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Thioredoxin-interacting protein is essential for memory T cell formation via the regulation of the redox metabolism

ABSTRACT: Thioredoxin-interacting protein is essential for memory T cell formation via the regulation of the redox metabolism

PROVIDER: PRJNA913845 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22810100.fastq.gz	Fastqsanger.gz
	SRR22810101.fastq.gz	Fastqsanger.gz
	SRR22810102.fastq.gz	Fastqsanger.gz
	SRR22810103.fastq.gz	Fastqsanger.gz
	SRR22810104.fastq.gz	Fastqsanger.gz

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Similar Datasets

Thioredoxin-interacting protein is essential for memory T cell formation via the regulation of the redox metabolism

Project description:CD4+ memory T cells are central to long-lasting protective immunity and are involved in shaping the pathophysiology of chronic inflammation. While metabolic reprogramming is critical for the generation of memory T cells, the mechanisms controlling the redox metabolism in memory T cell formation remain unclear. We found that reactive oxygen species (ROS) metabolism changed dramatically in T helper-2 (Th2) cells during the contraction phase in the process of memory T cell formation. Thioredoxin-interacting protein (Txnip), a regulator of oxidoreductase, regulated apoptosis by scavenging ROS via the nuclear factor erythroid 2-related factor 2 (Nrf2)-biliverdin reductase B (Blvrb) pathway. Txnip regulated the pathology of chronic airway inflammation in the lung by controlling the generation of allergen-specific pathogenic memory Th2 cells in vivo. Thus, the Txnip-Nrf2-Blvrb axis directs ROS metabolic reprogramming in Th2 cells and is a potential therapeutic target for intractable chronic inflammatory diseases.

2022-12-23 | GSE221291 | GEO

Thioredoxin-interacting protein is essential for memory T cell formation via the regulation of the redox metabolism.

| S-EPMC9926250 | biostudies-literature

Deletion of thioredoxin reductase disrupts redox homeostasis and impairs β-cell function

Project description:Reactive oxygen species (ROS) have been implicated as mediators of pancreatic β-cell damage. While β-cells are thought to be vulnerable to oxidative damage, we have shown, using inhibitors and acute depletions, that thioredoxin reductase, thioredoxin, and peroxiredoxins are the primary mediators of antioxidant defense in β-cells. However, the role of this antioxidant cycle in maintaining redox homeostasis and β-cell survival in vivo remains unclear. Here, we generated mice with a β-cell specific knockout of thioredoxin reductase 1 (Txnrd1.fl/fl; Ins1.Cre/+, βKO). Despite blunted glucose-stimulated insulin secretion, knockout mice maintain normal whole body glucose homeostasis. Unlike pancreatic islets with acute Txnrd1 inhibition, βKO islets do not demonstrate increased sensitivity to continuous ROS. RNA-sequencing analysis revealed that Txnrd1-deficient β-cells have increased expression of Nuclear factor erythroid 2-related factor 2 (Nrf2)-regulated genes, and altered expression of genes involved in heme and glutathione metabolism, suggesting an adaptive response. Txnrd1-deficient β-cells also have decreased expression of factors controlling β-cell function and identity which may explain the mild functional impairment. Together, these results suggest that Txnrd1-knockout β-cells compensate for loss of this essential antioxidant pathway by increasing expression of Nrf2-regulated antioxidant genes, allowing for protection from excess ROS at the expense of normal β-cell function and identity.

2022-07-05 | GSE200965 | GEO

Deletion of thioredoxin reductase disrupts redox homeostasis and impairs β-cell function

Project description:Deletion of thioredoxin reductase disrupts redox homeostasis and impairs β-cell function

| PRJNA827778 | ENA

Effects of redox modulation by inhibition of Thioredoxin reductase on radiosensitivity and gene expression

Project description:The involvement the thioredoxin system in radiation resistance was investigated in human lung cancer cells by a combination of ionizing radiation and specific thioredoxin reductase-inhibition by a phosphine gold compound. Gene expression profiles (Human Gene 1.0 ST) of lung cancer cells subjected to ionizing radiation and/or inhibition of thioredoxin reductase were studied. Data analyses were performed using the Affymetrix GeneChip Operating Software (GCOS) Version 1.4.

2010-12-03 | E-GEOD-25814 | biostudies-arrayexpress

Effects of redox modulation by inhibition of Thioredoxin reductase on radiosensitivity and gene expression

2010-12-03 | GSE25814 | GEO

Transcription profiling of Arabidopsis thioredoxin reductase knock-out mutant

Project description:Transcriptomic study of a thioredoxin reductase knock-out mutant. Biological question : Thioredoxins are small redox proteins implicated in crucial pathways of cell life. They are reduced by a conserved flavoprotein named NADPH-dependent thioredoxin reductase (NTR). In order to give an insight into the functions of the NTR/thioredoxin pathway in Arabidopsis, we have used a reverse genetic approch. Both NTR genes (NTRA and NTRB) have been inactivated in the double ntra ntrb mutant. T-DNA lines have been provided by the SALK library. Surprisingly, this mutant shows a limited phenotype suggested that some additional redox pathways are involved in compensating the inactivation of the NTR/thioredoxin pathway. In order to isolate compensatory genes that would be transcriptionally induced in the ntra ntrb mutant, we have performed this CATMA project. Seeds of the wild-type Col-0 ecotype and of the ntra ntrb homozygote double mutant were sowed in soil. Three replicates of lines were made (Col-0 1, 2 and 3 ntra ntrb 1, 2 and 3) : plants were put at different places of the greenhouse and grown at different times. Germination was synchronized by 4 days at 4C and plants were grown during 17 days, until they reached a 6 rosette leaves stage. Entire plants (30 plants per sample) were harvested, frozen in liquid nitrogen and stored at -80C until extraction.

2005-09-15 | E-MEXP-365 | biostudies-arrayexpress

Expression of thioredoxin-interacting protein (TXNIP) during megakaryopoiesis is indispensable for platelet biogenesis

Project description:Expression of thioredoxin-interacting protein (TXNIP) during megakaryopoiesis is indispensable for platelet biogenesis

| PRJNA773739 | ENA

Expression of thioredoxin-interacting protein (TXNIP) during megakaryopoiesis is indispensable for platelet biogenesis

Project description:Thioredoxin-interacting protein (TXNIP) is ubiquitously expressed in blood cells, including hematopoietic stem cells (HSCs), monocytes, and platelets. Here we report a novel finding that TXNIP plays a crucial role in megakaryopoiesis and platelet biogenesis via interacting with GATA1, a transcription factor for megakaryocyte-erythroid differentiation. Txnip-/- mice displayed immature megakaryocytes in the bone marrow with thrombocytopenia, which had gotten worse as the mice aged. Transcriptome analysis revealed that the transcriptional activity of GATA1 was significantly enhanced in the Txnip-/- megakaryocyte precursors (MkPs) than wild type (WT) cells. During megakaryopoiesis in ex vivo, Txnip-/- MkPs remained small in cell size with less mitochondrial mass, and more glycolysis for ATP production, as opposed to the normal megakaryocyte maturation. The effects of TXNIP in megakaryocytes were recapitulated in human cord blood CD34+ HSC-derived differentiation. Taken together, this study demonstrates the importance of spatiotemporal expression of TXNIP in platelet biogenesis. We propose for the first time that TXNIP might play a critical role in determining a lineage between megakaryocytes and erythroid cells from a common megakaryocyte-erythroid progenitor via regulation of transcriptional activity of GATA1.

2022-12-31 | GSE186400 | GEO

ntr-Transcriptomic study of a thioredoxin reductase knock-out mutant.

Project description:rs04-02_ntr - ntr - Thioredoxins are small redox proteins implicated in crucial pathways of cell life. They are reduced by a conserved flavoprotein named NADPH-dependent thioredoxin reductase (NTR). In order to give an insight into the functions of the NTR/thioredoxin pathway in Arabidopsis, we have used a reverse genetic approch. Both NTR genes (NTRA and NTRB) have been inactivated in the double ntra ntrb mutant. T-DNA lines have been provided by the SALK library. Surprisingly, this mutant shows a limited phenotype suggested that some additional redox pathways are involved in compensating the inactivation of the NTR/thioredoxin pathway. In order to isolate compensatory genes that would be transcriptionally induced in the ntra ntrb mutant, we have performed this CATMA project. - Comparison of the transcript profile of the ntra ntrb knock-out mutant vs Col-0 wild-type ecotype. Seeds of the wild-type Col-0 ecotype and of the ntra ntrb homozygote double mutant were sowed in soil. Three replicates of lines were made (Col-0 1, 2 and 3 ntra ntrb 1, 2 and 3) : plants were put at different places of the greenhouse and grown at different times. Germination was synchronized by 4 days at 4degreeC and plants were grown during 17 days, until they reached a 6 rosette leaves stage. Entire plants (30 plants per sample) were harvested, frozen in liquid nitrogen and stored at 80degreeC until extraction. Keywords: gene knock out,wt vs mutant comparison 3 dye-swap - CATMA arrays

2007-06-19 | E-GEOD-7998 | biostudies-arrayexpress

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