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ChIP-seq analysis of gene expression regulated by LSD1 in CD8+ T cells

ABSTRACT: ChIP-seq analysis of gene expression regulated by LSD1 in CD8+ T cells

PROVIDER: PRJNA1046394 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26979474_1.fastq.gz	Fastqsanger.gz
	SRR26979474_2.fastq.gz	Fastqsanger.gz
	SRR26979475_1.fastq.gz	Fastqsanger.gz
	SRR26979475_2.fastq.gz	Fastqsanger.gz
	SRR26979476_1.fastq.gz	Fastqsanger.gz

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ChIP-seq analysis of gene expression regulated by LSD1 in CD8+ T cells

Project description:ChIP-seq assay was performed with GSK- or Vehicle-treated CD8+ T cells to interrogate the genome-wide distribution of LSD1, H3K4me1, H3K4me2, H3K4me3, H3K27ac, and Pol II, and their alterations in response to LSD1 inhibition.

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RNA-seq analysis of gene expression regulated by LSD1 in CD8+ T cells

Project description:RNA-seq analysis of gene expression regulated by LSD1 in CD8+ T cells

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RNA-seq analysis of gene expression regulated by LSD1 in CD8+ TILs

Project description:T cell dysfunction is a hallmark of many cancers. Features of dysfunctional T cells and mechanisms leading to T cell dysfunction remain incompletely understood. Significant chromatin changes happen when T cells become dysfunctional, implicating a critical role of epigenetic regulators in such process. Here we study the role of LSD1 in regulating T cell function in cancer and perform a RNA-seq analysis of gene expression program controlled by LSD1.

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Analysis of miRNAs in MCF7 cells regulated by LSD1

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LNCaP LSD1 knockdown and SP-2509 treatment ChIP-seq data

Project description:LSD1 (also known as KDM1A) is a histone demethylase and a key regulator of gene expression in embryonic stem cells and cancer.1,2 LSD1 was initially identified as a transcriptional repressor via its demethylation of active histone H3 marks (di-methyl lysine 4 [2MK4]).1 In prostate cancer, specifically, LSD1 also co-localizes with the AR and demethylates repressive 2MK9 histone marks from androgen-responsive AR target genes, facilitating androgen-mediated induction of AR-regulated gene expression and androgen-induced proliferation in androgen-dependent cancers. We report here that the LSD1 protein is universally upregulated in human CRPC and promotes survival of CRPC cell lines. This effect is explained in part by LSD1-induced activation of cell cycle and embryonic stem cell gene setsâgene sets enriched in transcriptomal studies of lethal human tumors. Importantly, despite the fact that many of these genes are direct LSD1 targets, we did not observe histone methylation changes at the LSD1-bound regions, demonstrating non-canonical histone demethylation-independent mechanisms of gene regulation. This ChIP-seq dataset included H3K4me2 and H3K9me2 ChIP-seq data for siRNA target against LSD1 and non-targeting control, as well as SP2509 inhibition of LSD1 and mock treatment 4 conditions: siRNA against LSD1, siRNA against luciferase (non-targeting control); SP2509 inhibition of LSD1, mock treatment. There are 2 replicates per condition.

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Analysis of exosomal miRNAs in MCF7 cells regulated by LSD1

Project description:Lysine specific demethylase 1 (LSD1) is an important histone demethylase that mediates metastasis in luminal breast cancer. Exosomes play a major role in cell-to-cell communication. Thus, the characterization of miRNAs of exosome in MCF7 cells regulated by LSD1 is imperative in clarifying intercellular signaling.

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Analysis of miRNAs in MCF7 cells regulated by LSD1

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Analysis of exosomal miRNAs in MCF7 cells regulated by LSD1

Project description:Analysis of exosomal miRNAs in MCF7 cells regulated by LSD1

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LNCaP LSD1 knockdown and SP-2509 treatment ChIP-seq data

Project description:LSD1 (also known as KDM1A) is a histone demethylase and a key regulator of gene expression in embryonic stem cells and cancer.1,2 LSD1 was initially identified as a transcriptional repressor via its demethylation of active histone H3 marks (di-methyl lysine 4 [2MK4]).1 In prostate cancer, specifically, LSD1 also co-localizes with the AR and demethylates repressive 2MK9 histone marks from androgen-responsive AR target genes, facilitating androgen-mediated induction of AR-regulated gene expression and androgen-induced proliferation in androgen-dependent cancers. We report here that the LSD1 protein is universally upregulated in human CRPC and promotes survival of CRPC cell lines. This effect is explained in part by LSD1-induced activation of cell cycle and embryonic stem cell gene sets—gene sets enriched in transcriptomal studies of lethal human tumors. Importantly, despite the fact that many of these genes are direct LSD1 targets, we did not observe histone methylation changes at the LSD1-bound regions, demonstrating non-canonical histone demethylation-independent mechanisms of gene regulation. This ChIP-seq dataset included H3K4me2 and H3K9me2 ChIP-seq data for siRNA target against LSD1 and non-targeting control, as well as SP2509 inhibition of LSD1 and mock treatment

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