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Genome binding/occupancy profiling of Smad4 in Th17 cells cultured at 37°C and 39.5°C after 24 hours.

ABSTRACT: Genome binding/occupancy profiling of Smad4 in Th17 cells cultured at 37°C and 39.5°C after 24 hours.

PROVIDER: PRJNA515714 | ENA |

REPOSITORIES: ENA

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Genome binding/occupancy profiling of Smad4 in Th17 cells cultured at 37°C and 39.5°C after 24 hours.

Project description:Smad4 was required for febrile temperature enhanced Th17 differentiation. In order to further understand the mechanisms whereby Smad4 enhance Th17 differentiation, we conducted ChIP-seq analysis of Smad4 in Th17 cells cutured 37°C and 39.5°C after 24 hours.

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Global gene expression profile of wild type and Smad4-deficient Th17 cells cultured at 37°C and 39.5°C

Project description:Febrile temperature enhanced Th17 differentiation in Smad4 SUMOylation-dependent manner. Smad4-deficiency impaired the febrile temperature-enhanced Th17 differentiation. In order to understand how febrile temperature and Smad4 contribute to Th17 pathogenicity, we conducted transcriptional analysis of wild type and Smad4-deficient Th17 cells cultured at 37°C and 39.5°C (Day 3).

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Project description:ChIP-Seq of Smad4 in Th17 cells cultured at 37°C and 39.5°C and RNA-Seq of wild type and Smad4-deficient Th17 cells cultured at 37°C and 39.5°C

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2017-10-26 | PXD007172 | Pride

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Transcriptional profiling of THP-1 cells on treatment with LL-37 and nano conjugated LL-37

Project description:Gene expression in THP-1 cells treated for 6 hours with CNT and GNP conjugated with LL-37, LL-37 spiked as well as free LL-37: Reference (Total RNA Mixture of all samples) vs. treated cells

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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

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