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Acetate promotes T cell effector function during glucose restriction [ATAC-seq]

ABSTRACT: Acetate promotes T cell effector function during glucose restriction [ATAC-seq]

PROVIDER: PRJNA528258 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8756570_1.fastq.gz	Fastqsanger.gz
	SRR8756570_2.fastq.gz	Fastqsanger.gz
	SRR8756571_1.fastq.gz	Fastqsanger.gz
	SRR8756571_2.fastq.gz	Fastqsanger.gz
	SRR8756572_1.fastq.gz	Fastqsanger.gz

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Acetate promotes T cell effector function during glucose restriction

Project description:Acetate promotes T cell effector function during glucose restriction

| PRJNA528253 | ENA

Acetate promotes T cell effector function during glucose restriction [ATAC-seq]

Project description:Competition for nutrients like glucose can metabolically restrict T cells and contribute to their hyporesponsiveness during cancer. Metabolic adaptation to the surrounding microenvironment is therefore key for maintaining appropriate cell function. For instance, cancer cells use acetate as a substrate alternative to glucose to fuel metabolism and growth. Here we show that acetate rescued effector function in glucose-restricted CD8+ T cells. Mechanistically, acetate promoted histone acetylation and chromatin accessibility, and enhanced IFN-γ gene transcription and cytokine production in an acetyl-CoA synthetase (ACSS)-dependent manner. Ex vivo acetate treatment increased IFN-γ production by exhausted T cells, while reducing ACSS expression in T cells impaired IFN-γ production by tumor-infiltrating lymphocytes and tumor clearance. Thus, hyporesponsive T cells can be epigenetically remodeled and reactivated by acetate, suggesting that pathways regulating the use of substrates alternative to glucose could be therapeutically targeted to promote T cell function during cancer.

2019-05-14 | GSE128592 | GEO

Acetate promotes T cell effector function during glucose restriction [ChIP-seq]

Project description:Acetate promotes T cell effector function during glucose restriction [ChIP-seq]

| PRJNA528256 | ENA

Acetate promotes T cell effector function during glucose restriction [RNA-seq]

Project description:Acetate promotes T cell effector function during glucose restriction [RNA-seq]

| PRJNA528257 | ENA

Acetate promotes T cell effector function during glucose restriction [ChIP-seq]

2019-05-14 | GSE128593 | GEO

Acetate promotes T cell effector function during glucose restriction [RNA-seq]

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RNA-sequencing analysis of glucose and acetate regulated transcripts in glioblastoma cells

Project description:Our studies indicate that glucose and acetate can regulate histone acetylation by altering the acetyl-CoA concentrations in the cell. The purpose of this study was to to determine whether specific gene sets correlated with acetyl-CoA availability. We conclude that 10% of glucose-regulated genes are acetyl-CoA regulated genes (genes suppressed or induced by low glucose and reversed by acetate). Acetate usually regulated gene expression in the same direction as glucose, suggesting that acetyl-CoA is a key mediator of glucose-dependent gene expression.

2014-08-05 | GSE57488 | GEO

RNA sequencing of E. coli NCM3722 over the course of glucose to acetate growth transition

Project description:To understand the gene response during the glucose to acetate diauxic transition, we grew E. coli in minimal media with acetate and a small amount of glucose. Cells were collected and RNA was purified at different time points during the growth transition, including pre-shift (growth on glucose), 5 minutes, 15 minutes, 60 minutes and 120 minutes after glucose run-out, and steady state growth on acetate (post-shift).

2021-10-09 | GSE185426 | GEO

Acetate Promotes T Cell Effector Function during Glucose Restriction.

Project description:Competition for nutrients like glucose can metabolically restrict T cells and contribute to their hyporesponsiveness during cancer. Metabolic adaptation to the surrounding microenvironment is therefore key for maintaining appropriate cell function. For instance, cancer cells use acetate as a substrate alternative to glucose to fuel metabolism and growth. Here, we show that acetate rescues effector function in glucose-restricted CD8+ T cells. Mechanistically, acetate promotes histone acetylation and chromatin accessibility and enhances IFN-γ gene transcription and cytokine production in an acetyl-CoA synthetase (ACSS)-dependent manner. Ex vivo acetate treatment increases IFN-γ production by exhausted T cells, whereas reducing ACSS expression in T cells impairs IFN-γ production by tumor-infiltrating lymphocytes and tumor clearance. Thus, hyporesponsive T cells can be epigenetically remodeled and reactivated by acetate, suggesting that pathways regulating the use of substrates alternative to glucose could be therapeutically targeted to promote T cell function during cancer.

| S-EPMC6544383 | biostudies-literature

RNA-sequencing analysis of glucose and acetate regulated transcripts in glioblastoma cells

2014-08-05 | E-GEOD-57488 | biostudies-arrayexpress