Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MRNA-seq analysis of mouse cytotoxic T lymphocytes (CTLs) over-expressing Akt isoforms

ABSTRACT: mRNA-seq analysis of mouse cytotoxic T lymphocytes (CTLs) over-expressing Akt isoforms

PROVIDER: PRJNA634844 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11840704_1.fastq.gz	Fastqsanger.gz
	SRR11840704_2.fastq.gz	Fastqsanger.gz
	SRR11840705_1.fastq.gz	Fastqsanger.gz
	SRR11840705_2.fastq.gz	Fastqsanger.gz
	SRR11840706_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 36

Similar Datasets

mRNA-seq analysis of mouse cytotoxic T lymphocytes (CTLs) over-expressing Akt isoforms

Project description:PI3K/Akt pathway plays a central role in T-cell activation and is impaired in Ag-specific CTLs during chronic viral infections. In this study, we genetically engineered HBV-specific CTLs and adoptively transferred these Akt-expressing viral Ag-specific CTLs into HBV-infected mice and monitored the virological and immunological responses. In the meantime, we also analyzed the mRNA profiles of control-CTLs and CTLs-overexpressing Akt1 and Akt2, respectively before adoptive transfer and after in vitro restimulation. We expect to elucidate the potential mechanisms about how the Akt signaling in CTLs prevents T-cell exhaustion and enhance T-cell expansion in the liver during persistent HBV infection from this mRNA-seq analysis.

2025-01-03 | GSE151131 | GEO

RNA-seq of Cdc42 knockout murine cytotoxic T lymphocytes

Project description:This project explores the effects of Cdc42 gene-knock in effector cytotoxic T lymphocytes (CTLs). Effector CTLs were differentiated from OTI TCR transgenic mice for 5 days in vitro, then nucleofected with CRISPR/Cas9 RNPs targeting Cdc42 or non-targeting sequence.

2025-07-29 | E-MTAB-14519 | biostudies-arrayexpress

Actinomycin D treated cytotoxic T lymphocytes

Project description:Effector cytotoxic T lymphocytes (CTLs) are critical for ridding the body of infected or cancerous cells. Recognition of an antigenic ligand by the CTL’s T cell receptor (TCR) triggers a signalling cascade that ultimately results in the targeted release of cytolytic granules and/or secretion of cytokines and chemokines to alert and recruit additional immune cells. These signalling cascades are capable of initiating transcription, translation, and cytoskeletal rearrangements. While previous work has demonstrated how translation and intracellular reorganisation contribute to CTL effector responses, the role of transcription is less well studied. To address this, we examined the impact of blocking transcription on the CTL proteome during TCR stimulation. These data demonstrated a strong transcriptional requirement for expression of cytokines and chemokines but not cytolytic molecules. Together with functional studies, these data reveal differential molecular control of the cell-cell communication and cytolytic functions of effector CTLs. CTLs exhibit complete and persistent priming for cytolytic activity prior to target cell encounter, but they require de novo transcription to recruit additional immune cells that amplify the response.

2023-10-16 | PXD034920 | Pride

CMV-specific cytotoxic T lymphocytes (CTLs) RNA-seq at the late phase of allo-HCT

Project description:CMV-specific cytotoxic T lymphocytes (CTLs) RNA-seq at the late phase of allo-HCT

| PRJNA657205 | ENA

CMV-specific cytotoxic T lymphocytes (CTLs) RNA-seq at the early phase of allo-HCT

Project description:CMV-specific cytotoxic T lymphocytes (CTLs) RNA-seq at the early phase of allo-HCT

| PRJNA657236 | ENA

RNA-seq of murine cytotoxic T lymphocytes unstimulated and stimulated with anti-CD3 for 10, 20, 40 and 60 minutes

Project description:We wished to examine early transcriptional changes that occur after TCR engagement in CD8+ cytotoxic T lymphocytes (CTLs). To this end, we differentiated effector CTLs from OTI TCR transgenic mice for 7 days in vitro and then stimulated them with anti-CD3 for various times before lysing for RNA-seq. Results demonstrated significant transcriptional changes starting from 20 minutes. After 60 minutes, upregulated genes were most enriched for cytokines and transcriptional machinery.

2023-10-15 | E-MTAB-12083 | biostudies-arrayexpress

Transcriptome analysis of MAZR and/or Runx3-deficient cytotoxic T lymphocytes

Project description:We investigated transcriptional changes in MAZR-, Runx3- and MAZR/Runx3-deficient cytotoxic T lymphocytes (CTLs). This analysis revealed that MAZR plays a compensatory role in the Runx3-dependent transcriptional program of CTL differentiation.

2021-03-11 | GSE129772 | GEO

RNA-seq of murine cytotoxic T lymphocytes in response to myosin IIA inhibition using para-nitroblebbistatin

Project description:This project explores the effects of inhibiting myosin IIA using para-nitroblebbistatin (pNB) on effector cytotoxic T lymphocyte (CTL) activation. Effector CTLs were differentiated from OTI TCR transgenic mice for 7 days in vitro, then stimulated (or not stimulated) with anti-CD3 for 1 hour, treated with either pNB or DMSO control.

2025-09-27 | E-MTAB-14579 | biostudies-arrayexpress

Expression data from control and Phospholipid dependent kinase 1 (PDK1) null cytotoxic T-lymphocytes (CTL) and from control and Akt inhibitor treated CTL

Project description:In cytotoxic T cells (CTL), Protein Kinase B /Akt is activated by the T cell antigen receptor (TCR) and the cytokine Interleukin 2 (IL2), in part by phosophorylation of Akt by Phospholipid dependent kinase 1 (PDK1). The role of PDK1 and Akt in CTL has however not been fully defined. In order to explore the relative roles of these kinases in CTL we used microarrays to profile the gene expression of control and PDK1 null CTL. In separate experiments we compared the gene expression profiles of control and Akt inhibitor treated CTL. CTL were generated from 3 mice each carrying two loxP flanked PDK1 alleles plus a tamoxifen inducible Cre transgene. PDK1 was then deleted from these CTL by tamoxifen treatment and the gene expression pattern determined by microarray. Tamoxifen treated PDK1wt/wt TamoxCre+ CTL generated from 3 PDK1wt/wt TamocCre+ mice were used as a control. In separate experiments CTL were were generated from 3 wild-type mice and then half the CTL generated from each mouse were treated with the Akt inhibitor AktI-1/2. The gene expression patterns of the AktI treated and the untreated CTL were then compared by microarray.

2011-02-01 | E-GEOD-26290 | biostudies-arrayexpress

Doxycycline treated cytotoxic T lymphocytes

Project description:Recent work in immunometabolism has emphasised the role of mitochondria in both the innate and adaptive immune system. Mitochondria are important in T cell development and differentiation, but less is known about their role in CD8+ effector T cells (CTLs). We found that CTLs that lack the mitochondrial deubiquitinase USP30 undergo promiscuous mitophagy, destroying most of the cellular mitochondria. Surprisingly, this results in a markedly diminished killing capacity, while motility, signalling and secretion remain intact. This study uses quantitative DIA proteomics to measure the impact of USP30 deficiency on the global proteome of IL-2 maintained, 4.5 h TCR retriggered and 4.5 h TCR retriggered + cycloheximide CTL. We also measured the impact of pharmacologically inhibiting mitochondrial translation by performing Quantitative DIA proteomics on IL2 maintained or TCR retriggered CTL treated with the mitochondrial translation inhibitor doxycycline for 4.5 hrs. Unexpectedly, inhibition of mitochondrial translation, through genetic or pharmacologic methods, was the mechanism by which CTL killing was impaired. Reduced mitochondrial translation triggered attenuated cytosolic translation which precluded replenishment of secreted effector molecules thereby limiting the capacity of CTLs to serially kill multiple targets. Thus, mitochondria emerge as a previously unappreciated homeostatic regulator of protein translation required for serial CTL killing.

2022-06-09 | PXD026948 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data