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ATAC-seq of cholangiocytes treated with TGFbeta

ABSTRACT: ATAC-seq of cholangiocytes treated with TGFbeta

PROVIDER: PRJNA606518 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11080029_1.fastq.gz	Fastqsanger.gz
	SRR11080029_2.fastq.gz	Fastqsanger.gz
	SRR11080030_1.fastq.gz	Fastqsanger.gz
	SRR11080030_2.fastq.gz	Fastqsanger.gz
	SRR11080031_1.fastq.gz	Fastqsanger.gz

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Project description:TGF beta has profound effects on global gene expression changes. To understand the epigenetic changes associated with TGF beta stimulation, we performed ATAC-seq of cholangiocytes to understand the changes in chromatin accessibility associated with TGF beta. We also wanted to determine if H3K9ac played a role in TGF beta induced changes in chromatin accessibility. Therefore, H3K9ac inhibitor CPTH6 was used to treat cells.

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Project description:TGF beta has profound effects on global gene expression changes. To understand the epigenetic mechanisms associated with TGF beta stimulation, we performed ChIP-seq of cholangiocytes to understand the changes in histone modifications associated with TGF beta. We choose H3K27ac and H3K9ac, histone modification associated with gene expression. These histone modifications were correlated with SMAD3 occupancy, which is a canonical downstream mediator of TGF beta signaling.

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cholangiocytes treated with TGFbeta

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

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Expression data from TGFbeta-treated control or aPKC silenced A549 cells

Project description:Aberrant TGFbeta signalling is a hallmark of epithelial derived tumours. Signalling patterns can depend on the membrane trafficking and internalization of the TGFbeta receptors. Protein kinase C (PKC), particularly the atypical PKC isoforms, alter the trafficking of TGFbeta receptors and can alter TGFbeta induced gene expression. We used microarrays to detail the programme of gene expression underlying TGFbeta induction between control or aPKC silenced A549 cells. Control or aPKC silenced A549 cells were serum starved and treated with TGFbeta for 1 hour. Total RNA was extracted from untreated or TGFbeta treated cells after 8 and 24 hours and analyzed using Affymetrix microarrays. We sought to assess TGFbeta gene expression in aPKC silenced lung cancer cells, as we found that knockdown of aPKC extends TGFbeta signalling as assessed by phospho Smad2 levels. Furthermore, increased expression and oncogenic activity of aPKC (PKCiota) has been reported in lung cancer cells.

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