Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A Treg specific long non-coding RNA maintains immune-metabolic homeostasis in ageing liver

ABSTRACT: A Treg specific long non-coding RNA maintains immune-metabolic homeostasis in ageing liver

PROVIDER: PRJNA947156 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

A Treg specific long non-coding RNA maintains immune-metabolic homeostasis in ageing liver [Young Treg]

Project description:A Treg specific long non-coding RNA maintains immune-metabolic homeostasis in ageing liver [Young Treg]

| PRJNA954301 | ENA

PARK7/DJ-1 promotes pyruvate dehydrogenase activity and maintains Treg homeostasis during ageing

Project description:PARK7/DJ-1 promotes pyruvate dehydrogenase activity and maintains Treg homeostasis during ageing

| PRJNA474438 | ENA

A Treg specific long non-coding RNA maintains immune-metabolic homeostasis in ageing liver [Altre-WT and Altre-KO]

Project description:A Treg specific long non-coding RNA maintains immune-metabolic homeostasis in ageing liver [Altre-WT and Altre-KO]

| PRJNA947081 | ENA

A Treg specific long non-coding RNA maintains immune-metabolic homeostasis in ageing liver [Naive T cells, Th17 and Tregs]

Project description:A Treg specific long non-coding RNA maintains immune-metabolic homeostasis in ageing liver [Naive T cells, Th17 and Tregs]

| PRJNA947159 | ENA

PARK7/DJ-1 promotes pyruvate dehydrogenase activity and maintains Treg homeostasis during ageing

Project description:Pyruvate dehydrogenase (PDH) is the gatekeeper enzyme of the tricarboxylic acid (TCA) cycle. Here we show that the deglycase DJ-1 (encoded by PARK7, a key familial Parkinson's disease gene) is a pacemaker regulating PDH activity in CD4+ regulatory T cells (Treg cells). DJ-1 binds to PDHE1-β (PDHB), inhibiting phosphorylation of PDHE1-α (PDHA), thus promoting PDH activity and oxidative phosphorylation (OXPHOS). Park7 (Dj-1) deletion impairs Treg survival starting in young mice and reduces Treg homeostatic proliferation and cellularity only in aged mice. This leads to increased severity in aged mice during the remission of experimental autoimmune encephalomyelitis (EAE). Dj-1 deletion also compromises differentiation of inducible Treg cells especially in aged mice, and the impairment occurs via regulation of PDHB. These findings provide unforeseen insight into the complicated regulatory machinery of the PDH complex. As Treg homeostasis is dysregulated in many complex diseases, the DJ-1-PDHB axis represents a potential target to maintain or re-establish Treg homeostasis.

2022-04-19 | GSE115269 | GEO

A Treg specific long non-coding RNA maintains immune-metabolic homeostasis in ageing liver

Project description:To find specific transcription factors (TFs) interact with Altre to regulate target gene expression by Cis- or Trans- action on chromatin.

2023-05-18 | PXD041040 | Pride

H2R signaling maintains neutrophil homeostasis

Project description:H2R signaling maintains neutrophil homeostasis

| PRJNA683590 | ENA

KMT2D maintains Treg homeostasis and protects against inflammatory diseases by regulating the purinergic channel P2X7

Project description:Regulatory T (Treg) cells are essential for maintaining immune homeostasis and tolerance through the prevention of inflammatory and autoimmune responses. The histone methyltransferase KMT2D is indispensable for induced Treg (iTreg) cell differentiation, its role in the differentiation and function of Treg cells in vivo has remained largely unknown. Here, we demonstrate that KMT2D is critical for the differentiation and function of effector activated Treg (aTreg) cells. We found that KMT2D deficiency in Treg cells impairs aTreg generation and exacerbates inflammatory conditions, such as allergic airway inflammation and colitis. Mechanistically, KMT2D regulates aTreg differentiation through TCR signaling. Furthermore, KMT2D modulates Ca2+ influx by promoting the expression of purinergic receptor P2X7 through H3K4me3 deposition. Collectively, our fundings highlight a pivotal role for KMT2D in Treg cell homeostasis and function, potentially offering a new therapeutic strategy for treating inflammatory diseases.

2026-01-16 | GSE316150 | GEO

Stem cell competition orchestrates skin homeostasis and ageing

Project description:Stem cells underlie tissue homeostasis, but their dynamics during ageing—and the relevance of these dynamics to organ ageing—remain unknown. Here we report that the expression of the hemidesmosome component collagen XVII (COL17A1) by epidermal stem cells fluctuates physiologically through genomic/oxidative stress-induced proteolysis, and that the resulting differential expression of COL17A1 in individual stem cells generates a driving force for cell competition. In vivo clonal analysis in mice and in vitro 3D modelling show that clones that express high levels of COL17A1, which divide symmetrically, outcompete and eliminate adjacent stressed clones that express low levels of COL17A1, which divide asymmetrically. Stem cells with higher potential or quality are thus selected for homeostasis, but their eventual loss of COL17A1 limits their competition, thereby causing ageing. The resultant hemidesmosome fragility and stem cell delamination deplete adjacent melanocytes and fibroblasts to promote skin ageing. Conversely, the forced maintenance of COL17A1 rescues skin organ ageing, thereby indicating potential angles for anti-ageing therapeutic intervention.

2019-04-05 | GSE111825 | GEO

KMT2D maintains Treg homeostasis and protects against inflammatory diseases by regulating the purinergic channel P2X7

Project description:KMT2D maintains Treg homeostasis and protects against inflammatory diseases by regulating the purinergic channel P2X7

| PRJNA1401737 | ENA