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Regnase-1 suppresses TCF-1+ precursor exhausted T cell formation to limit CAR T cell responses against ALL [Microarray Expression]

ABSTRACT: Regnase-1 suppresses TCF-1+ precursor exhausted T cell formation to limit CAR T cell responses against ALL [Microarray Expression]

PROVIDER: PRJNA647751 | ENA |

REPOSITORIES: ENA

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Regnase-1 suppresses TCF-1+ precursor exhausted T cell formation to limit CAR T cell responses against ALL

Project description:Regnase-1 suppresses TCF-1+ precursor exhausted T cell formation to limit CAR T cell responses against ALL

| PRJNA648158 | ENA

Regnase-1 suppresses TCF-1+ precursor exhausted T cell formation to limit CAR T cell responses against ALL [WGBS]

Project description:Regnase-1 suppresses TCF-1+ precursor exhausted T cell formation to limit CAR T cell responses against ALL [WGBS]

| PRJNA719647 | ENA

Regnase-1 suppresses TCF-1+ precursor exhausted T cell formation to limit CAR T cell responses against ALL [WGBS]

Project description:Defciency of Regnase-1 enhances CAR-T cell persistence and anti-tumor ability

2021-07-21 | GSE171442 | GEO

Regnase-1 suppresses TCF-1+ precursor exhausted T cell formation to limit CAR T cell responses against ALL [Microarray Expression]

Project description:transcriptional profiling was performed on WT and KO CAR T cells isolated 7 days after co-transfer into mice with or without tumors. Regnase-1 KO CAR T cells undergoing a tumor-dependent shift from an effector to memory-like phenotype

2021-07-08 | GSE154859 | GEO

Regnase-1 suppresses TCF-1+ precursor exhausted T-cell formation to limit CAR-T-cell responses against ALL.

Project description: Not available

| S-EPMC8288655 | biostudies-literature

Improved persistence and expanded TPEX formation in Regnase-1 KO CAR T cells is TCF-1-dependent

Project description:transcriptional profiling was performed on Regnase-1 KO CAR and Regnase-1 TCF-1 DKO CAR T cells isolated 7days after co-transfer into tumor bearing mice. TCF-1 deficiency in Regnase-1 KO CAR T cells led to reduced long-term persistence and memory-like phenotype.

2021-04-07 | GSE155020 | GEO

Regnase-1 suppresses TCF-1+ precursor exhausted T cell formation to limit CAR T cell responses against ALL

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-04-07 | GSE155021 | GEO

Single-cell RNA-seq of human breast tumor samples with exhausted and non-exhausted immune environments

Project description:Fresh human breast tumor tissue was dissociated into single cells and viably frozen. Patient samples were annotated as having an ""exhausted"" or ""non-exhausted"" immune environment based on CyTOF characterization of T cell phenotypes (Wagner et al, Cell 2019). 14 samples (7 exhausted, 7 non-exhausted) were selected for scRNA-seq (without prior cell type enrichment) with the goal to compare the two immune environment types and to comprehensively characterize exhaustion-associated features of the tumor microenvironment.

2023-08-25 | E-MTAB-10607 | biostudies-arrayexpress

Effect of loss of Regnase-1 and Regnase-3 on the transcriptional profile in mouse Lin–Sca1+Kit+ (LSK) cells

Project description:Regulation of lineage biases in hematopoietic stem and progenitor cells (HSPCs) is pivotal for balanced hematopoietic output. However, little is known about the mechanism behind lineage choice in HSPCs. Here, we show that mRNA decay factors Regnase-1 (Zc3h12a) and Regnase-3 (Zc3h12c) are critical for induction of myeloid lineage priming, restricting lymphoid differentiation in HSPCs. Regnase-1- and Regnase-3-mediated control of mRNA encoding Nfkbiz, a transcriptional and epigenetic regulator, was essential for balancing lymphoid/myeloid lineage output in HSPCs in vivo. Furthermore, single cell-assay for transposase-accessible chromatin sequencing (scATAC-seq) analysis revealed that Regnase-1 and Regnase-3 control the epigenetic landscape on myeloid-related gene loci in hematopoietic stem cells (HSCs) via Nfkbiz. Consistently, an antisense oligonucleotide designed to inhibit Regnase-1- and Regnase-3-mediated Nfkbiz mRNA degradation primed HSCs toward myeloid lineages by enhancing Nfkbiz expression. Collectively, the collaboration between post-transcriptional control and chromatin remodeling by the Regnase-1/Regnase-3-Nfkbiz axis governs lineage priming, instructing HSC lineage specification.

2024-02-09 | GSE228923 | GEO

Effect of Regnase-2/MCPIP2/ZC3H12B overexpression in human glioblastoma U-251 MG cell line.

Project description:Regnase-2/MCPIP2/ZC3H12B is a protein belonging to the ZC3H12 protein family. There are three other proteins of this family present in humans of which Regnase-1/MCPIP1/ZC3H12A is the founder member as well as the best-described protein. All proteins of this family contain a NYN domain with endoribonuclease activity and a CCCH-type zinc finger responsible for interaction with substrate RNA. Although the NYN domain has a high degree of similarity across all four members the in vitro RNase activity was shown only for two of them, namely Regnase-1 and Regnase-3. Interestingly the ZC3H12 family proteins have unique expression patterns with Regnase-2 being expressed almost solely in the central nervous system. What is more, Regnase-2 is downregulated in human glioblastoma, and its expression is inversely correlated with tumor grade. To decipher the role of Regnase-2 in human glioblastoma we performed RNA sequencing of U-251 MG cells overexpressing Regnase-2 and control, mock-transfected cells.

2024-01-24 | GSE248634 | GEO

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