Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Non-oxidative pentose phosphate pathway controls regulatory T cell function by integrating metabolism and epigenetics

ABSTRACT: Non-oxidative pentose phosphate pathway controls regulatory T cell function by integrating metabolism and epigenetics

PROVIDER: PRJNA817804 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18362963.fastq.gz	Fastqsanger.gz
	SRR18362964.fastq.gz	Fastqsanger.gz
	SRR18362965.fastq.gz	Fastqsanger.gz
	SRR18362966.fastq.gz	Fastqsanger.gz
	SRR18362967.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Non-oxidative pentose phosphate pathway controls regulatory T cell function by integrating metabolism and epigenetics

Project description:Regulatory T cells (Tregs) are critical for maintaining immune homeostasis and preventing autoimmunity. Here, we show that the non-oxidative pentose phosphate pathway (PPP) regulates Treg function to prevent autoimmunity. Deletion of transketolase (TKT), an indispensable enzyme of non-oxidative PPP, in Tregs causes a fatal autoimmune disease in mice, with impaired Treg suppressive capability despite regular Treg numbers and normal Foxp3 expression levels. Mechanistically, reduced glycolysis and enhanced oxidative stress induced by TKT deficiency triggers excessive fatty acid and amino acid catabolism, resulting in uncontrolled oxidative phosphorylation and impaired mitochondrial fitness. Reduced -KG levels as a result of reductive TCA cycle activity leads to DNA hypermethylation, thereby limiting functional gene expression and suppressive activity of TKT-deficient Tregs. We also find that TKT levels are frequently downregulated in Tregs of patients with autoimmune disorders. Our study identifies the non-oxidative PPP as an integrator of metabolic and epigenetic processes that control Treg function.

2022-03-31 | GSE198995 | GEO

Control of regulatory T cell function by the non-oxidative pentose phosphate pathway [ATAC-seq]

Project description:Non-oxidative pentose phosphate pathway (PPP) is a crucial gatekeeper of glucose catabolism in metabolic tissues. However, its role in regulatory T cells (Tregs) remains unknown. Here we report deleting transketolase (TKT), an indispensable enzyme of non-oxidative PPP, in Tregs caused a fatal auto-immune disease in mice. TKT deletion impaired suppressive capability without disturbing Treg cell number. Mechanistically, TKT deficiency caused Treg metabolic remodeling with decreased glucose catabolism, activated fatty acid and amino acid catabolism and uncontrolled oxidative phosphorylation. Moreover, excessive ammonia from deregulated amino acid catabolism impaired mitochondrial fitness while reduced α-ketoglutarate/succinate ratio led to DNA hypermethylation, limiting functional gene expression and suppressive activity of TKT-deficient Tregs. Therefore, our study identifies non-oxidative PPP as a new pathway for controlling Treg function.

2022-03-31 | GSE172047 | GEO

Control of regulatory T cell function by the non-oxidative pentose phosphate pathway [RNA-Seq]

2022-03-31 | GSE171675 | GEO

Control of regulatory T cell function by the non-oxidative pentose phosphate pathway

Project description:Control of regulatory T cell function by the non-oxidative pentose phosphate pathway

| PRJNA721880 | ENA

Anaerobic fermentative metabolism of Corynebacterium glutamicum is hampered by a functional oxidative pentose phosphate pathway

Project description:Anaerobic fermentative metabolism of Corynebacterium glutamicum is hampered by a functional oxidative pentose phosphate pathway

| PRJNA602423 | ENA

Control of regulatory T cell function by the non-oxidative pentose phosphate pathway [ATAC-seq]

Project description:Control of regulatory T cell function by the non-oxidative pentose phosphate pathway [ATAC-seq]

| PRJNA721882 | ENA

Control of regulatory T cell function by the non-oxidative pentose phosphate pathway [RNA-Seq]

Project description:Control of regulatory T cell function by the non-oxidative pentose phosphate pathway [RNA-Seq]

| PRJNA720550 | ENA

High concentration of prolactin induce oxidative stress in ovine ovarian GCs by the pentose phosphate pathway through regulating the ROS and mitophagy pathways

Project description:High concentration of prolactin induce oxidative stress in ovine ovarian GCs by the pentose phosphate pathway through regulating the ROS and mitophagy pathways.

2022-10-23 | PXD037645 |

Progesterone increases metabolism via the pentose phosphate pathway in bovine uterine epithelial cells

Project description:During early pregnancy, glucose is essential for the uterine epithelium and the developing embryo. In cows, studies have shown that progesterone increases the secretion of glucose into the uterine lumen. Nevertheless, how progesterone affects glucose metabolism in the uterine epithelium has been sparsely investigated. Therefore, our objective was to investigate how progesterone influences glucose metabolism in immortalized bovine uterine epithelial (BUTE) cells. Progesterone treatment (10 μM) increased glucose consumption. To gain a more global picture of the effects of progesterone, RNAseq was performed after BUTE cells were treated with vehicle (DMSO) or 10 μM for 24 hours. KEGG analysis indicated that progesterone altered genes associated with metabolic pathways and glutathione metabolism. Manually examining genes unique to specific glucose metabolic pathways identified an increase in the rate-limiting enzyme in the pentose phosphate pathway—glucose-6-phosphate dehydrogenase. Functionally, a major product of the pentose phosphate pathway is NADPH, and progesterone treatment increased NADPH concentrations in BUTE cells. In cows, immunohistochemistry confirmed that glucose-6-phosphate dehydrogenase levels were higher in the uterine epithelium in the luteal phase when progesterone concentrations are high. In conclusion, progesterone increased glucose-6-phosphate dehydrogenase expression and metabolism via the pentose phosphate pathway in the bovine uterine epithelium. This metabolism could provide substrates for cell proliferation, molecules to be secreted into the uterine lumen that supports embryonic development, or maintain reduction/oxidation balance in the uterine epithelium.

2024-10-09 | GSE269076 | GEO

The Pentose Phosphate Pathway in pathogenic Francisella

Project description:Metabolic pathways are now considered as intrinsic virulence attributes of pathogenic bacteria and hence represent potential targets for anti-bacterial strategies. Here, we addressed the role of the pentose phosphate pathway (PPP) and its connections with other metabolic pathways in the pathophysiology of Francisella novicida. We have previously shown that this intracellular bacterial pathogen used gluconeogenesis to metabolize host-derived nutrients in the cytosolic compartment of infected macrophages. Francisella species, which lacks the oxidative branch of the PPP, are equipped with all the genes of the non-oxidative branch (i.e. tktA, tal, rpiA and rpe, encoding transketolase, transaldolase, ribose-phosphate isomerase and ribulose phosphate epimerase, respectively). The involvement of the PPP in the early stage of intracellular life cycle of F. novicida was first demonstrated with the study of PPP inactivation mutants. Indeed, inactivation of tktA, rpiA or rpe genes, severely impaired intramacrophagic multiplication during the first 24–hours. However, time-lapse video microscopy demonstrated that rpiA and rpe mutants were able to resume late intracellular bacterial multiplication. To get further insight into the links between the PPP and other metabolic networks of the bacterium, we next performed a thorough proteo-metabolomic analysis of these mutants. We show that the PPP constitutes a major bacterial metabolic hub with multiple connections with glycolysis, tricarboxylic acid cycle and other metabolic pathways, such as fatty acid degradation and sulfur metabolism. Hence, our study highlights how, by its multiple connections with other metabolic pathways, PPP is instrumental to Francisella pathogenesis and growth in its intracellular niche.

2021-07-27 | PXD023550 | 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