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Genome-wide maps of H3K27ac ocupancy on chromatin in murine acinar cell line upon EGF treatment and Arid1a silencing

ABSTRACT: Genome-wide maps of H3K27ac ocupancy on chromatin in murine acinar cell line upon EGF treatment and Arid1a silencing

PROVIDER: PRJNA700524 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13649947.fastq.gz	Fastqsanger.gz
	SRR13649948.fastq.gz	Fastqsanger.gz
	SRR13649949.fastq.gz	Fastqsanger.gz
	SRR13649950.fastq.gz	Fastqsanger.gz
	SRR13649951.fastq.gz	Fastqsanger.gz

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Genome-wide maps of H3K27ac ocupancy on chromatin in murine acinar cell line upon EGF treatment and Arid1a silencing

Project description:Chromatin Immunoprecipitation-based sequencing (ChIP-seq) of H3K27ac was conduced in murine Kras-mutant acinar cell line 266-6 in the context of Arid1a-knockdown and/or EGF treatment. We found EGFR signaling activation as well as Arid1a silencing leads to additional increase of H3K27ac level genome-widely. And the maximal H3K27ac was achieved by the combined- EGF treatment and Arid1a knockdown.

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Genome-wide occupancy profile of ARID1A in the presence and absence of epidermal growth factor stimulation in murine acinar cell line 266-6 (ChIP-seq)

Project description:We identified the genome binding profile of SWI/SNF complex component ARID1A in pancreatic acinar cells. By comparing the genomic occupancy profiles, we found that EGF strikingly diminished ARID1A genome-wide affinity to the chromatin.

2023-05-31 | GSE166330 | GEO

Arid1a restrains Kras-dependent changes in acinar cell identity

Project description:Mutations in members of the SWI/SNF chromatin remodeling family are common events in human cancer, but the mechanisms whereby disruption of SWI/SNF components alters tumorigenesis remain poorly understood. To model the effect of loss of function mutations in the SWI/SNF subunit Arid1a in pancreatic ductal adenocarcinoma (PDAC) initiation, we directed shRNA triggered, inducible and reversible suppression of Arid1a to the pancreas of mice in the setting of oncogenic KrasG12D. Arid1a cooperates with Kras in the adult pancreas as postnatal silencing of Arid1a following sustained KrasG12D expression induces rapid and irreversible reprogramming of acinar cells into mucinous PDAC precursor lesions. In contrast, Arid1a silencing during embryogenesis, concurrent with KrasG12D activation, leads to retention of acinar cell fate. Together, our results demonstrate Arid1a as a critical modulator of Kras-dependent changes in acinar cell identity, and underscore an unanticipated influence of timing and genetic context on the effects of SWI/SNF complex alterations in epithelial tumorigenesis.

2018-07-03 | GSE114576 | GEO

Arid1a restrains Kras-dependent changes in acinar cell identity

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Project description:mRNA expression profiles were generated from primary pancreatic acinar cells of Arid1a-deficient and Arid1a-wildtype mice. Arid1a depletion leads to transcription activation to the majority of genes.

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Analysis of chromatin accessibility in Arid1a-deficient murine primary pancreatic acinar cells using ATAC-seq

Project description:To gain insight into how the loss of SWI/SNF component ARID1A affects the chromatin accessibility, primary acinar cells were isolated from Arid1a-knockout and control mice and subjected to ATAC-sequencing.

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Arid1a restrains Kras-dependent changes in acinar cell identity

Project description:Arid1a restrains Kras-dependent changes in acinar cell identity

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Arid1a restrains Kras-dependent changes in acinar cell identity

Project description:Arid1a restrains Kras-dependent changes in acinar cell identity

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High throughput sequencing in ARID1A knockout MDA-MB-231 cells [H3K27ac histone modification ChIP-seq]

Project description:ARID1A has been suggested as a key regulator for anti-tumor immunity. In the present study, we evaluated the role of ARID1A deficiency in inducing adaptive immune resistance in triple negative breast cancer. To explore global transcriptional activity, we performed chromatin immunoprecipitation followed by high throughput sequencing (ChIP–seq) to investigate H3K27ac histone modification of ARID1A knockout and control MDA-MB-231 cells.

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Project description:Arid1a is the subunit of SWI/SNF complex, which was reported to guide SWI/SNF to DNA. Here, we found that loss of Arid1a in the liver results in improved liver regeneration after partial hepatectomy.Genome-wide analysis showed that after hepatectomy,loss of Arid1a reduces the recruitment and activity of E2F4 on target promoters, resulting in expression programs that favor regeneration during injury. Correspondingly, these promoters showed increased H3k4me2 and H3k27ac marks, indicating de-repression of these E2f target genes. The post partial hepatectomy mice liver cells were fixed and isolated, analysis of genomic occupancy of E2f4,H3K4me2,H3K27ac in hepatocytes from Arid1a WT and Arid1a liver specific KO mice by ChIP-seq.

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