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High-throughput sequencing in ARID1A knockout MDA-MB-231 cells [H3K4me3 histone modification ChIP-seq]

ABSTRACT: High-throughput sequencing in ARID1A knockout MDA-MB-231 cells [H3K4me3 histone modification ChIP-seq]

PROVIDER: PRJNA980245 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24830559_1.fastq.gz	Fastqsanger.gz
	SRR24830559_2.fastq.gz	Fastqsanger.gz
	SRR24830560_1.fastq.gz	Fastqsanger.gz
	SRR24830560_2.fastq.gz	Fastqsanger.gz
	SRR24830561_1.fastq.gz	Fastqsanger.gz

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High-throughput sequencing in ARID1A knockout MDA-MB-231 cells [H3K4me3 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 H3K4me3 histone modification of ARID1A knockout and control MDA-MB-231 cells.

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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 investigate global chromatin remodeling, we performed ATAC–seq in ARID1A knockout and control MDA-MB-231 cells.

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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. Next-generation sequencing analysis was performed in control and ARID1A knockout MDA-MB-231 cells to investigate global gene expression changes.

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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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High throughput sequencing in ARID1A knockout MDA-MB-231 cells [H3K4me1 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 H3K4me1 histone modification of ARID1A knockout and control MDA-MB-231 cells.

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The miRNA profiling in MDA-MB-231, MDA-MB-231/E1A and knockdown of Dicer in MDA-MB-231/E1A cells

Project description:Dicer, RNase III endonuclease, is an essential enzyme in miRNA biogenesis that regulates target gene expression, and it has been reported that aberrant expressions of Dicer associate with the clinical outcomes of patients in various cancers. To explore the miRNA differencial expression regulated by Dicer in MDA-MB-231/E1A cells, the microarray profiling analysis was employed to conduct differentially expressed miRNAs in stable MDA-MB-231/vector, MDA-MB-231/E1A, and MDA-MB-231/E1A/shDicer cells.

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Expression profiles of MDA-MB-231, MDA-231 S1a and S1b

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The miRNA profiling in MDA-MB-231, MDA-MB-231/E1A and knockdown of Dicer in MDA-MB-231/E1A cells

2016-01-16 | E-GEOD-76924 | biostudies-arrayexpress

High-throughput sequencing in ARID1A knockout MDA-MB-231 cells

Project description:High-throughput sequencing in ARID1A knockout MDA-MB-231 cells

| PRJNA980238 | ENA

Expression profiles of MDA-MB-231, MDA-231 S1a and S1b

Project description:Identification of genes that are involved in self-seeding by comparing gene expression profiles between parental MDA-MB-231 cells and seeder cells (MDA-231-S1a and S1b)

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