Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17195353.fastq.gz | Fastqsanger.gz | |||
| SRR17195354.fastq.gz | Fastqsanger.gz | |||
| SRR17195355.fastq.gz | Fastqsanger.gz | |||
| SRR17195356.fastq.gz | Fastqsanger.gz | |||
| SRR17259676.fastq.gz | Fastqsanger.gz |
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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
Project description:Hut78 cell line was used as Sezary syndrome cell model. Comparative transcriptome profiles of SATB1 transduced Hut78 cells (Hut78-SATB1) relative to empty MIG vector transduced control Hut78 cells (Hut78-MIG) were analyzed. The primary goal is to establish a list of genes with differential expression between SATB1 transduced Hut78 cells and control Hut78 cells to identify the gene expression regulation effect of SATB1 expression in Sezary cells. Two color experiment, 3 biological replicates (3 unique cell clones) with Hut78 cells, each compared with a distinct individual clone from cells transduced with empty MIG vector.
2011-12-01 | E-GEOD-24951 | biostudies-arrayexpress
Project description:Hut78 cell line was used as Sezary syndrome cell model. Comparative transcriptome profiles of SATB1 transduced Hut78 cells (Hut78-SATB1) relative to empty MIG vector transduced control Hut78 cells (Hut78-MIG) were analyzed. The primary goal is to establish a list of genes with differential expression between SATB1 transduced Hut78 cells and control Hut78 cells to identify the gene expression regulation effect of SATB1 expression in Sezary cells.
2011-12-01 | GSE24951 | GEO
Project description:Satb1 and Satb2 are regulators of higher order chromatin in T cells and osteoblasts repectively. We were interested if Satb1 and Satb2 play a role in the regulation of gene expression in ES cells. In this experiment, we compared the transcriptome of wild type and Satb1-/- ES cells. Interestingly Satb1-/- ES cells display an impaired differentiation potential. WT and Satb1-/- ES cells were grown for 3 days in the presence of LIF and selected for Oct4-expression cells by the addition of hygromycin to the culture medium. Previously the cells had been engineered so that they contain a selectable HygroTK reporter in the the Oct4 locus. Total RNA was harvested and used for hybridization.
2009-09-01 | E-GEOD-17487 | biostudies-arrayexpress
Project description:Satb1 and Satb2 are regulators of higher order chromatin in T cells and osteoblasts repectively. We were interested if Satb1 and Satb2 play a role in the regulation of gene expression in ES cells. This SuperSeries is composed of the following subset Series: GSE17487: Expression data in WT and Satb1-/- ES cells GSE17488: Expression data in WT and ES cells overexpressing Satb1 GSE17489: Expression data in WT and ES cells overexpressing Satb2 Refer to individual Series
2009-09-01 | E-GEOD-17490 | biostudies-arrayexpress
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
Project description:Satb1 and Satb2 are regulators of higher order chromatin in T cells and osteoblasts repectively. We were interested if Satb1 and Satb2 play a role in the regulation of gene expression in ES cells. In this experiment, we compared the transcriptome of wild type and Satb1-/- ES cells. Interestingly Satb1-/- ES cells display an impaired differentiation potential.
2009-09-01 | GSE17487 | GEO
Project description:Three-dimensional (3D) genome folding, which is highly cell type-specific, plays a crucial role in orchestrating spatiotemporal gene expression. Although factors such as CTCF have been extensively studied in the hierarchical regulation of 3D chromatin organization, the mechanisms driving dynamic genome folding during T cell fate transitions remain incompletely defined. In this study, we reveal that Satb1, a chromatin organizer enriched in the T cell lineage, co-occupies genomic regions with the cohesin complex and Ctcf in double-positive (DP) thymocytes, where chromatin interactions are notably increased. We show that Satb1 physically interacts with the cohesin subunit Smc1a, and its deletion results in aberrant Smc1a binding and reduced chromatin contacts at sites co-occupied by Satb1 and cohesin. In both DP and immature CD4 single-positive (SP) T cells, Satb1 is essential for proper T cell activation and cytokine signaling. At the Cd3 locus, Satb1 and cohesin collaboratively regulate gene expression, with Satb1 loss leading to disrupted Smc1a occupancy and compromised chromatin interactions. Furthermore, Satb1 shows in vitro properties consistent with liquid-liquid phase separation, and disease-associated mutations impair these properties. Together, our findings uncover a molecular mechanism in which Satb1 facilitates chromatin looping through direct interaction with the cohesin complex and its ability to form nuclear condensates, thereby governing transcriptional regulation during T cell development.
2026-06-25 | GSE301980 | GEO
Project description:To understand gene expression signatures between wild-type and Satb1-deficient cells To examine genes regulated by Satb1 expression, sets of microarrays were conducted with Lin- c-kitHi Sca-1+ Flt3- HSC-enriched cells, Lin- c-kitHi Sca-1+ Flt3+LMPP-enriched cells, and Lin- c-kitLo Sca-1Lo IL7Rα+ CLP-enriched cells derived from E18.5 FL of Satb1-null mice or their WT littermates.
2013-03-20 | E-GEOD-45299 | biostudies-arrayexpress
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 | GSE250578 | GEO