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MessengerRNA-seq of wild type, GLUT3-deficient and ACLY-deficient T helper 17 (Th17) cells

ABSTRACT: messengerRNA-seq of wild type, GLUT3-deficient and ACLY-deficient T helper 17 (Th17) cells

PROVIDER: PRJNA792580 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17335416.fastq.gz	Fastqsanger.gz
	SRR17335417.fastq.gz	Fastqsanger.gz
	SRR17335418.fastq.gz	Fastqsanger.gz
	SRR17335419.fastq.gz	Fastqsanger.gz
	SRR17335420.fastq.gz	Fastqsanger.gz

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RNA-seq of wild type and GLUT3-deficient T helper 17 (Th17) cells

Project description:RNA-seq of wild type and GLUT3-deficient T helper 17 (Th17) cells

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Histone H3 K9/14 acetylation of wild type and GLUT3-deficient T helper 17 (Th17) cells

Project description:Histone H3 K9/14 acetylation of wild type and GLUT3-deficient T helper 17 (Th17) cells

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messengerRNA-seq of wild type, GLUT3-deficient and ACLY-deficient T helper 17 (Th17) cells

Project description:messengerRNA-sequencing and analysis of in vitro differentiated Th17 cells isolated from WT, Slc2a3-fl/fl Cd4-cre or Acöy-fl/fl Cd4-cre mice in the presence or absence of 20 mM acetate for 24h.

2022-02-13 | GSE192663 | GEO

RNA-seq of wild type and GLUT3-deficient T helper 17 (Th17) cells

Project description:RNA-sequencing and analysis of in vitro differentiated Th1 and Th17 cells isolated from WT and Slc2a3-fl/fl Cd4-cre mice.

2022-02-13 | GSE192659 | GEO

CIP2A negatively regulates Th17 differentiation

Project description:Interleukin 17 (IL-17) producing T helper 17 (Th17) cells are critical drivers of pathogenesis in a variety of autoimmune and inflammatory diseases. Strategies to mitigate excessive Th17 response thus remain an attractive target for immunotherapies. Here we report that Cancerous Inhibitor of Protein Phosphatase 2A (CIP2A) regulates IL-17 production by Th17 cells in human and mouse. Using CIP2A knock-out (KO) mice and siRNA-mediated CIP2A silencing in human primary CD4+ T cells, we demonstrated that CIP2A silencing results in a significant increase in IL-17 production. Interestingly, CIP2A deficient Th17 cells were characterized by increased strength and duration of STAT3 (Y705) phosphorylation. Genome-wide gene expression profile as well as the p-STAT3 (Y705) interactome of CIP2A deficient Th17 cells identified that CIP2A regulates the strength of the interaction between Acylglycerol kinase (AGK) and STAT3, and thereby, modulates STAT3 phosphorylation as well as expression of IL-17 in Th17 cells. Our results uncover the physiological function of CIP2A in Th17 cells and provides new opportunities for therapeutic intervention in Th17 cell mediated diseases.

2020-05-26 | PXD010612 | Pride

Histone H3 K9/14 acetylation of wild type and GLUT3-deficient T helper 17 (Th17) cells

Project description:Examination of histone acetlytion in Th17 cells

2022-02-13 | GSE193515 | GEO

Expression data by ACLY knockdown

Project description:De novo lipogenesis is activated in most cancers. Several lipogenic enzymes are implicated in oncogenesis and represent potential cancer therapeutic targets. RNA interference-mediated depletion of ATP citrate lyase (ACLY), the enzyme that catalyzes the first step of de novo lipogenesis, leads to growth suppression in a subset of human cancer cells. Here we demonstrate the molecular basis and potential biomarkers for ACLY-targeting therapy. First, suppression of cancer cell growth by ACLY depletion involves down-regulation of fatty acid elongase ELOVL6 at the transcriptional level. Lipid profiling revealed that ACLY depletion alters fatty acid composition in triglyceride; increased palmitate and decreased longer fatty acids, in accordance with ELOVL6 down-regulation. Second, ACLY depletion increases reactive oxygen species (ROS), whereas addition of antioxidant reduces ROS and attenuates the growth suppression. Third, ACLY depletion or ROS stimulation induce phosphorylation of AMP-activated protein kinase (AMPK), a sensor of energy and lipid metabolism. Analysis of various cancer cell lines revealed that the levels of AMPK phosphorylation (p-AMPK) correlate with the basal ROS levels, and that cancer cells with low basal p-AMPK (i.e., low basal ROS) levels are highly susceptible to ACLY depletion-mediated growth suppression. Finally, in clinical colon cancer tissues, p-AMPK levels are significantly decreased in aggressive tumors and correlate with the levels of 8-hydroxydeoxyguanosine, a hallmark of ROS stimulation. Together, these data suggest that ACLY inhibition suppresses cancer growth via palmitate-mediated lipotoxicity, and p-AMPK could be a predictive biomarker for its therapeutic outcome. Two cell lines are treated with ACLY siRNA. The samples include controls of each cell line.

2014-04-13 | E-GEOD-37243 | biostudies-arrayexpress

The AP-1 Transcription Factor JunB Is Required for Th17 Cell Differentiation

Project description:Interleukin (IL)-17-producing T helper (Th17) cells are crucial for host defense against extracellular microbes and pathogenesis of autoimmune diseases. Here we show that the AP-1 transcription factor JunB is required for Th17 cell development. Junb-deficient CD4+ T cells are able to develop in vitro into various helper T subsets except Th17. The RNA-seq transcriptome analysis reveals that JunB is crucial for the Th17-specific gene expression program. Junb-deficient mice are completely resistant to experimental autoimmune encephalomyelitis, a Th17-mediated inflammatory disease, and naive T helper cells from such mice fail to differentiate into Th17 cells. JunB appears to activate Th17 signature genes by forming a heterodimer with BATF, another AP-1 factor essential for Th17 differentiation. The mechanism whereby JunB controls Th17 cell development likely involves activation of the genes for the Th17 lineage-specifying orphan receptors RORt and ROR and reduced expression of Foxp3, a transcription factor known to antagonize RORt function.

2018-02-15 | GSE98242 | GEO

Mouse gene expression in wild-type Th17 cells and Pten deficient Th17 cells

Project description:Transcriptional profiling of mouse Th17 cells comparing WT Th17 cells with Pten-deficient Th17 cells. Naïve CD4 T cells from each mice were cultured Th17 polarizing condition for 3 days. Goal was to determine the effects of Pten on global gene expression.

2017-08-10 | GSE102414 | GEO

Compare gene expression profiles of TCR transgenic CD4+ T helper type 1 (Th1) vs. type 17 (Th17) cells optimally stimulated by antigen and differentiated under Th1 or Th17 conditions.

Project description:The comparison of Th1 vs. Th17 cell expression profile has been plagued by 1) rarely use of physiologically relevant antigen-driven T helper cell differentiation; and 2) cell lineage tracking system to enrich highly pure Th subsets. We began our attempt to produce large numbers of antigen-specific T helper subsets for expression profiling, when Foxp3GFP knockin mice were first made by our laboratory in 2005. We crossed this line with syngeneic TEa TCR transgenic mice in C57BL/6 background, and use FACS to sort optimally stimulated, highly pure GFP(Foxp3)-negative populations for Th1 vs. Th17 expression profile comparison.

2019-03-15 | E-MTAB-7661 | biostudies-arrayexpress

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