enhancers in different TLR activated control CD8α+ DCs as well as to understand the role of NCoR1 in regulating TLR specific enhacner activity using H3K27ac ChIP-seq performed in NCoR1 KD DCs. MutuDC1940 cell line were treated with TLR3 ligand poly I:C, TLR9 ligand CpG-B and combined stimulation of TLR9 , TLR3, and IFNg for 2hr and 6hr. Recombinant Anti-Histone H3 (acetyl K27) antibody was used to pull down chromatin regions having active enhacner mark in each unstimulated and stimulated condition.

2025-12-03 | E-MTAB-10992 | biostudies-arrayexpress

Genomic analysis reveals HDAC1 regulates clinically relevant transcriptional programs in Pancreatic cancer

Project description:We performed ChIP-seq analysis on H3K27ac in MIA PaCa-2 cells with HDAC1 overexpression using the antibody Abcam H3K27ac (Abcam, ab4729), a non-targeting scrableled sgRNA control, and two replicates for each.

2023-05-31 | GSE209895 | GEO

Enhancer landscape of mouse developing midbrain at 11.5 dpc embryos

Project description:We report the distribution of histone H3K4me1 and H3K27ac within the genome of mouse embryonic midbrain. We prepared the chromatin from 11 dpc embryonic midbrain and made chromatin precipitation with antibody against H3K4me1 and H3K27ac (rabbit polyclonal antibody). High-throughput sequencing applied for the ChIP analysis revealed the differential distribution of modified histone within developing midbrain. ChIP analysis of mouse 11 dpc embryonic midbrain and forelimb buds against anti-H3K4me1 and H3K27ac antibody.

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