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Effect of deletion of UTX expression in NY8.3 progenitor CD8+ T cells

ABSTRACT: Effect of deletion of UTX expression in NY8.3 progenitor CD8+ T cells

PROVIDER: PRJNA1187616 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31385515_1.fastq.gz	Fastqsanger.gz
	SRR31385515_2.fastq.gz	Fastqsanger.gz
	SRR31385516_1.fastq.gz	Fastqsanger.gz
	SRR31385516_2.fastq.gz	Fastqsanger.gz
	SRR31385517_1.fastq.gz	Fastqsanger.gz

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Effect of deletion of UTX expression in NY8.3 progenitor CD8+ T cells

Project description:Type 1 diabetes (T1D) is a chronic autoimmune disease resulting from the destruction of insulin-producing beta cells. This persistence is due to the continual replenishment of short-live effector CD8+ T cells (autoimmune mediators, Tmed) in the pancreatic lymph nodes (pLNs) by a long-lived reservoir of stem-like memory CD8+ T cells (autoimmune progenitors, Tprog). We are investigating an epigenetic regulator UTX playing the role in Tprog to Tmed conversion. The NOD mice with T cell-specific UTX deficiency (UTXTCD mice) were protected from T1D. In addition, the deletion of UTX in CD8+ T cells resulted in the accumulation of Tprog and loss of Tmed populations in pLNs. The function of UTX is to demethylate the histone mark, H3K27 tri-methylation, leading to the open chromatin accessibility for gene expression. ATAC-seq and RNA-seq of antigen specific Tprog cells revealed a role of UTX in closing chromatin at progenitor gene loci while enforcing accessibility at effector gene loci. Taken together, these findings point to the potential of targeting UTX-mediated conversion of Tprog into Tmed for interrupting the T1D autoimmune response.

2024-11-25 | GSE282227 | GEO

Utx interactome in mouse myeloid progenitor cells

Project description:Immunoprecipitation of Utx followed by mass spectrometry analysis to identify Utx binding partners in mouse myeloid progenitor cells.

2018-04-30 | PXD005011 | Pride

Analysis of gene expression sigunature in Utx KO CD8 T cells

Project description:To elucidate the effect of Utx, histone demethylase, on CD8 Tcell diferentiation, The gene expression were measured in WT and Utx KO CD8 T cells.

2023-07-12 | GSE214673 | GEO

UTX constrains antiviral CD8+ T cell responses during chronic virus infection

Project description:Persistent virus infections can cause pathogenesis that is debilitating or lethal. During these infections, virus-specific T cells fail to protect due to weakened antiviral activity or failure to persist. These outcomes are governed epigenetically, though it is unknown which enzymes contribute to T cell loss or impaired function over time. Here, we show that T cell receptor-stimulated CD8+ T cells increase their expression of UTX (Ubiquitously transcribed Tetratricopeptide repeat, X-chromosome), an enzyme involved in demethylating histone-3 lysine-27 (H3K27), and reduce genome-wide H3K27-me3. UTX limits the frequency and durability of virus-specific CD8+ T cells during chronic lymphocytic choriomeningitis virus (LCMV) infection in mice by promoting inhibitory receptor expression and apoptosis. UTX also increases effector gene expression to improve CTL-mediated protection, a process corresponding to reduced H3K27me3 at effector gene bodies. Thus, UTX guides gene expression patterns in CD8+ T cells, promoting antiviral activity while reducing CD8+ T cell durability.

2021-02-09 | GSE143736 | GEO

Utx

Project description:Drosophila melanogaster Utx, Utx histone demethylase, is differentially expressed in 12 experiment(s);

| FBgn0260749 | ExpressionAtlas

Utx

Project description:Drosophila melanogaster Utx, Utx histone demethylase, is expressed in 3 baseline experiment(s);

| FBgn0260749 | ExpressionAtlas

Deletion of UTX, a histone demethylase interacting with MLL2, in three patients with Kabuki syndrome.

Project description:Kabuki syndrome (KS) is a rare multiple congenital anomalies/mental retardation (MCA/MR) syndrome described in 19811,2. In 2010, exome sequencing identified MLL2 mutations in patients with KS3. Since then, 5 studies identified a mutation in MLL2 in 56-75,6% of KS patients3-7. Here, we describe 2 KS and 1 KS-like patient with a de novo partial or complete deletion of UTX, a histone demethylase interacting with MLL2 in gene regulation. UTX locates on the X chromosome and we showed that the X chromosome with the deleted copy of UTX is preferentially inactivated despite the fact that UTX escapes X-inactivation. This study unveiled deletion of UTX as a second cause of KS and highlights the growing role of histone methylase/demethylase in MCA/MR syndrome. Two patients were analysed by Agilent array CGH 244K (AMADID: 014693) Three patients DNA were analyzed by CGH on custom targeted array 44K (AMADID: 032482). Two of them were initially analyzed using 244K Whole genome Arrays (AMADID: 014693). One third patient was selected given suspicion of deletion in one of the targeted gene (KDM6A) as amplification of some exons performed in our lab to sequence this gene failed.

2012-01-01 | E-GEOD-32567 | biostudies-arrayexpress

Deletion of UTX, a histone demethylase interacting with MLL2, in three patients with Kabuki syndrome.

2012-01-01 | GSE32567 | GEO

Gene expression profiling in mature OT-II TCR transgenic CD4 SP thymocytes, either Jmjd3- and Utx-deficient or -sufficient.

Project description:The biological functions of histone demethylases Jmjd3 and Utx remain poorly understood. We assessed such functions in developing T cells, using conditional (CD4-Cre-mediated) gene disruption, by inactivating Kdm6a and Kdm6b, respectively encoding Utx and Jmjd3, in immature CD4+CD8+ thymocytes. We compared microarray gene expression in mature (Va2hi CD24lo) mutant and wild-type CD4+CD8- thymocytes carrying the OT-II TCR transgene. We show that Jmjd3 and Utx redundantly promote H3K27Me3 removal at, and expression of, a specific subset of genes involved in terminal thymocyte differentiation, especially S1pr1, encoding a sphingosine-phosphate receptor required for thymocyte egress. Mature (Va2hi CD24lo) CD4 thymocytes were sorted from freshly prepared single-cell suspensions OT-II TCR transgenic thymocytes deficient for Utx and Jmjd3 (dKO, CD4-Cre conditional deletion of floxed Kdm6a and Kdm6b alleles), and from Cre-negative controls (wild-type). Total RNA was extracted from sorted thymocytes using the RNeasy Plus Mini Kit (Qiagen) and processed for microarray analyses (Affymetrix Mouse Exon 1.0 ST array) at the NCI microarray facility, following the manufacturer’s recommendation. Data is generated from 3 replicates from each experiment.

2015-09-17 | E-GEOD-70363 | biostudies-arrayexpress

JMJD3 and UTX Determine Fidelity and Lineage Specification of Human Neural Progenitor Cells [UTX ChIP]

Project description:JMJD3 and UTX Determine Fidelity and Lineage Specification of Human Neural Progenitor Cells [UTX ChIP]

| PRJNA550392 | ENA