Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E4BP4 is a transcriptional brake in Tfh cell differentiation

ABSTRACT: E4BP4 is a transcriptional brake in Tfh cell differentiation

PROVIDER: PRJNA497241 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8069700_1.fastq.gz	Fastqsanger.gz
	SRR8069700_2.fastq.gz	Fastqsanger.gz
	SRR8069696.fastq.gz	Fastqsanger.gz
	SRR8069697_1.fastq.gz	Fastqsanger.gz
	SRR8069697_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 9

Similar Datasets

ChIP-seq for E4BP4 in CD4+ T cell

Project description:Here, using ChIP-seq, we demonstrate that the transcriptional repressor Adenovirus E4 promoter-binding protein (E4BP4) binds directly to the Bcl6 promoter, which a key transcription factor controlling Tfh cell differentiation. By obtaining sequence from chromatin immunoprecipitated DNA of E4BP4 overexpressing CD4+T cells, we generated genome-wide binding gene spectrums of E4BP4. These results reveal that E4BP4 interacts with BCL6 and E4BP4 directly modulated the expression of Bcl6 to reveal the mechanism downstream of E4BP4 that regulates Tfh cell differentiation.

2021-01-19 | GSE121387 | GEO

RNA-seq analysis of the effects of E4BP4 in Tfh cells

Project description:The goal of this experiment is to measure the changes in gene expression in E4BP4 deficient in vitro induced mice Tfh cells.

2021-01-19 | GSE121388 | GEO

E4BP4 is a transcriptional brake in Tfh cell differentiation

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-01-19 | GSE121389 | GEO

RNA-seq analysis of the effects of E4BP4 in Tfh cells

Project description:RNA-seq analysis of the effects of E4BP4 in Tfh cells

| PRJNA497244 | ENA

Regulation of Tfh differentiation by Mettl3 [RNA-seq]

Project description:T follicular helper (Tfh) cells are a specialized subset of CD4 T cells that are essential for most antibody productions and humoral responses. It is well characterized that transcriptional network exerts indispensable roles in Tfh cell differentiation. However, how post-transcriptional regulation controls Tfh biology has largely remained unclear. Multiple mice models were used here by a series of experimental approaches to illustrate m6A methyltransferase Mettl3 programs Tfh cell differentiation at post-transcriptional layer.

2021-01-19 | GSE129648 | GEO

Novel Roles for the Transcriptional Repressor E4BP4 in Both Cardiac Physiology and Pathophysiology

Project description:Circadian clocks temporally orchestrate biological processes critical for cellular/organ function. For example, the cardiomyocyte circadian clock modulates cardiac metabolism, signaling, and electrophysiology over the course of the day, such that, disruption of the clock leads to age-onset cardiomyopathy (through unknown mechanisms). Here, we report that genetic disruption of the cardiomyocyte clock results in chronic induction of the transcriptional repressor E4BP4. Importantly, E4BP4 deletion prevents age-onset cardiomyopathy following clock disruption. These studies also indicate that E4BP4 regulates both cardiac metabolism (eg, fatty acid oxidation) and electrophysiology (eg, QT interval). Collectively, these studies reveal that E4BP4 is a novel regulator of both cardiac physiology and pathophysiology.

2023-08-11 | GSE240149 | GEO

Regulation of Tfh differentiation by PDK1

Project description:Follicular helper T (Tfh) cells, as important effector CD4+ T cells, are able to regulate antigen-specific B cell immunity in vivo. It is well characterized that transcription factors, cytokines, microRNA, epigenetic modifications exerts important roles in Tfh differentiation and function. Howerer, the regulatory mechanism of the major signaling pathways driving Tfh cell differentiation remains unclear. Multiple mice models were used by a series of experimental approaches to illustrate PDK1 signaling programs Tfh differentiation and function.

2021-02-15 | GSE154976 | GEO

TCF1 is required for the differentiation of T follicular helper (TFH) cells during viral infections

Project description:TFH and Th1 cells generated after viral or intracellular bacterial infections are critical for the control of infections and the development of immunological memories. However, the mechanisms that govern the choice of activated CD4 T cells to the two alternative fates remain unclear. Here, we found that reciprocal expression of TCF1 and Blimp1 between viral-specific TFH and Th1 cells started early after infection. TCF1 was intrinsically required for the differentiation of TFH cells. In the absence of TCF1, TFH cells failed to maintain their transcriptional and metabolic signatures, distinct from those in Th1 cells. Mechanistically, TCF1 functioned through forming negative feedback loops with IL-2 and Blimp1 signaling. Thus, we have demonstrated an essential role of TCF1 in TFH-cell differentiation. Tcf7 deficient and WT SMARTA CD4 T cells were isolated from mice 8 days after Lymphocytic Choriomeningitis Virus (LCMV) infection. TFH and Th1 cells were separated by FACS.

2015-09-18 | E-GEOD-65660 | biostudies-arrayexpress

Regulation of Tfh differentiation by PDK1

Project description:Regulation of Tfh differentiation by PDK1

| PRJNA648089 | ENA

Foxp1 is a rate-limiting and essential negative regulator of Tfh cell differentiation

Project description:CD4+ T follicular helper (Tfh) cells are essential for germinal center (GC) and high-affinity antibody responses. Yet the regulation that determines the initial development of Tfh cells is still largely unknown. Here we find that transcription factor Foxp1, previously shown to be essential in maintaining T cell quiescence, is a rate-limiting and essential negative regulator of Tfh cell differentiation. NaM-CM-/ve CD4+ T cells constitutively express Foxp1A, and stimulation through the T cell receptor (TCR) transiently induces the expression of a shorter Foxp1D isoform. In T cell-dependent (TD) humoral responses, CD4+ T cells deficient in all Foxp1 isoforms preferentially differentiate into Tfh cells, resulting in substantially increased GC and antibody responses. This negative regulation of Foxp1 on Tfh cell differentiation shows profound dominance: even in the absence of B cells, Foxp1-deficient CD4+ T cells differentiate into Tfh cells with high frequencies and sustained Bcl6 expression. Further, in the absence of Foxp1, Tfh cells are generated in higher frequencies than seen with Bcl6 overexpression and Tfh cell differentiation becomes significantly resistant to Blimp1-mediated repression. Finally, our experiments reveal specific roles of Foxp1A and Foxp1D in inhibiting Tfh cell differentiation: TCR-induced Foxp1D functions as a M-bM-^@M-^XgatekeeperM-bM-^@M-^Y to block the initial Tfh cell development, and together Foxp1A and Foxp1D proteins inversely determine Tfh cell generation in a dosage-dependent manner. Our study suggests that two Foxp1 isoforms provide a M-bM-^@M-^\double checkM-bM-^@M-^] mechanism as fundamental regulators in Tfh cell differentiation and humoral responses. Gene expression analysis of ex vivo OT-II Foxp1-WT Tfh cells and OT-II Foxp-conditional knockout (CKO) Tfh cells 5 days after immunization.

2014-05-18 | E-GEOD-50725 | 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