Similar studies for GEO DataSets (Select 200086499) - GEO DataSets

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Items: 20

Select item 2000864991.

JunB is essential for IL-23-dependent pathogenicity of Th17 cells.

(Submitter supplied) To understand molecular mechanisms by which JunB regulates Th17 differentiation, we performed microarray analyses of JunB-deficient and control Th17 cells.

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL6246
12 Samples

Download data: CEL

Series

Accession:: GSE86499

ID:: 200086499

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 2000865352.

JunB is essential for IL-23-dependent pathogenicity of Th17 cells.

(Submitter supplied) To understand molecular mechanisms by which JunB regulates Th17 differentiation, we performed ChIP-seq analyses of JunB-deficient and control Th17 cells.

Organism:: Mus musculus

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL21103
8 Samples

Download data: BED

Series

Accession:: GSE86535

ID:: 200086535

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2000982423.

The AP-1 Transcription Factor JunB Is Required for Th17 Cell Differentiation

(Submitter supplied) Interleukin (IL)-17-producing T helper (Th17) cells are crucial for host defense against extracellular microbes and pathogenesis of autoimmune diseases. Here we show that the AP-1 transcription factor JunB is required for Th17 cell development. Junb-deficient CD4+ T cells are able to develop in vitro into various helper T subsets except Th17. The RNA-seq transcriptome analysis reveals that JunB is crucial for the Th17-specific gene expression program. more...

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL17021
8 Samples

Download data: TXT

Series

Accession:: GSE98242

ID:: 200098242

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2000534554.

Expression profiling comparisons of human CD4+ T cells treated with RORgt inhibitors

(Submitter supplied) The aim of this study was to identify differential gene expression resulting from the inhibition of RORgt in human CD4+ T cells.

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL6244
20 Samples

Download data: CEL

Series

Accession:: GSE53455

ID:: 200053455

Select item 2000984145.

Role of JunB in Th17 cell effector stability

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:: GPL21103 GPL13112
14 Samples

Download data: XLS

Series

Accession:: GSE98414

ID:: 200098414

PubMed Full text in PMC Similar studies

Select item 2000984136.

Role of JunB in Th17 cell effector stability [RNA-seq]

(Submitter supplied) Here we identify the activator protein-1 (AP-1) factor JunB as an essential regulator of Th17 cell identity. JunB activates the expression of Th17 lineage-specifying genes, and coordinately represses genes controlling Th1 and Treg fate. Through regulatory analysis, we find that JunB is a core regulator of global transcriptional programs that promote Th17 cell identity and restrict alternative CD4+ T cell potential.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL13112
4 Samples

Download data: TAB

Series

Accession:: GSE98413

ID:: 200098413

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2000984127.

Role of JunB in Th17 cell effector stability [ChIP-seq]

Organism:: Mus musculus

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platforms:: GPL21103 GPL13112
10 Samples

Download data: XLS

Series

Accession:: GSE98412

ID:: 200098412

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2000722718.

The nuclear receptor REV-ERBa modulates Th17 cell differentiation and function by competing with RORgt

(Submitter supplied) T helper 17 (Th17) cells produce interleukin-17 (IL-17) cytokines and drive inflammatory responses in autoimmune diseases such as multiple sclerosis and rheumatoid arthritis. The differentiation of Th17 cells is dependent on the retinoic acid receptor-related orphan nuclear receptor RORgt. Here we identify REV-ERBa (encoded by Nr1d1), a member of the nuclear hormone receptor family (NHR), as a transcriptional repressor that antagonizes RORgt function in Th17 cells. more...

Organism:: Mus musculus

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL17021
2 Samples

Download data: BEDGRAPH, TXT

Series

Accession:: GSE72271

ID:: 200072271

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2001085989.

Epigenetic activation during Th17 cell differentiation is impaired after TRIM28 deletion

(Submitter supplied) Cell fate decision is mediated by epigenetic mechanisms. We have analyzed naive T cell differentiation into Th17 cells, which is regulated by environmental cytokines and their downstream transcription factors. RORγt is a lineage-specific master transcription factor for Th17 cells. Although epigenetic mechanisms have been implicated in Th17 cell differentiation, how transcription factors interact to activate epigenetic program is unclear. more...

Organism:: Mus musculus

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL13112
8 Samples

Download data: WIG

Series

Accession:: GSE108598

ID:: 200108598

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20009842710.

Epigenetic activation during Th17 cell differentiation is impaired after TRIM28 deletion

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL17021
8 Samples

Download data: TDF, TXT, WIG

Series

Accession:: GSE98427

ID:: 200098427

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20005501311.

Profiling of in vitro differentiated activated T helper cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Mus musculus; synthetic construct

Type:: Expression profiling by array; Non-coding RNA profiling by array

Platforms:: GPL16570 GPL16384
20 Samples

Download data: CEL, XLSX

Series

Accession:: GSE55013

ID:: 200055013

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20005501212.

microRNA cluster 106a~363 is involved in T helper 17 cell differentiation

(Submitter supplied) Combined analysis of mRNA and miRNA transcriptoms revealed a complex network regulating major immune regulatory signaling pathways

Organism:: Mus musculus; synthetic construct

Type:: Non-coding RNA profiling by array

Platform:: GPL16384
10 Samples

Download data: CEL

Series

Accession:: GSE55012

ID:: 200055012

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20005501113.

Profiling of in vitro differentiated activated T helper cells [mRNA]

(Submitter supplied) Combined analysis of mRNA and miRNA transcriptoms revealed a complex network regulating major immune regulatory signaling pathways

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL16570
10 Samples

Download data: CEL

Series

Accession:: GSE55011

ID:: 200055011

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20015344214.

ATAC-seq of wild type and Stat3-deficient or Rorgt-deficient Th17 cells

(Submitter supplied) STAT3 has a more profound effect on chromatin accessibility regulation than RORgt during Th17 cell differentiation.

Organism:: Mus musculus

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL21273
4 Samples

Download data: BW

Series

Accession:: GSE153442

ID:: 200153442

PubMed Similar studies SRA Run Selector

Select item 20002368115.

Enhanced Pathogenicity of Th17 cells Generated in the Absence of Transforming Growth Factor-β Signaling: ChIPSeq

(Submitter supplied) CD4+ T cells that selectively produce interleukin (IL)-17, are critical for host defense and autoimmunity. Crucial for T helper17 (Th17) cells in vivo, IL-23 has been thought to be incapable of driving initial differentiation. Rather, IL-6 and transforming growth factor (TGF)-β1 have been argued to be the factors responsible for initiating specification. Herein, we show that Th17 differentiation occurs in the absence of TGF-β signaling. more...

Organism:: Mus musculus

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL9185
3 Samples

Download data: BED, BEDGRAPH

Series

Accession:: GSE23681

ID:: 200023681

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20002350516.

Enhanced Pathogenicity of Th17 cells Generated in the Absence of Transforming Growth Factor-β Signaling

(Submitter supplied) CD4+ T cells that selectively produce interleukin (IL)-17, are critical for host defense and autoimmunity1-4. Crucial for T helper17 (Th17) cells in vivo5,6, IL-23 has been thought to be incapable of driving initial differentiation. Rather, IL-6 and transforming growth factor (TGF)-β1 have been argued to be the factors responsible for initiating specification7-10. Herein, we show that Th17 differentiation occurs in the absence of TGF-β signaling. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL1261
10 Samples

Download data: CEL

Series

Accession:: GSE23505

ID:: 200023505

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20012272617.

REV-ERBa regulates TH17 cell development and autoimmunity

(Submitter supplied) RORγt is well recognized as the lineage defining transcription factor for TH17 cell development. However, the cell-intrinsic mechanisms that negatively regulate TH17 cell development and autoimmunity remain poorly understood. Here we demonstrate that the transcriptional repressor REV-ERBa is exclusively expressed in TH17 cells, competes with RORγt for their shared DNA consensus sequence, and negatively regulates TH17 cell development via repression of genes traditionally characterized as RORγt-dependent, including Il17a. more...

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL19057
10 Samples

Download data: XLSX

Series

Accession:: GSE122726

ID:: 200122726

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20013318018.

Microglia and infiltrating monocytes gene expression profiling during EAE progress

(Submitter supplied) The project was designed to figure out the role of microglia in brain inflammation (EAE model). The first step was to find genes/pathways that are upregulated in the microglia during EAE progress but absent in the infiltrating monocytes. These genes/pathways may provide clues for studying the unique function of microglia in the brain inflammation that is disctinct from the infiltrating monocytes.