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Histone H3K27 acetylation at CTCF sites mediates cell type-specific chromatin interactions between them

ABSTRACT: Histone H3K27 acetylation at CTCF sites mediates cell type-specific chromatin interactions between them

PROVIDER: PRJNA612834 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11311767.fastq.gz	Fastqsanger.gz
	SRR11311768.fastq.gz	Fastqsanger.gz

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Histone H3K27 acetylation at CTCF sites mediates cell type-specific chromatin interactions between them.

Project description:Histone H3K27 acetylation at CTCF sites mediates cell type-specific chromatin interactions between them.

| PRJNA612057 | ENA

Histone H3K27 acetylation at CTCF sites mediates cell type-specific chromatin interactions between them.

Project description:We found that CTCF sites was acetylated at H3K27 and this modification was decreased by histone acetyltransferases and depletion of GATA-1.

2021-03-12 | GSE146827 | GEO

Histone H3K27 acetylation at CTCF sites mediates cell type-specific chromatin interactions between them

Project description:We found that H3K27ac at CTCF sites was decreased around the β-globin locus by loss of GATA-1 binding.

2021-03-15 | GSE147037 | GEO

H3K27 and H3K9 Methylation Mask Potential CTCF Binding Sites to Maintain 3D Genome Integrity

Project description:The three-dimensional (3D) genome structure is essential for gene regulation and various genomic functions. CTCF plays a key role in organizing Topologically Associated Domains (TADs) and promoter-enhancer loops, contributing to proper cell differentiation and development. Although CTCF binds the genome with high sequence specificity, its binding sites are dynamically regulated during development, and aberrant CTCF binding is linked to diseases such as cancer and neurological disorders, and aging. However, the mechanisms controlling CTCF binding remain unclear. Here, we investigated the role of repressive chromatin modifications in CTCF binding using H3K9 methyltransferase-deficient immortalized mouse embryonic fibroblasts (iMEFs) and H3K27 methyltransferase EZH1/2 inhibitor. We found that H3K9 and H3K27 methylation regulate CTCF binding at distinct genomic regions, and their simultaneous loss induces drastic changes in CTCF binding. These changes were associated with alterations in 3D genome architecture and gene expression, suggesting that repressive chromatin modifications preserve proper chromatin organization by preventing aberrant CTCF binding. Additionally, while CTCF binding sites repressed by H3K9 methylation were bound by CTCF in early mouse embryos, those repressed by both H3K9 and H3K27 methylation remained inaccessible, with early embryonic-specific H3K27 methylation forming at these sites. These findings implicate that H3K27 methylation prevents abnormal CTCF binding in early embryos, ensuring proper genome organization during development.

2025-07-17 | GSE293581 | GEO

H3K27 and H3K9 Methylation Mask Potential CTCF Binding Sites to Maintain 3D Genome Integrity [ChIP-Seq]

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CBP/P300 Dependent Histone H3K27 Acetylation

Project description:Enhancer Activity Requires CBP/P300 Bromodomain Dependent Histone H3K27 Acetylation

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H3K27 acetylation and gene expression during late spermatogenesis

Project description:H3K27 acetylation and gene expression during late spermatogenesis

| PRJNA420064 | ENA

H3K27 acetylation and gene expression during late spermatogenesis

Project description:ChIP-seq for H3K27 acetylation and RNA-seq were performed during spermatogenesis. We analyzed two representative stages of spermatogenesis: purified pachytene spermatocytes (PS) undergoing meiosis; and postmeiotic round spermatids (RS) from adult testes.

2018-02-05 | GSE107398 | GEO

H3K27 acetylation profiling of B cells from Mb1Cre and Mct1f/fMb1Cre mice

Project description:Using ChIP-seq we identified H3K27 acetylation loci in B cells from Mb1Cre and Mct1f/fMb1Cre mice

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H3K27 Acetylation profile of hypothyroid NCoR1KO mice

Project description:We ablated the expression of the Nuclear Receptor Corepressor 1 specifically in mice livers and rendered them hypothyroid. Then we performed H3K27 acetylation CHIP-Seq. We found decreased H3K27ac in the livers of hypothyroid wild type and NCoR1KO mice. Therefore, we concluded that the thyroid hormone receptor may recruit histone deacetilases independently of NCoR1.

2017-09-18 | GSE99475 | GEO

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