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Next Generation Sequencing analysis using splenic cells freshly isolated from Wild Type-OT-I (WT) and OTUB1-CD4Cre-OT-I (KO) mice

ABSTRACT: Next Generation Sequencing analysis using splenic cells freshly isolated from Wild Type-OT-I (WT) and OTUB1-CD4Cre-OT-I (KO) mice

PROVIDER: PRJNA523247 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8592470_1.fastq.gz	Fastqsanger.gz
	SRR8592470_2.fastq.gz	Fastqsanger.gz
	SRR8592471_1.fastq.gz	Fastqsanger.gz
	SRR8592471_2.fastq.gz	Fastqsanger.gz
	SRR8592472_1.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing analysis using splenic cells freshly isolated from Wild Type-OT-I (WT) and OTUB1-CD4Cre-OT-I (KO) mice

Project description:CD8 T cells play a central role in immune responses against pathogens and cancer; however, CD8 T cells are typically rendered hypofunctional in tumor microenvironment due to tolerance to cancer cells and functional exhaustion. How to overcome CD8 T cell tolerance and stimulate strong antitumor responses has become an important issue for cancer immunotherapy 1,2. Here we identified the atypical deubiquitinase Otub1 as a pivotal regulator of CD8 T cell self-tolerance and antigen-stimulated responses. T cell-specific deletion of Otub1 in mice breaks CD8 T cell self-tolerance and promotes the metabolic reprograming and effector functions of activated CD8 T cells, resulting in profoundly stronger immunity against infections and tumorigenesis. The Otub1 deletion also synergizes with an immune checkpoint inhibitor in inducing tumor rejection and greatly increases the efficiency of an adoptive T cell transfer model of cancer immunotherapy. In line with these findings, the expression level of Otub1 is inversely associated with the abundance of CD8 effector T cell signature gene expression and patient survival in human melanoma. Mechanistically, Otub1 negatively regulates activation of AKT, a kinase that integrates the T cell receptor (TCR) and cytokine signals and mediates CD8 T cell metabolism and effector functions. Otub1 deficiency greatly promotes AKT activation by both the TCR signal and the immunostimulatory cytokine IL-15. Otub1 inhibits AKT ubiquitination and, thereby, suppresses its interaction with the membrane lipid phosphoinositol 3,4,5 triphosphate required for membrane translocation. These results demonstrate a ubiquitin-dependent mechanism that controls CD8 T cell responses and implicate Otub1 as a potential therapeutic target for cancer immunotherapy.

2019-05-16 | GSE126777 | GEO

Next Generation Sequencing analysis using splenic CD8 T cells isolated from Wild Type-OT-I (WT) and NIK -CD4Cre-OT-I (KO) mice

Project description:Next Generation Sequencing analysis using splenic CD8 T cells isolated from Wild Type-OT-I (WT) and NIK -CD4Cre-OT-I (KO) mice

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The deubiquitylase Otub1 regulates the chemotactic response in splenic B cells by modulating the stability of the g-subunit Gng2

Project description:The ubiquitin (Ub) proteasome system (UPS) performs the covalent attachment of lysine 48-linked poly-Ub chains to substrate proteins, thereby targeting them for degradation, while deubiquitylating enzymes (DUBs) reverse this process. This post-translational modification system regulates many processes in the innate and adaptive immune system. Here we show that loss of one of the most highly expressed DUBs, Otub1, results in changes in splenic B cell subsets, leading to a significant increase in marginal zone and transitional B cells and a decrease in follicular B cells. We demonstrate that Otub1 interacts with and modulates the ubiquitylation status of the heterotrimeric G-protein g-subunit Gng2, thereby regulating Gng2 stability. Proximal mapping of Gng2 revealed an enrichment in partners associated with cell migration and chemokine signaling. Indeed, Otub1-deficient B cells exhibited sustained chemokine receptor signaling and increased chemokine responsiveness towards Cxcl12, Cxcl13 and S1P in vitro, which manifested in vivo as a defect in the localization of splenic B cells. Together, our data establishes Otub1 as a novel regulator of G-protein coupled receptor signaling (GPCR) in B cells, altering their positioning and differentiation.

2023-02-08 | MSV000091229 | MassIVE

RNA sequencing data of OTUB1-knockdown in PDGF-BB-treated HASMCs

Project description:We report the high-throughput RNA sequencing on human aortic smooth muscle cells (HASMCs) transfected with siRNA targeting OTUB1 (si-OTUB1) or control siRNA (si-NC). Cells were treated with PDGF-BB for 48 hours.

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RNA sequencing of naïve, Th1 and Th2 polarised live CD4+ T cells from CD4Cre+ and CD4Cre+DOT1LFL/FL mice

Project description:RNA sequencing of naïve, Th1 and Th2 polarised live CD4+ T cells from CD4Cre+ and CD4Cre+DOT1LFL/FL mice

2020-12-15 | GSE123966 | GEO

Deubiquitinase OTUB1 regulates doxorubicin-induced cardiotoxicity

Project description:Wild-type (WT) and Otub1-heterozygously knock-out mice were applied in the study. Doxorubicin (DOX)-induced subacute cardiotoxicity mouse model was established by 6 intraperitoneal injections during a 2-week period. The differentially expressed genes were analyzed by RNA-sequencing and clustering analyses.

2024-08-16 | GSE240959 | GEO

OTUB1 catalytic-independently deubiquitinates TGFBI and mediates the angiogenesis in infantile hemangioma by regulating glycolysis

Project description:To investigate the role of Ubiquitination in the progression of infantile hemangioma. And to investigate the role of OTUB1 in infantile hemangioma

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Project description:Desulfosporosinus sp. OT genome sequencing

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Comparison of gene transcription in Ly49G versus Ly49I positive splenic NK cells

Project description:We report RNA seq of mature, freshly isolated splenic NK cells sorted for the expression of Ly49G or Ly49I.

2017-03-08 | GSE83153 | GEO

Deubiquitinase OTUB1 regulates doxorubicin-induced cardiotoxicity

Project description:Deubiquitinase OTUB1 regulates doxorubicin-induced cardiotoxicity

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