Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Nuclear receptor coregulator NRIP1 R448G modulates T cell gut-homing and Teff:Treg balance to control intestinal inflammation [scRNA-seq]

ABSTRACT: Nuclear receptors (NRs) are crucial to integrate metabolite sensing and immune responses in the gut. Nuclear receptor-interacting protein 1 (NRIP1) is an important coregulator of various NRs that has been implicated in inflammatory bowel disease risk, but mechanistic details of how NRIP1 controls NR activities mediating immune homeostasis and inflammation remain elusive. We unveil pleiotropic functions of NRIP1 in distinct CD4+ T cell subsets during intestinal inflammation. We demonstrate that a coding risk variant, NRIP1 R448G, promotes activated CD4+ T cell gut homing and inflammatory cytokine production but impairs regulatory T cell stability, ultimately leading to exacerbated intestinal inflammation. Mechanistically, NRIP1 acts as a corepressor in retinoic acid signaling by modulating VDR (vitamin D receptor) expression and BATF (Basic leucine zipper transcription factor, ATF-like) activity. Our study reveals the impacts of NRIP1 on CD4+ T cells in immune regulation during intestinal inflammation, providing insights into mechanisms by which an NR coregulator controls immune homeostasis and tissue inflammation.

ORGANISM(S): Mus musculus

PROVIDER: GSE236565 | GEO | 2025/09/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Nuclear receptor coregulator NRIP1 R448G modulates T cell gut-homing and Teff:Treg balance to control intestinal inflammation [scATAC-Seq]

Project description:Nuclear receptors (NRs) are crucial to integrate metabolite sensing and immune responses in the gut. Nuclear receptor-interacting protein 1 (NRIP1) is an important coregulator of various NRs that has been implicated in inflammatory bowel disease risk, but mechanistic details of how NRIP1 controls NR activities mediating immune homeostasis and inflammation remain elusive. We unveil pleiotropic functions of NRIP1 in distinct CD4+ T cell subsets during intestinal inflammation. We demonstrate that a coding risk variant, NRIP1 R448G, promotes activated CD4+ T cell gut homing and inflammatory cytokine production but impairs regulatory T cell stability, ultimately leading to exacerbated intestinal inflammation. Mechanistically, NRIP1 acts as a corepressor in retinoic acid signaling by modulating VDR (vitamin D receptor) expression and BATF (Basic leucine zipper transcription factor, ATF-like) activity. Our study reveals the impacts of NRIP1 on CD4+ T cells in immune regulation during intestinal inflammation, providing insights into mechanisms by which an NR coregulator controls immune homeostasis and tissue inflammation.

2025-09-03 | GSE236564 | GEO

Nuclear receptor coregulator NRIP1 R448G modulates T cell gut-homing and Teff:Treg balance to control intestinal inflammation.

Project description:Nuclear receptor coregulator NRIP1 R448G modulates T cell gut-homing and Teff:Treg balance to control intestinal inflammation.

| PRJNA991565 | ENA

Nuclear receptor coregulator NRIP1 R448G modulates T cell gut-homing and Teff:Treg balance to control intestinal inflammation [scATAC-Seq]

Project description:Nuclear receptor coregulator NRIP1 R448G modulates T cell gut-homing and Teff:Treg balance to control intestinal inflammation [scATAC-Seq]

| PRJNA991570 | ENA

Nuclear receptor coregulator NRIP1 R448G modulates T cell gut-homing and Teff:Treg balance to control intestinal inflammation [scRNA-seq]

Project description:Nuclear receptor coregulator NRIP1 R448G modulates T cell gut-homing and Teff:Treg balance to control intestinal inflammation [scRNA-seq]

| PRJNA991571 | ENA

Effect of DC-SCRIPT expression in MCF7 breast cancer cell line

Project description:Breast cancer is one of the most common causes of cancer-related deaths in women. Nuclear receptors (NR) and their regulators are well known for their role in breast cancer. Especially ligands for the type I NRs, Estrogen Receptor (ER) and Progesterone Receptor have growth promoting effects in breast cancer cells. The NR coregulator DC-SCRIPT (ZNF366) has been found to be a strong and independent prognostic marker in ER positive (ESR1) breast cancer patients. DC-SCRIPT modulates the function of multiple NRs and has opposing effects on type I versus type II NRs. It represses the function of the growth promoting type I NRs, whereas it enhances the mainly anti-proliferative type II NRs. In this study we aimed to gain further insight into the functional role of DC-SCRIPT in breast cancer cells. Therefore, the effect of DC-SCRIPT expression on breast cancer cell gene expression was investigated using a novel DC-SCRIPT-inducible MCF7 breast cancer cell line model. In the presence of DC-SCRIPT, multiple cell cycle related genes were differentially expressed, including the tumor suppressor gene CDKN2B.

2015-08-01 | GSE59995 | GEO

Effect of DC-SCRIPT expression in MCF7 breast cancer cell line

2015-08-01 | E-GEOD-59995 | biostudies-arrayexpress

CpG ODN-functionalized gold nanorods for better immune activation and its potential mechanism

Project description:Background: Immune escape in the treatment by functionalized gold nanorods (Au NRs) should not be ignored. Whether CpG ODN, an immune adjuvant, can synergize with Au NRs to activate the immune response and its potential mechanism is not clear. Methods: The expression of CD8+ T cells, macrophage, NK cells, Th17, and Treg was detected by flow cytometry. Expression levels of IL-1, IL-6, IL-17, and TNF-α were assessed by ELISA. Subsequently, transcriptome sequencing analysis was performed to identify DEGs. GO, KEGG and PPI analyses explored the mechanism. The immune activation properties of antibody functionalization-associated Au NR were then compared. Results: Flow cytometry and ELISA analyses indicate that both Au NRs and CpG ODN promote the proliferation of inflammatory factors and immune activation. However, the CpG ODN-coupled Au NRs (Au NRs-C) demonstrated superior immune activation potential. Furthermore, Au NRs stimulate the expression of Treg, while Au NRs-C significantly inhibited this effect. This suggests that the conjugation of CpG ODN with Au NRs not only greatly enhances the immune activation but also compensates for their deficiencies in eliciting immune responses. Transcriptome sequencing uncovered DEGs mainly localized to immune and pro-inflammatory cytokine pathways. PPI analysis identified six hub genes: FOXM1, HMOX1, UBE2C, E2F1, PECAM1, and FCGR3A. Moreover, CpG conjugation with antibody-associated Au NRs enhances immune stimulation. Conclusion: Au NRs-C may upregulate the E2F1 and downregulate the PECAM1, which promotes MHC antigen presentation and Toll-like receptor-mediated immune processes while inhibiting CXCR receptor binding and immune negative regulation, thereby resulting in a stronger immune activation.

2025-09-11 | GSE285375 | GEO

Boosting NAD preferentially blunts TH17 inflammation via arginine biosynthesis and redox regulatory control in control and psoriasis subjects [NR or placebo]

Project description:To evaluate whether NAD+-boosting modulates adaptive immunity, primary CD4+ T cells from healthy control and psoriasis subjects were exposed to vehicle or nicotinamide riboside (NR) supplementation. NR blunts IFNg and IL-17 secretion with greater effects on TH17 polarization. RNA-seq analysis implicates NR blunting of sequestosome 1 (SQSTM1/p62)-coupled oxidative stress. NR administration increases SQSTM1 and reduces reactive oxygen species (ROS) levels. Furthermore NR activates NRF2, and genetic knockdown of NRF2 and of the NRF2-dependent gene, SQSTM1 diminish NR amelioratory effects. Metabolomic analysis identify that NAD+-boosting increases arginine and fumarate biosynthesis and genetic knockdown of argininosuccinate lyase ameliorates NR-effects on IL-17 production. Hence, NR via amino acid metabolites orchestrate NRF2 activation, augments CD4+ T cell antioxidant defenses and attenuates TH17 responsiveness. Oral NR supplementation in healthy volunteers similarly increase serum arginine, SQSTM1 and antioxidant enzyme gene expression and blunts TH17 immune responsiveness, supporting evaluation of NAD+-boosting in CD4+ T cell linked inflammation.

2023-07-18 | GSE237555 | GEO

Boosting NAD preferentially blunts TH17 inflammation via arginine biosynthesis and redox regulatory control in control and psoriasis subjects [healthy or psoriasis]

2023-07-18 | GSE237552 | GEO

Comprehensive Study of Nuclear Receptor DNA Binding Provides a Revised Framework for Understanding Receptor Specificity

Project description:The type II nuclear receptors (NRs) function as heterodimeric transcription factors with the retinoid X receptor (RXR) to regulate diverse biological processes in response to endogenous ligands and therapeutic drugs. DNA-binding specificity has been proposed as a primary mechanism for NR gene regulatory specificity. We use protein-binding microarrays (PBMs) to comprehensively analyze the DNA binding of 12 NR:RXRα heterodimers. We find more promiscuous NR-DNA binding than has been reported, challenging the view that NR binding specificity is defined by half-site spacing. We show that NRs bind DNA using two distinct modes, explaining widespread NR binding to half-sites in vivo. Finally, we show that the current models of NR specificity better reflect binding-site activity rather than binding-site affinity. Our rich dataset and revised NR binding models provide a framework for understanding NR regulatory specificity and will facilitate more accurate analyses of genomic datasets.

2019-01-12 | GSE124910 | GEO

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