Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription factor TFII-I fine tunes innate properties of B lymphocytes

ABSTRACT: Transcription factor TFII-I fine tunes innate properties of B lymphocytes

PROVIDER: PRJNA919016 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22999048.fastq.gz	Fastqsanger.gz
	SRR22999049.fastq.gz	Fastqsanger.gz
	SRR22999050.fastq.gz	Fastqsanger.gz
	SRR22999051.fastq.gz	Fastqsanger.gz
	SRR22999052.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Transcription factor TFII-I fine tunes innate properties of B lymphocytes

Project description:The ubiquitously expressed transcription factor TFII-I is a multifunctional protein with pleiotropic roles in gene regulation. TFII-I associated polymorphisms are implicated in Sjögren’s syndrome and Lupus in humans and, germline deletion of the Gtf2i gene in mice leads to embryonic lethality. Here we report a unique role for TFII-I in homeostasis of innate properties of B lymphocytes. Loss of Gtf2i in murine B lineage cells leads to an alteration in transcriptome, chromatin landscape and associated transcription factor binding sites, which exhibits myeloid like features and coincides with enhanced sensitivity to LPS induced gene expression. TFII-I deficient B cells also show increased switching to IgG3, a phenotype associated with inflammation. These results demonstrate a role for TFII-I in maintaining immune homeostasis and provide clues for GTF2I polymorphisms associated with B cell dominated autoimmune diseases in humans.

2023-01-06 | GSE222325 | GEO

Transcription factor TFII-I fine tunes innate properties of B lymphocytes

Project description:The ubiquitously expressed transcription factor TFII-I is a multifunctional protein with pleiotropic roles in gene regulation. TFII-I associated polymorphisms are implicated in Sjögren’s syndrome and Lupus in humans and, germline deletion of the Gtf2i gene in mice leads to embryonic lethality. Here we report a unique role for TFII-I in homeostasis of innate properties of B lymphocytes. Loss of Gtf2i in murine B lineage cells leads to an alteration in transcriptome, chromatin landscape and associated transcription factor binding sites, which exhibits myeloid-like features and coincides with enhanced sensitivity to LPS induced gene expression. TFII-I deficient B cells also show increased switching to IgG3, a phenotype associated with inflammation. These results demonstrate a role for TFII-I in maintaining immune homeostasis and provide clues for GTF2I polymorphisms associated with B cell dominated autoimmune diseases in humans.

| S-EPMC9900109 | biostudies-literature

Mecp2 fine-tunes quiescence exit by targeting nuclear receptors

Project description:Mecp2 fine-tunes quiescence exit by targeting nuclear receptors

| PRJNA946716 | ENA

Mnx1 fine tunes neuronal gene expression in motor neurons

Project description:Mnx1 fine tunes neuronal gene expression in motor neurons

| PRJNA599127 | ENA

A PP2A-Integrator complex fine-tunes transcription by opposing CDK9

Project description:A PP2A-Integrator complex fine-tunes transcription by opposing CDK9

| PRJNA687654 | ENA

Orphan nuclear receptor COUP-TFII enhances myofibroblasts glycolysis leading to kidney fibrosis

Project description:Recent studies demonstrated that metabolic disturbance, such as augmented glycolysis, contributes to fibrosis. The molecular regulation of this metabolic perturbation in fibrosis, however, has been elusive. COUP-TFII (also known as NR2F2) is an important regulator of glucose and lipid metabolism. Its contribution to organ fibrosis is undefined. Here, we found increased COUP-TFII expression in myofibroblasts in human fibrotic kidneys, lungs, kidney organoids, and mouse kidneys after injury. Genetic ablation of COUP-TFII in mice resulted in attenuation of injury-induced kidney fibrosis. A non-biased proteomic study revealed the suppression of fatty acid oxidation and the enhancement of glycolysis pathways in COUP-TFII overexpressing fibroblasts. Overexpression of COUP-TFII in fibroblasts induced augmented glycolysis and production of alpha smooth muscle actin (αSMA) and collagen1. Knockout of COUP-TFII decreased glycolysis and collagen1 levels in fibroblasts. Chip-qPCR revealed the binding of COUP-TFII on the promoter of PGC1α. Overexpression of COUP-TFII reduced the cellular level of PGC1α. Targeting COUP-TFII serves as a novel treatment approach for mitigating fibrosis in chronic kidney disease and potentially fibrosis in other organs.

2021-04-27 | PXD024035 | Pride

TBX3 is dynamically expressed in pancreatic organogenesis and fine-tunes regeneration

Project description:TBX3 is dynamically expressed in pancreatic organogenesis and fine-tunes regeneration

| PRJNA896121 | ENA

Mecp2 fine-tunes quiescence exit by targeting nuclear receptors [ChIP-Seq]

Project description:Mecp2 fine-tunes quiescence exit by targeting nuclear receptors [ChIP-Seq]

| PRJNA946720 | ENA

Mecp2 fine-tunes quiescence exit by targeting nuclear receptors [RNA-Seq]

Project description:Mecp2 fine-tunes quiescence exit by targeting nuclear receptors [RNA-Seq]

| PRJNA946719 | ENA

Genes regulated by COUP-TFII inhibitor

Project description:The orphan nuclear receptor COUP-TFII is expressed at a low level in adult tissues, but its expression is increased and shown to promote progression of multiple diseases including prostate cancer, heart failure and muscular dystrophy. Suppression of COUP-TFII slows disease progression, making it an intriguing therapeutic target. Here, we identified a potent and specific COUP-TFII inhibitor through high-throughput screening. The inhibitor specifically suppressed COUP-TFII activity to regulate its target genes.

2020-05-12 | GSE142475 | 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