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Transcriptome analysis of activated CD4+ T cells deficient for Zfp36 or Zfp36l1

ABSTRACT: Transcriptome analysis of activated CD4+ T cells deficient for Zfp36 or Zfp36l1

PROVIDER: PRJNA885048 | ENA |

REPOSITORIES: ENA

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Transcriptome analysis of activated CD4+ T cells deficient for Zfp36 or Zfp36l1

Project description:Characterisation of the effects on the transcriptome of deleting the Zfp36 or Zfp36l1 genes in activated CD4+ T cells

2022-10-01 | GSE214350 | GEO

Multiomics analysis couples mRNA turnover and translational control of glutamine metabolism to the differentiation of the activated CD4+ T cell

Project description:The ZFP36 family of RNA-binding proteins acts post-transcriptionally to repress translation and promote RNA decay. Studies of genes and pathways regulated by the ZFP36 family in CD4+ T cells have focussed largely on cytokines, but their impact on metabolic reprogramming and differentiation is unclear. Using CD4+ T cells lacking Zfp36 and Zfp36l1, we combined the quantification of mRNA transcription, stability, abundance and translation with crosslinking immunoprecipitation and metabolic profiling to determine how they regulate T cell metabolism and differentiation. Our results suggest that ZFP36 and ZFP36L1 act directly to limit the expression of genes driving anabolic processes by two distinct routes: by targeting transcription factors and by targeting transcripts encoding rate-limiting enzymes. These enzymes span numerous metabolic pathways including glycolysis, one-carbon metabolism and glutaminolysis. Direct binding and repression of transcripts encoding glutamine transporter SLC38A2 correlated with increased cellular glutamine content in ZFP36/ZFP36L1-deficient T cells. Increased conversion of glutamine to α-ketoglutarate in these cells was consistent with direct binding of ZFP36/ZFP36L1 to Gls (encoding glutaminase) and Glud1 (encoding glutamate dehydrogenase). We propose that ZFP36 and ZFP36L1 as well as glutamine and α-ketoglutarate are limiting factors for the acquisition of the cytotoxic CD4+ T cell fate. Our data implicate ZFP36 and ZFP36L1 in limiting glutamine anaplerosis and differentiation of activated CD4+ T cells, likely mediated by direct binding to transcripts of critical genes that drive these processes.

2021-04-28 | GSE155087 | GEO

Transcriptome of ZFP36L1-sufficient and ZFP36L1-deficient Fo B cells

Project description:High-throughput sequencing analysis of transcriptome from LPS-activated B cells from Lymph node of Zfp36l1(fl/fl) and Zfp36l1(fl/fl) x Cd79a(Cre/+) mice

2020-11-20 | GSE146073 | GEO

Transcriptome of ZFP36L1-sufficient and ZFP36L1-deficient Fo B cells

Project description:Transcriptome of ZFP36L1-sufficient and ZFP36L1-deficient Fo B cells

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The effect of ZFP36L1 deficiency on gene expression in the U2OS osteosarcoma cancer cell line

Project description:Post-transcriptional regulation of gene expression by RNA binding proteins (RBPs), one of the major classes of proteins encoded by the human genome, is well established. ZFP36L1 and its protein family members, ZFP36 and ZFP36L2, function as RBPs that primarily regulate gene expression at the post-transcriptional level by binding to adenine uridine (AU) rich elements (AREs) in the 3′ untranslated region (3′UTR) of certain mRNAs and mediating ARE-dependent mRNA decay. In this study, using CRISPR/Cas9 ZFP36L1 gene-editing, we generated ZFP36L1 deficient U2OS cellular models. The aim of the RNASeq experiment was to compare the gene expression profile in wild-type U2OS cells compared to ZFP36L1 deficient U2OS cells. Loss of functional ZFP36L1 leads to widespread changes in gene expression that are associated with dysregulation of KRAS signalling.

2024-06-04 | GSE268088 | GEO

Zfp36l1 overexpression/knockdown effect on primary mouse articular chondrocytes

Project description:Gene expression profiling of primary mouse articular chondrocyte infected with recombinant adenovirus expressing mouse ZFP36 Ring Finger Protein Like 1(Zfp36l1) or recombinant adenovirus expressing mouse small hairpin RNA of Zfp36l1. In this study, we have attempted to explore the effects of Zfp36l1 gene overexpression or knockdown on mouse transcriptome and have identified numerous genes which are involved in osteoarthritis pathogenesis.

2018-02-14 | GSE110581 | GEO

ZFP36L1

Project description:ZFP36L1

| PRJNA834739 | ENA

Effect of restoring endogenous ZFP36L1 expression in CORL47 SCLC Cells that are CRISPR activated for ZFP36L1 (sgZFP36L1-1 and sgZFP36L1-2) or a non-targeting sgRNA (sgControl)

Project description:To investigate the impact of restoring endogenous ZFP36L1 expression in CORL47 SCLC Cells on neuroendocrine cell state We performed RNA-sequencing on CORL47 SCLC Cells that are CRISPR activated for ZFP36L1 (sgZFP36L1-1 and sgZFP36L1-2) or a non-targeting sgRNA (sgControl)

2022-05-06 | GSE202114 | GEO

RNAseq of naive CD4 T cells deficient for Elp3 activated for 18h against WT control

Project description:CD4 T cell deficient for the Elp3 gene have a delayed cell cycle entry. We explored by RNAseq by which molecular pathway the absence of Elp3 delayed the cell cycle entry. Naive T cell from CD4-cre Elp3 fl/fl mice and WT littermate were purified and activated in vitro with CD3 and CD28 antibodies for 18h.

2020-07-31 | E-MTAB-9057 | biostudies-arrayexpress

RNAseq profiling of miR-132/212-deficient CD4+ T cells activated in vitro and in vivo.

Project description:Transcriptomic profiling of miR-132/212-deficient and WT CD4 T cells isolated from spleens of L donovani infected mice (d28) to determine the effects of miR-132/212 on CD4 T cell activation in vivo. This was combined by transcriptomic analysis of early stage in vitro activated WT and miR-132/212-deficient CD4 T cells to identify direct miR-132/212 targets in CD4 T cells.

2019-03-22 | GSE125268 | GEO

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