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RNA-seq of Satb1 conditional KO in CD4+ na ve T cells reveals role of Satb1 in developing Th17 T cells through suppression of IL-2 expression

ABSTRACT: RNA-seq of Satb1 conditional KO in CD4+ na ve T cells reveals role of Satb1 in developing Th17 T cells through suppression of IL-2 expression

PROVIDER: PRJNA1054567 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27292081.fastq.gz	Fastqsanger.gz
	SRR27292082.fastq.gz	Fastqsanger.gz
	SRR27292083.fastq.gz	Fastqsanger.gz
	SRR27292084.fastq.gz	Fastqsanger.gz
	SRR27292085.fastq.gz	Fastqsanger.gz

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RNA-seq of Satb1 conditional KO in CD4+ na ve T cells reveals role of Satb1 in developing Th17 T cells through suppression of IL-2 expression

Project description:TH17 cells play an important role in host defense especially in barrier organs. Altered functionality of TH17 cells is associated with dysregulated tissue homeostasis resulting in an increased susceptibility for the development of autoimmune diseases. Thus, it is critical to identify mechanisms governing physiological as well as pathophysiological TH17 cell differentiation and identify strategies targeting TH17 cell differentiation in disease settings. Here, we identified the genome organizer Special AT-rich sequence-binding protein 1 (Satb1) as a pioneering factor for TH17 cell development. Satb1 is highly expressed in TH17 cells and loss of Satb1 prevents the differentiation of TH17 cells. As a consequence, expression of Satb1 in CD4+ T cells is required for the formation of TH17 cell-driven autoimmune diseases. Mechanistically, Satb1 mediates TH17 cell development through regulating accessibility of the Il2 gene locus and thereby preventing IL-2 signaling early during TH17 cell differentiation. Thus, Satb1 is critical by suppressing IL-2 expression during the formation of TH17 cells and may be a novel therapeutic target for the treatment of TH17 cell-driven autoimmune diseases.

2025-05-20 | GSE250577 | GEO

ATAC-seq of Satb1 conditional KO in CD4+ naïve T cells reveals epigenetic role of Satb1 in developing Th17 T cells by controlling the accessibility of Il2, thereby inhibiting IL-2 signaling in the initial stages of T cell differentiation.

2025-05-20 | GSE250576 | GEO

Satb1 directs the differentiation of TH17 cells through suppression of IL-2 expression [scMultiom ATAC/RNA-seq]

2025-05-20 | GSE290258 | GEO

Single-cell RNA-seq of CNS T cells derived from Satb1-deficient and Satb1-sufficient animals in EAE model

2025-05-20 | GSE250578 | GEO

Transcription factor Satb1 modulates the functionality of peripheral Treg cells

Project description:Transcription factor Satb1 plays important roles in the development of various immune cells. By utilizing genetic tools such as conditional knockout in mice have provided valuable information about its roles in T cell development. For example, CD4-cre transgenic mouse has been extensively used to delete Satb1 gene from T cells. While CD4-cre is useful to knockout a target gene floxed by LoxP sites from T cells, its expression lacks tissue specificity. To decipher the specific roles of Satb1 in T cells, we generated Satb1 conditional knockout mice with ThPOK-cre and E8I-cre to delete Satb1 from peripheral CD4+ and CD8+ T cells, respectively. Subsequently, total RNA-seq was performed to examine changes in transcriptome in the absence of Satb1 from peripheral T cells.

2024-08-01 | GSE190914 | GEO

Transcription factor Satb1 modulates the functionality of peripheral T cells

2024-08-01 | GSE190629 | GEO

Satb1 Overexpression Drives Tumor-Promoting Activities In Cancer-Associated Dendritic Cells

Project description:Special AT-rich sequence-binding protein-1 (Satb1) governs genome-wide transcriptional programs. Using a new conditional knockout mouse, we found that Satb1 is required for normal differentiation of conventional dendritic cells (DCs). Furthermore, Satb1 governs the differentiation of inflammatory DCs by regulating MHC-II expression through Notch1 signaling. Mechanistically, Satb1 binds to the Notch1 promoter, activating Notch expression and driving RBPJ occupancy of the H2-Ab1 promoter, which activates MHC-II transcription. However, tumor-driven, unremitting expression of Satb1 in activated Zbtb46+ inflammatory DCs that universally infiltrate ovarian tumors results in an immunosuppressive phenotype characterized by increased secretion of tumor-promoting Galectin-1 and IL-6. Correspondingly, specific in vivo silencing of Satb1 in tumor-associated DCs reverses their tumorigenic activity and boosts protective immunity. Therefore, dynamic fluctuations in Satb1 expression govern the generation and immunostimulatory activity of steady-state and inflammatory DCs, but relentless Satb1 overexpression in differentiated DCs converts them into tolerogenic/pro-inflammatory cells that contribute to malignant progression. RNA-seq with whild type and knocked-down Satb1

2016-01-13 | E-GEOD-76776 | biostudies-arrayexpress

Transcription factor Satb1 modulates the functionality of in vitro stimulated CD8+ T cells

2024-08-01 | GSE190948 | GEO

Transcriptome analysis of SATB1- and SATB1+ Hematopoietic stem cells.

Project description:Hematopoietic stem cells (HSCs) are now recognized as a heterogeneous population in self-renewing and differentiation capabilities. However, fundamental mechanisms governing the heterogeneity remain uncertain. We here show that special AT-rich sequence-binding protein 1 (SATB1), a global chromatin organizer, is involved in the mechanisms. Analyzing hematological lineage-restricted SATB1 knock out mice proved that SATB1 is indispensable for both self-renewal and normal differentiation of adult HSCs. Using SATB1/Tomato knock-in mice, we subdivided HSCs according to SATB1 intensity. Culture experiments and RNA-sequencing revealed essential differences between SATB1- and SATB1+ HSCs regarding lineage potential.

2018-06-14 | GSE94630 | GEO

Satb1

Project description:Satb1

| PRJNA788921 | ENA