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Links from GEO DataSets

Items: 20

1.

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
2.

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
3.

Role of JunB in Th17 cell effector stability [ChIP-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:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL21103 GPL13112
10 Samples
Download data: XLS
Series
Accession:
GSE98412
ID:
200098412
4.

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
5.

JunB modulates an IRF4-dependent transcriptional program to regulate homeostasis and suppressive functions of effector regulatory T cells

(Submitter supplied) To understand molecular mechanisms by which JunB regulates Treg function, we performed RNA-seq and ChIP-seq analyses of JunB-deficient and control Treg cells (CD4+ CD25hi). 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
Platform:
GPL21103
10 Samples
Download data: BED
Series
Accession:
GSE121295
ID:
200121295
6.

JunB modulates an IRF4-dependent transcriptional program to regulate homeostasis and suppressive functions of effector regulatory T cells [ChIP-Seq]

(Submitter supplied) To understand molecular mechanisms by which JunB regulates Treg function, we performed ChIP-seq analysis of JunB-deficient and control Treg cells (CD4+ CD25hi).
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21103
4 Samples
Download data: BED
Series
Accession:
GSE121294
ID:
200121294
7.

JunB modulates an IRF4-dependent transcriptional program to regulate homeostasis and suppressive functions of effector regulatory T cells [RNA-Seq]

(Submitter supplied) To understand molecular mechanisms by which JunB regulates Treg function, we performed RNA-seq analysis of JunB-deficient and control Treg cells (CD4+ CD25hi).
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
6 Samples
Download data: XLSX
Series
Accession:
GSE121293
ID:
200121293
8.

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
9.

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
10.

JunB-dependent expression in colonic and Peyer's patch regulatory T cells

(Submitter supplied) Foxp3-expressing regulatory T (Treg) cells are critical mediators of immunological tolerance to both self and microbial antigens. Tregs activate context-dependent transcriptional programs to adapt effector function to specific tissues; however, the factors controlling tissue-specific gene expression in Tregs remain unclear. Here, we find that the AP-1 transcription factor JunB regulates the intestinal adaptation of Tregs by controlling select gene expression programs in multiple Treg subsets. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
14 Samples
Download data: TXT
Series
Accession:
GSE145888
ID:
200145888
11.

Network Analysis Reveals a Novel Role for the AP-1 Transcription Factor JUNB in Classical and Alternative Macrophage Activation

(Submitter supplied) Bone marrow-derived macrophages were generated from wild type and Junb knockout mice and tested for their responses to LPS treatment.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL13912
15 Samples
Download data: TXT
Series
Accession:
GSE50542
ID:
200050542
12.

Bach2 represses effector programmes to stabilize Treg-mediated immune homeostasis

(Submitter supplied) Through their functional diversification, CD4+ T cells play key roles in both driving and constraining immune-mediated pathology. Transcription factors are critical in the generation and maintenance of cellular diversity and negative regulators antagonistic to alternate fates often act in conjunction with positive regulators to stabilize lineage specification1. Polymorphisms within the locus encoding a transcription factor BACH2 are associated with diverse immune-mediated diseases including asthma2, multiple sclerosis3, Crohn¹s disease4-5, coeliac disease6, vitiligo7 and type 1 diabetes8. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
12 Samples
Download data: RPKM, TXT, WIG
Series
Accession:
GSE45975
ID:
200045975
13.

Gene expression in Bach2-deficient and wildtype CD4 single-positive thymocytes from mixed chimeric animals

(Submitter supplied) The role of FoxP3+ regulatory T (Treg) cells in the maintenance of immunological tolerance is well established. Recently, genome-wide association studies (GWAS) in humans have associated polymorphisms within the BACH2 locus encoding the transcription factor BTB and CNC homology 1, basic leucine zipper transcription factor 2 (Bach2) with diverse allergic and autoimmune diseases including asthma, multiple sclerosis, Crohn's disease, celiac disease, generalized vitiligo and type 1 diabetes. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
6 Samples
Download data: CEL
Series
Accession:
GSE42598
ID:
200042598
14.

JunB regulates the common and lineage-specific transcriptional programs of distinct CD4+ effector T cells

(Submitter supplied) IRF4 is critical for differentiation of various CD4+ effector T cells, such as T helper 1 (Th1), Th2, and Th17 subsets, through interaction with BATF-containing AP-1 heterodimers. A major BATF heterodimeric partner, JunB, regulates Th17 differentiation, but the role of JunB in other CD4+ effector T subsets is not fully understood. Here we demonstrate that JunB is essential for accumulation of Th1 and Th2 cells, as well as Th17 cells, both in vitro and in vivo. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL21103 GPL24247
28 Samples
Download data: CSV, TXT
Series
Accession:
GSE172490
ID:
200172490
15.

Metabolic heterogeneity underlies reciprocal fates of TH17 cell stemness and plasticity

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL21103
24 Samples
Download data: MTX, TSV
Series
Accession:
GSE121599
ID:
200121599
16.

Metabolic heterogeneity underlies reciprocal fates of TH17 cell stemness and plasticity [scRNA-seq]

(Submitter supplied) TH17 cells in autoimmune disease are functionally and metabolically heterogeneous and contain a subset with stemness-associated features but lower anabolic metabolism and a reciprocal subset with higher metabolic activity that supports the transdifferentiation into TH1 cells.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
6 Samples
Download data: MTX, TSV
Series
Accession:
GSE121598
ID:
200121598
17.

Metabolic heterogeneity underlies reciprocal fates of TH17 cell stemness and plasticity [ATAC-seq]

(Submitter supplied) TH17 cells in autoimmune disease are functionally and metabolically heterogeneous and contain a subset with stemness-associated features but lower anabolic metabolism and a reciprocal subset with higher metabolic activity that supports the transdifferentiation into TH1 cells.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21103
18 Samples
Download data: CSV
Series
Accession:
GSE121597
ID:
200121597
18.

Transcription profiles of fate mapped IL17aiCre+flox/stop/flox-YFP+ TH17 cells, CD44intCD27+ TH17 cells and CD44hiCD27- TH17 cells from WT or Raptor-ko (flox/flox) mice after immunization with Myelin Oligodendrocyte Glycoprotein (MOG)

(Submitter supplied) Mechanisms governing memory responses in IL-17 secreting CD4+ T cells (TH17), especially in autoimmune disorders, remain poorly understood. TH17 cells play pleiotropic roles in autoimmunity and tissue inflammation and are characterized by inherent plasticity, although how plasticity is regulated remains elusive. We investigated the transcriptional profiles of fate mapped (IL17aiCre-flox/stop/flox-YFP) TH17 cells and WT and Raptor-ko (flox/flox) TH17 cells (both IL17aiCre-flox/stop/flox-YFP) as well as sorted within CD27+ and CD27- subsets of WT in experimental autoimmune encephalomyelitis, a human model for human multiple sclerosis. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
18 Samples
Download data: CEL
Series
Accession:
GSE107521
ID:
200107521
19.

Comparison of gene expression profiles of naïve and in vitro effector CD8+ T cells from wild-type and BATF-/- mice

(Submitter supplied) The transcription factor BATF is required for Th17 and TFH differentiation. Here, we show that BATF also has a fundamental role in regulating effector CD8+ T cell differentiation. BATF-deficient CD8+ T cells show profound defects in effector expansion and undergo proliferative and metabolic catastrophe early after antigen encounter. BATF, together with IRF4 and Jun proteins, binds to and promotes early expression of genes encoding lineage-specific transcription-factors (T-bet and Blimp-1) and cytokine receptors, while paradoxically repressing genes encoding effector molecules (IFNg and granzyme B). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
13 Samples
Download data: CEL
Series
Accession:
GSE54215
ID:
200054215
20.

ChIP-Seq analysis of BATF, IRF4, the Jun proteins, and histone modifications in effector CD8+ T cells

(Submitter supplied) The transcription factor BATF is required for Th17 and TFH differentiation. Here, we show that BATF also has a fundamental role in regulating effector CD8+ T cell differentiation. BATF-deficient CD8+ T cells show profound defects in effector expansion and undergo proliferative and metabolic catastrophe early after antigen encounter. BATF, together with IRF4 and Jun proteins, binds to and promotes early expression of genes encoding lineage-specific transcription-factors (T-bet and Blimp-1) and cytokine receptors, while paradoxically repressing genes encoding effector molecules (IFNg and granzyme B). more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
23 Samples
Download data: BW
Series
Accession:
GSE54191
ID:
200054191
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