Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: The Effect of Asparagine Deprivation on CD8+ T Cell Activation

PROVIDER: PRJNA1219535 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR32238517_1.fastq.gz	Fastqsanger.gz
	SRR32238517_2.fastq.gz	Fastqsanger.gz
	SRR32238518_1.fastq.gz	Fastqsanger.gz
	SRR32238518_2.fastq.gz	Fastqsanger.gz
	SRR32238519_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Project description:Effects of Asparagine Deprivation on CD8+ T Cell Activation

| PRJNA1219369 | ENA

Asparagine availability controlsgerminal centre B cell homeostasis

Project description:Germinal centre (GC) B cells proliferate at some of the highest rates of any mammalian cell. Yet the metabolic processes which enable this are poorly understood. We performed integrated metabolomic and transcriptomic profiling of GC B cells, and found that asparagine metabolism is highly upregulated. Asparagine is conditionally essential to B cells, and its synthetic enzyme, asparagine synthetase (ASNS) is markedly upregulated following their activation, through the integrated stress response sensor general control non-derepressible 2 (GCN2). When Asns is deleted, B cell survival in low asparagine conditions is severely impaired. Using stable isotope tracing, we found that metabolic adaptation to the absence of asparagine requires ASNS, and that the synthesis of nucleotides is particularly sensitive to asparagine deprivation. Conditional deletion of Asns in B cells selectively impairs GC formation, associated with a reduction in RNA synthesis rates. Finally, removal of environmental asparagine by asparaginase was found to also severely compromise the GC reaction.

2024-04-03 | GSE228845 | GEO

Human CD8 T cell IL2 deprivation time course

Project description:IL2 deprivation time course for day 8 human CD8 T cells activated for 3 days with TransAct T-cell activation beads. PBMC (Cambridge Bio) were defrosted and CD8+ T-cells isolated using a human CD8+ T-cell isolation kit. CD8+ T-cells were activated at 1 x 106 cells/mL with 1 in 100 TransAct T-cell activation beads (Miltenyi) and 20 ng/mL IL-2 in complete RMPI (RMPI 1640, 10% FBS, penicillin/streptomycin) for three days. Cells were then washed out of activation and then maintained in complete RMPI with 20 ng/mL IL-2 for five days. To remove IL-2 for IL-2 deprivation, cells were washed twice in pre-warmed media, then replated in complete media without IL-2. Cells were deprived of IL-2 for 1hr, 3hrs, 5hrs, 8hrs, 24hrs or 48hrs.

2024-10-10 | PXD056475 | Pride

Oncogenic KRAS mediates amino acid metabolism during nutrient stress via regulation of NRF2 and ATF4 in NSCLC [shKRAS low Q]

Project description:Glutamine is a key nutrient for tumor cells that supports nucleotide and amino acid biosynthesis, replenishes the TCA cycle intermediates and contributes to redox metabolism. We identified oncogenic KRAS as a critical regulator of the response to glutamine deprivation in NSCLC. Full activation of the ATF4 stress response pathway is dependent on expression of NRF2 downstream of oncogenic KRAS in NSCLC. Through this mechanism, KRAS alters amino acid uptake and metabolism and sustains mTORC1 signaling during nutrient stress. Furthermore, we identified regulation of asparagine synthetase (ASNS) as a key effect of oncogenic KRAS signaling via ATF4 during glutamine deprivation, and a potential therapeutic target in KRAS mutant NSCLC.

2017-12-30 | GSE81643 | GEO

Oncogenic KRAS mediates amino acid metabolism during nutrient stress via regulation of NRF2 and ATF4 in NSCLC [shKRAS high Q]

2017-12-30 | GSE81642 | GEO

Oncogenic KRAS mediates amino acid metabolism during nutrient stress via regulation of NRF2 and ATF4 in NSCLC [low versus high Q]

2017-12-30 | GSE81641 | GEO

Asparagine availability controls B cell homeostasis

Project description:Study of the effects of asparagine deprivation on germinal centre B cells.

2025-03-21 | GSE277338 | GEO

Molecular effects of ISRIB during asparagine deprivation

Project description:Molecular effects of ISRIB during asparagine deprivation

| PRJNA521363 | ENA

Chromatin accessibility profiling by ATAC-seq in LNCaP-shNT and LNCaP-shTP53 cells

Project description:The TP53 tumor suppressor is frequently altered in lethal, castration-resistant prostate cancer (CRPC). However, to date there are no effective treatments that specifically target TP53 alterations. Using transcriptomic and metabolomic analyses, we show here that TP53-altered prostate cancer (PCa) exhibits an increased dependency on asparagine and overexpresses asparagine synthetase (ASNS, the enzyme catalyzing the synthesis of asparagine). Mechanistically, loss/mutation of TP53 transcriptionally activate ASNS expression, directly as well as via ATF4, driving de novo asparagine biosynthesis to support CRPC growth. TP53-altered CRPC cells are sensitive to asparagine restriction by knockdown of ASNS and L-asparaginase treatment to deplete the intracellular and extracellular sources of asparagine respectively. This effect was rescued by asparagine addition. Notably, pharmacological inhibition of intracellular asparagine biosynthesis using a glutaminase (GLS) inhibitor and depletion of extracellular asparagine with L-asparaginase significantly reduced asparagine production and effectively impaired CRPC growth. This study highlights the significance of ASNS-mediated metabolic adaptation as a synthetic vulnerability in CRPC with TP53 alterations, providing a rationale for co-targeting intracellular and extracellular asparagine production to treat these lethal prostate cancers.

2024-02-29 | GSE255000 | GEO

Transcriptional regulators of the amino acid response pathway in leukemia

Project description:CRISPR/Cas9-based genetic screening revealed ZBTB1 as a critical mediator of the response of T-ALL cells to asparagine deprivation. ZBTB1 regulates the transcription of ASNS, a transcriptional target of ATF4. Loss of ZBTB1 results in decreased transcription and expression of ASNS. ChIP-Sequencing reveals that both ATF4 and ZBTB1 enrich in the promoter of ASNS. This dataset contains the RNA-Seq, ChIP-Seq and ATAC-Seq data on three different cell lines (WT Jurkat cells, ZBTB1 knockout Jurkat cells and ZBTB1 knockout Jurkat cells expressing ZBTB1 cDNA) in support of these findings.

2020-03-31 | GSE145783 | GEO

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