Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mutations from IPEX patients elicit a range of phenotypes in mice [RNAseq]

ABSTRACT: RNAseq analysis of mouse Treg from Foxp3 missense mutant mice hemizygous male and heterozygous female : R51Q, C168Y, K199del, R309Q, F324L, R337Q

ORGANISM(S): Mus musculus

PROVIDER: GSE225891 | GEO | 2023/10/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Mutations from IPEX patients elicit a range of phenotypes in mice [scATAC-Seq]

Project description:scATAC analysis of mouse Treg from Foxp3 missense mutant mice heterozygous females : R51Q, K199del, R51Q, WT

2023-10-20 | GSE237198 | GEO

Mutations from IPEX patients elicit a range of phenotypes in mice

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

2023-10-20 | GSE237199 | GEO

PDK1 is required for maintenance of CD4+ FoxP3+ regulatory T cell function [Hemizygous]

Project description:The goal of this study was to determine the effect of Treg-specific Pdpk1 (PDK1) deletion on the transcriptome of Treg cells. CD4+ YFP+ Treg cells from spleens and peripheral lymph nodes of hemizygous Foxp3 YFP-Cre/0 Pdpk1 +/+ (WT) and Foxp3 YFP-Cre/0 Pdpk1 FL/FL (KO) were sorted, RNA was isolated and RNA-seq libraries were constructed and sequenced by Hiseq2000. Note companion data set using Pdpk1-deleted Treg from Cre-heterozygous mice, which do not develop spontaneous inflammation.

2021-02-11 | GSE163662 | GEO

PDK1 is required for maintenance of CD4+ FoxP3+ regulatory T cell function [heterozygous]

Project description:The goal of this study was to determine the effect of Treg-specific Pdpk1 (PDK1) deletion on the transcriptome of Treg cells in the absence of inflammatory conditions. CD4+ YFP+ Treg cells from spleens and peripheral lymph nodes of Cre-heterozygous Foxp3 YFP-Cre/+ Pdpk1 +/+ (WT) and Foxp3 YFP-Cre/+ Pdpk1 FL/FL (KO) were sorted, RNA was isolated and RNA-seq libraries were constructed and sequenced by Hiseq2500. Note companion data set using hemizygous Cre (induces spontaneous inflammation).

2021-02-11 | GSE163659 | GEO

Mutations from IPEX patients elicit a range of phenotypes in mice

Project description:Mutations from IPEX patients elicit a range of phenotypes in mice

| PRJNA994155 | ENA

Mutations from IPEX patients elicit a range of phenotypes in mice [RNAseq]

Project description:Mutations from IPEX patients elicit a range of phenotypes in mice [RNAseq]

| PRJNA937782 | ENA

Mutations from IPEX patients elicit a range of phenotypes in mice [scATAC-Seq]

Project description:Mutations from IPEX patients elicit a range of phenotypes in mice [scATAC-Seq]

| PRJNA994157 | ENA

FoxP3 scanning mutagenesis reveals functional variegation and mild mutations with atypical autoimmune phenotypes [microarray]

Project description:Microarray profiles of M176, M354 and WT FoxP3 -transdued (in vitro) and -Treg from mice

2017-09-28 | GSE104345 | GEO

Expression data from Treg cells expressing mutant FoxP3

Project description:FoxP3 is a central regulator of immunological tolerance, controlling the development and function of regulatory T (Treg) cells. To dissect the complex processes orchestrated by FoxP3, we investigated impacts of three autoimmune disease-associated missense FoxP3 mutations (i.e., I363V, A384T, R397W) through knock-in mutagenesis in mice. We investigated the impacts of these mutations on Treg cell transcriptome by microarray analysis.

2017-08-01 | GSE89654 | GEO

Nemo-like kinase drives Foxp3 stability and is critical for maintenance of immune tolerance by regulatory T cells

Project description:The Foxp3 transcription factor is a crucial determinant of both regulatory T (TREG) cell development and their functional maintenance. Appropriate modulation of tolerogenic immune responses therefore requires tight regulation of Foxp3 transcriptional output, and this involves both transcriptional and post-translational regulation. Here, we show that during T cell activation, phosphorylation of Foxp3 in TREG cells can be regulated by a TGFβ Activated Kinase 1 (TAK1)-Nemo Like Kinase (NLK) signaling pathway. NLK interacts with Foxp3 in TREG cells and directly phosphorylates Foxp3 on multiple serine residues. This phosphorylation results in stabilization of Foxp3 protein levels by preventing association with the STUB1 E3-ubiquitin protein ligase, resulting in both reduced ubiquitination and proteasome-mediated degradation. Conditional TREG cell NLK-knockout (NLKTREG) results in decreased TREG cell-mediated immunosuppression in vivo and NLK-deficient TREG cell animals develop more severe experimental autoimmune encephalomyelitis. Our data suggest a molecular mechanism, in which stimulation of TCR-mediated signaling can induce a TAK1-NLK pathway to sustain Foxp3 transcriptional activity through stabilization of protein levels, thereby maintaining TREG cell suppressive function. Pharmacological manipulation of this phosphorylation-ubiquitination axis may provide therapeutic opportunities for regulating TREG cell function, for example during cancer immunotherapy.

2019-09-02 | PXD011164 | Pride

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