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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)

ABSTRACT: 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)

PROVIDER: PRJNA700523 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13649743.fastq.gz	Fastqsanger.gz
	SRR13649744.fastq.gz	Fastqsanger.gz
	SRR13649745.fastq.gz	Fastqsanger.gz
	SRR13649746.fastq.gz	Fastqsanger.gz

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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.

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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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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 | GSE114567 | GEO

Arid1a restrains Kras-dependent changes in acinar cell identity

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Transcriptome analysis of murine primary pancreatic acinar cells in the context of Arid1a deficiency

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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Interplay of EGFR signaling and ARID1A in regulating transcriptome of celllular-plasticity genes

Project description:mRNA expression profiles of Arid1a-wildtype and Arid1a-knockdown murine 266-6 cells were generated, in the presence or absence of EGF. We found that EGFR signaling activation and Arid1a loss cooperatively upregulate a subset of genes which are involved in cellular palsticity regulation.

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Epigenetic reprogramming in pancreatic acinar cell in the absence of MIST1

Project description:Epigenetic profile of tissues is reprogrammed under diseased conditions. H3K4Me3 and H3K27Me3 represent active and repressive epigenetic marks, respectively. ChIP-seq is an effective tool to study global protein-DNA interactions. To study global epigenetic differences, we used H3K4Me3 antibody to evaluate its enrichment in pancreatic acinar cells of WT and Mist1-/- mice followed by next generation sequencing. We found specific hotspots that showed differential enrichment for H3K4Me3 both in WT and Mist1-/- mice. The data show that pancreatic acinar cells are epigenetically reprogrammed under stressed cellular conditions. Global H3K4Me3 profiling of WT and Mist1-/- pancreatic acinar cells using ChIP-seq.

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