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ChIP-seq analysis reveals alteration of H3K4 trimethylation occupancy of cancer-related genes by cold atmospheric plasma

ABSTRACT: ChIP-seq analysis reveals alteration of H3K4 trimethylation occupancy of cancer-related genes by cold atmospheric plasma

PROVIDER: PRJNA482967 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7602020.fastq.gz	Fastqsanger.gz
	SRR7602017_1.fastq.gz	Fastqsanger.gz
	SRR7602017_2.fastq.gz	Fastqsanger.gz
	SRR7602018_1.fastq.gz	Fastqsanger.gz
	SRR7602018_2.fastq.gz	Fastqsanger.gz

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ChIP-seq analysis reveals alteration of H3K4 trimethylation occupancy in cancer-related genes by cold atmospheric plasma

Project description:ChIP-seq analysis reveals alteration of H3K4 trimethylation occupancy in cancer-related genes by cold atmospheric plasma

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ChIP-seq analysis reveals alteration of H3K4 trimethylation occupancy of cancer-related genes by cold atmospheric plasma

Project description:Cold atmospheric plasma (CAP) has obtained credits for cancer treatment by its ability to preferentially induce cancer cell death, while its molecular mechanism is under elucidation. Here, an epigenetic effect of CAP on cancer cell was examined by performing a genome-wide ChIP-seq for H3K4me3 in the MCF-7 breast cancer cell.

2019-07-26 | GSE117698 | GEO

ChIP-seq analysis reveals alteration of H3K4 trimethylation occupancy in cancer-related genes by cold atmospheric plasma

Project description:This SuperSeries is composed of the SubSeries listed below.

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H3K4 trimethylation is required for postnatal pancreatic endocrine cell functional maturation

Project description:During pancreas development, endocrine progenitors differentiate into the islet-cell subtypes, which undergo further functional maturation in postnatal islet development. In islet b-cells, genes involved in glucose-stimulated insulin secretion are activated and glucose exposure increases the insulin response as b-cells mature. Here, we investigated the role of H3K4 trimethylation in endocrine cell differentiation and functional maturation by disrupting TrxG complex histone methyltransferase activity in mouse endocrine progenitors. In the embryo, genetic inactivation of TrxG component Dpy30 in NEUROG3+ cells did not affect the number of endocrine progenitors or endocrine cell differentiation. H3K4 trimethylation was progressively lost in postnatal islets and the mice displayed elevated non-fasting and fasting glycemia, as well as impaired glucose tolerance by postnatal day 24. Although postnatal endocrine cell proportions were equivalent to controls, islet RNA-sequencing revealed a downregulation of genes involved in glucose-stimulated insulin secretion and an upregulation of immature b-cell genes. Comparison of histone modification enrichment profiles in NEUROG3+ endocrine progenitors and mature islets suggested that genes downregulated by loss of H3K4 trimethylation more frequently acquire active histone modifications during maturation. Taken together, these findings suggest that H3K4 trimethylation is required for the activation of genes involved in the functional maturation of pancreatic islet endocrine cells.

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The alteration of gene expression in fulvestrant resistant breast cancer cell by cold atmospheric plasma (CAP)

Project description:Cold atmospheric plasma (CAP) contributes to recovery of fulvestrant sensitivity in fulvestarnt resistant breast cancer cell.

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Arginine methylation at histone H3R2 controls deposition of H3K4 trimethylation

Project description:Modifications on histones control important biological processes through their effects on chromatin structure. Methylation at histone H3 lysine 4 (H3K4) by Set1p is found at the 5’end of active genes and contributes to transcriptional activation by recruiting chromatin remodeling enzymes. An adjacent arginine residue (H3R2) is also known to be asymmetrically dimethylated (H3R2me2a) in mammalian cells6, but its location within genes and its function in transcription are unknown. Here we show that H3R2 is also methylated in budding yeast. Using an antibody specific for H3R2me2a in ChIP-on-Chip analysis we determine the distribution of this modification on the entire yeast genome. We find that H3R2me2a is enriched at all heterochromatic loci, at inactive euchromatic genes and at the 3’-end of moderately transcribed genes. In all cases the pattern of H3R2 methylation is mutually exclusive with the presence of trimethylation at H3K4 (H3K4me3). The inverse correlation reflects the fact that methylation at H3R2 disrupts the ability of the Set1-complex to methylate H3K4. H3R2m2a inhibits specifically the trimethylation of H3K4 because it prevents Spp1 (a Set1-methyltranferase subunit) from binding to histone H3. These results indicate that methylation at H3R2 controls the global distribution of H3K4me3 and provides the first mechanistic insight into the function of arginine methylation on chromatin. Keywords: ChIP-chip

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H3K4 trimethylation is required for postnatal pancreatic endocrine cell functional maturation

Project description:H3K4 trimethylation is required for postnatal pancreatic endocrine cell functional maturation

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H3K4 trimethylation ChIP - wild-type

Project description:Genome-wide location analysis of histone H3 lysine-4 trimethylation in wild-type strain Keywords: repeat

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