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ATAC-seq in ARID1A WT or KO OVCA429 Cells after interferron treatment

ABSTRACT: ATAC-seq in ARID1A WT or KO OVCA429 Cells after interferron treatment

PROVIDER: PRJNA545316 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9151880_1.fastq.gz	Fastqsanger.gz
	SRR9151880_2.fastq.gz	Fastqsanger.gz
	SRR9151881_1.fastq.gz	Fastqsanger.gz
	SRR9151881_2.fastq.gz	Fastqsanger.gz
	SRR9151882_1.fastq.gz	Fastqsanger.gz

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RNA-seq in ARID1A WT, KO OVCA429 Cells after IFNγ treatment

Project description:RNA-seq in ARID1A WT, KO OVCA429 Cells after IFNγ treatment

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RNA-seq transcriptonal profiling in partial hepatectomy liver tissues in Arid1a WT and liver specific KO mice.

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.RNAseq shows transcriptional profiling in WT and Arid1a LKO livers pre- and post-hepatectomy, which confirmed the E2F4 target genes and cell cycle genes were upregulated after hepatectomy. After partial hepatectomy, liver transcriptional profiling in WT and Arid1a liver specific KO mice were generated by RNA-seq analysis.

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Effect of Arid1a deletion on chromatin accessibility in antiviral effector CD8+ T cells. [ATAC-Seq]

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ATAC-seq in ARID1A WT or KO OVCA429 Cells after interferron treatment

Project description:Whether cancer driver mutation(s) directly drives cancer immune phenotype and immune tolerance remains a standing question. ARID1A is a core member of the polymorphic BAF chromatin remodeling complex. ARID1A mutations frequently occur in human cancers and drive cancer development. Here, we studied the molecular, cellular, and clinical impact of ARID1A gene status on cancer immunity. We demonstrate that ARID1A mutations, limited expression, and deficiency impair interferon(IFN)-responsive gene chromatin accessibility and expression, resulting in anemic T cell tumor infiltration, weakened tumor immunity, and shortened host survival in many human cancer histologies as well as in murine cancer models, and are negatively associated with immunotherapy response. Mechanistically, ARID1A interacts with EZH2 via its carboxyl terminal and antagonizes EZH2-mediated IFN responsiveness. Thus, the interaction between ARID1A and EZH2 defines cancer IFN-responsiveness and immune evasion. Our work indicates that cancer epigenetic driver mutations can shape cancer immune phenotype and immunotherapy.

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Project description:Assess chromatin accessibility in WT, p53-ko, Ezh2-ko primary macrophages using ATAC-seq.

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ATAC-seq in WT, p53-ko, Ezh2-ko primary macrophages

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