Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PTPMT1 is critical for both expansion and differentiation of activated CD8 T cells

ABSTRACT: PTPMT1 is critical for both expansion and differentiation of activated CD8 T cells

PROVIDER: PRJNA894154 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22028430_1.fastq.gz	Fastqsanger.gz
	SRR22028430_2.fastq.gz	Fastqsanger.gz
	SRR22028431_1.fastq.gz	Fastqsanger.gz
	SRR22028431_2.fastq.gz	Fastqsanger.gz
	SRR22028432_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

PTPMT1 is critical for both expansion and differentiation of activated CD8 T cells

Project description:To understand the function of PTPMT1 in CD8 T cells responses, we characterized the transcriptomes of activated CD8+ T cells from PTPMT1 wildtype and knockout mice

2023-11-21 | GSE216523 | GEO

Pharmacological targeting of the mitochondrial phosphatase PTPMT1 sensitizes hepatocellular carcinoma to ferroptosis

Project description:Protein tyrosine phosphatase mitochondrial 1 (PTPMT1), is a member of the protein tyrosine phosphatase superfamily localized on the mitochondrial inner membrane, and regulates the biosynthesis of cardiolipin. Given the important position of PTPMT1 in mitochondrial function and metabolism, pharmacological targeting of PTPMT1 is considered a promising manner in disease treatments. In this study, we mainly investigated the role of PTPMT1 in hepatocellular carcinoma (HCC) ferroptosis, a new type of cell death accompanied by significant iron accumulation and lipid peroxidation. Herein, the pharmacological inhibition of PTPMT1 was induced by alexidine dihydrochloride (AD, a dibiguanide compound).

2025-05-07 | PXD058606 | Pride

Effect of PTPMT1 deficiency on regulatory T cells

Project description:CD4 T cells were isolated from Wt and PTPMT1 DT mice. Cells were activated in vitro and differentiated into regulatory T cells for 4 days. At this time point WT and KO cells were harvested and analysed by proteomics.

2026-03-25 | GSE288709 | GEO

PTPMT1-dependent regulatory T cells mediate immunological tolerance to gut pathobionts

Project description:Mitochondrial dysfunctions are emerging as key drivers of gut inflammation, colitis, and IBD, yet their role in regulating immune tolerance remains unclear. Meanwhile, pathobiont infections, such as those caused by Helicobacter species, affect nearly half the global population, with symptoms manifesting in only 20%, adding a new layer of complexity. The genetic and environmental factors that disrupt gut tolerogenic mechanisms, tipping the balance toward disease in symptomatic infections, are not fully understood. Here, we show that PTPMT1 impairs tolerance to Helicobacter via Treg cells, independently from T cell-generated Type I or Type II interferons. Without cardiolipin, Treg cells lose metabolic fitness and immunosuppressive potential, unleashing pro-inflammatory myeloid cells in the gut. As a result, PTPMT1 ΔT mice are highly vulnerable to pathobiont infections even without microbiome imbalance. Inflammation and helper T cell imbalance are conserved in Barth syndrome, linked to cardiolipin deficiency from TAFAZZIN mutations. Overall, we propose that T cell-specific PTPMT1 governs the balance between tolerance and inflammation in the gut, dictating outcomes in pathobiont infections.

2026-04-01 | GSE288641 | GEO

Proteomic dataset of Wt, PTPMT1 KO, CHOP KO and PTPMT1 CHOP double KO regulatory T cells

Project description:Mitochondrial defects are emerging as key drivers of gut inflammation, colitis, and IBD. Yet, their role in regulating immune tolerance, fine-tuned by helper T cells, is unclear. Understanding how metabolic changes in T cells impact gut tolerogenic mechanisms, including gut colonization and the balance between tolerance and disease, remains, therefore, a critical challenge. Here, we show that cardiolipin deficiency impairs tolerance to Helicobacter due to loss of regulatory T (Treg) cell function. Without cardiolipin, Treg cells lose metabolic fitness and immunosuppressive capacity igniting inflammation, particularly in the gut. Hence, mice with a T cell-specific deletion of the enzyme PTPMT1, essential for cardiolipin synthesis, are highly vulnerable to pathobiont infections even without microbiome imbalance. Notably, patients affected by Barth syndrome, a genetic disease characterized by severe cardiolipin deficiency, also exhibit inflammation and helper T cell imbalance. Overall, we found that cardiolipin in T cells preserves gut-immune homeostasis, dictating outcomes in pathobiont infections.

2026-04-14 | PXD071483 | Pride

Gene expression profile at Ptpmt1 cardiomyocytes-specific Knockout mcie, Eif2a mutant mice, Gcn2 Knockout mice, and Hri Knockout mice

Project description:To study the mitochondrial stress response HRI-eIF2a-ATF4 signaling pathway in mitochondrial cardiomyopathy , we generated Ptpmt1 cardiomyocytes-specific Knockout mcie, Eif2a mutant mcie, Gcn2 Knockout mcie, and Hri Knockout mcie

2022-04-21 | GSE201042 | GEO

Effect of PTPMT1 deficiency on regulatory T cells

Project description:Effect of PTPMT1 deficiency on regulatory T cells

| PRJNA1219111 | ENA

Proteomic dataset of Wt and PTPMT1 KO regulatory T cells

2026-04-14 | PXD060518 | Pride

PTPMT1-dependent regulatory T cells mediate immunological tolerance to gut pathobionts

Project description:PTPMT1-dependent regulatory T cells mediate immunological tolerance to gut pathobionts

| PRJNA1218772 | ENA

TRNP1 regulates expansion and folding of the mammalian cerebral cortex by control of radial glial fate

Project description:Evolution of the mammalian brain encompassed a remarkable increase in size of cerebral cortex, including tangential and radial expansion, but the mechanisms underlying these key parameters are still largely unknown. Here, we identified the novel DNA associated protein TRNP1 as a regulator of cerebral cortical expansion in both these dimensions. Gain and loss of function experiments in the mouse cerebral cortex in vivo demonstrate that high Trnp1 levels promote neural stem cell self-renewal and tangential expansion, while lower levels promote radial expansion resulting in a potent increase in the generation of intermediate progenitors and outer radial glial cells resulting in folding of the otherwise smooth murine cerebral cortex. Remarkably, TRNP1 expression levels exhibit regional differences also in the cerebral cortex of human fetuses anticipating radial or tangential expansion respectively. Thus, the dynamic regulation of TRNP1 is critical to regulate tangential and radial expansion of the cerebral cortex in mammals. We performed gene expression microarray analysis on embryonic mouse cerebral cortex derived from Trnp1 knockdown and control animals.

2013-04-26 | E-GEOD-40582 | biostudies-arrayexpress

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