Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [IEC bulk RNA-seq]

ABSTRACT: Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [IEC bulk RNA-seq]

PROVIDER: PRJNA1220150 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR32258800_1.fastq.gz	Fastqsanger.gz
	SRR32258800_2.fastq.gz	Fastqsanger.gz
	SRR32258801_1.fastq.gz	Fastqsanger.gz
	SRR32258801_2.fastq.gz	Fastqsanger.gz
	SRR32258802_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [IEC bulk RNA-seq]

Project description:Necrotizing enterocolitis (NEC) is a prevalent pediatric emergency characterized by the sudden onset of intestinal ischemia and necrosis resulting from hyperinflammation.The interactions between the bile acid receptor FXR with gut microbiota and mucosal immunity in early postnatal life, and its exact role in the pathogenesis of NEC, are unknown.Here we analyze the role of FXR in IECs under NEC.

2025-02-06 | GSE288979 | GEO

Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [SI bulk RNA-seq]

2025-02-02 | GSE288274 | GEO

Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [ILC3s bulk RNA-seq]

2025-02-06 | GSE288754 | GEO

Blocking NKp46-CCR6-ILC3 autophagy alleviates necrotizing enterocolitis by restoring energy metabolism balance [RNA-seq]

Project description:Group 3 innate lymphoid cells (ILC3s) play a crucial role in intestinal inflammatory disorders such as necrotizing enterocolitis (NEC) in neonates; however, the mechanisms by which ILC3s contribute to NEC remain unclear. In this study, single-cell transcriptomics, in vivo experiments on T cell-deficient mice, and targeted cell interventions demonstrated that NKp46−CCR6− (double-negative, DN) ILC3 autophagy significantly impacts NEC development by regulating intracellular metabolism. Mice lacking ATG5 or treated with autophagy inhibitors exhibited reduced ILC3 abundance and impaired ILC3 function, alleviating NEC. Mechanistically, ATG5 deficiency enhanced fatty acid metabolism while reducing glycolysis. Conversely, inhibiting fatty acid oxidation or supplementing with lactate restored the quantity and functionality of ATG5-deficient DN ILC3s, exacerbating NEC. Lipid metabolism analyses combined with a mouse model of NEC indicated that phosphatidylcholine supplementation alleviated intestinal inflammation by inhibiting DN ILC3 autophagy. Clinically, patients with NEC showed elevated ILC3 levels and significant enrichment of autophagy genes. These findings highlight the importance of DN ILC3 autophagy in metabolic adaptation, suggesting potential strategies for managing NEC.

2026-04-12 | GSE306398 | GEO

Blocking NKp46-CCR6-ILC3 autophagy alleviates necrotizing enterocolitis by restoring energy metabolism balance [ATAC-Seq]

2026-04-12 | GSE319269 | GEO

Blocking NKp46-CCR6-ILC3 autophagy alleviates necrotizing enterocolitis by restoring energy metabolism balance [scRNA-seq]

2026-04-12 | GSE306522 | GEO

Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [scRNA-seq]

Project description:Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [scRNA-seq]

| PRJNA1219193 | ENA

Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [ILC3s bulk RNA-seq]

Project description:Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [ILC3s bulk RNA-seq]

| PRJNA1219195 | ENA

Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [SI bulk RNA-seq]

Project description:Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [SI bulk RNA-seq]

| PRJNA1216659 | ENA

Blocking NKp46-CCR6-ILC3 autophagy alleviates necrotizing enterocolitis by restoring energy metabolism balance

Project description:<p>Group 3 innate lymphoid cells (ILC3s) play a crucial role in intestinal inflammatory disorders such as necrotizing enterocolitis (NEC) in neonates; however, the mechanisms by which ILC3s contribute to NEC remain unclear. In this study, single-cell transcriptomics, in vivo experiments on T cell-deficient mice, and targeted cell interventions demonstrated that NKp46CCR6 (double-negative, DN) ILC3 autophagy significantly impacts NEC development by regulating intracellular metabolism. Mice lacking ATG5 or treated with autophagy inhibitors exhibited reduced ILC3 abundance and impaired ILC3 function, alleviating NEC. Mechanistically, ATG5 deficiency enhanced fatty acid metabolism while reducing glycolysis. Conversely, inhibiting fatty acid oxidation or supplementing with lactate restored the quantity and functionality of ATG5-deficient DN ILC3s, exacerbating NEC. Lipid metabolism analyses combined with a mouse model of NEC indicated that phosphatidylcholine supplementation alleviated intestinal inflammation by inhibiting DN ILC3 autophagy. Clinically, patients with NEC showed elevated ILC3 levels and significant enrichment of autophagy genes. These findings highlight the importance of DN ILC3 autophagy in metabolic adaptation, suggesting potential strategies for managing NEC.</p>

2026-04-12 | MTBLS12891 | MetaboLights

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