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Thinking out of the box to evaluate the performance of engineered SOX17 in pluripotency reprogramming (ATAC-Seq)

ABSTRACT: Thinking out of the box to evaluate the performance of engineered SOX17 in pluripotency reprogramming (ATAC-Seq)

PROVIDER: PRJNA946704 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23921096_1.fastq.gz	Fastqsanger.gz
	SRR23921096_2.fastq.gz	Fastqsanger.gz
	SRR23921097_1.fastq.gz	Fastqsanger.gz
	SRR23921097_2.fastq.gz	Fastqsanger.gz
	SRR23921098_1.fastq.gz	Fastqsanger.gz

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Thinking out of the box to evaluate the performance of engineered SOX17 in pluripotency reprogramming

Project description:Thinking out of the box to evaluate the performance of engineered SOX17 in pluripotency reprogramming

| PRJNA947150 | ENA

Thinking out of the box to evaluate the performance of engineered SOX17 in pluripotency reprogramming (RNA-Seq)

Project description:Thinking out of the box to evaluate the performance of engineered SOX17 in pluripotency reprogramming (RNA-Seq)

| PRJNA844076 | ENA

Thinking out of the box to evaluate the performance of engineered SOX17 in pluripotency reprogramming (ATAC-Seq)

Project description:The SOX17 triple-mutant SOX17FNV is a more potent inducer of pluripotency than wild-type SOX2 for unknown features outside its DNA binding high mobility group box domain. Using an inducible reprogramming system, we verified that wild-type SOX17 is not capable to induce pluripotency but SOX17FNV outperforms SOX2 in mouse and human. In mature pluripotent stem cells, SOX17FNV can fully replace SOX2 without compromising self-renewal and pluripotency despite considerable sequence variation. Binding assays using full length proteins expressed in mammalian cells show that SOX17FNV and SOX17 co-bind OCT4 more tightly than SOX2 albeit with switched preferences for composite DNA motifs. Through the systematic analyses of domain deletions, we found that the N-terminus is dispensable for the reprogramming activity of SOX17FNV whilst the C-terminus encodes for essential as well as superfluous domains. Domains have non-additive and partially compensatory effects suggesting that versatile multivalent interaction drive transactivation and reprogramming. We define a minimal SOX17FNV (miniSOX) that can support reprogramming without loss in activity enabling payload reduction within reprogramming cassettes. The definition, functional evaluation and utilisation of potent effector domains that are optimised to pioneer cell fate transition will open up new avenues to enhance cellular reprogramming and stem cell engineering with synthetic transcription factors.

2023-08-01 | GSE227716 | GEO

Thinking out of the box to evaluate the performance of engineered SOX17 in pluripotency reprogramming (RNA-Seq)

2023-08-01 | GSE205192 | GEO

Thinking out of the box to evaluate the performance of engineered SOX17 in pluripotency reprogramming

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

2023-08-01 | GSE227830 | GEO

Gene expression profiles of SOX17 overexpression in the KYSE170 luciferase cell

Project description:SOX17 is a transcriptional factor containing DNA-binding domain HMG box, we hypothesized that there are more genes other than in Wnt singnaling pathway to be transcriptionally regulated by SOX17 in esophageal squamous cell carcinoma. We performed the GeneChips expression array analyses to reveal more transcriptional target for SOX17. In this study, the esophageal cancer cell line, KYSE170-luc, were transfection with empty vector and expression plasmids of SOX17 for 12 hours. Total RNA were prepared for microarray assays.

2014-02-12 | E-GEOD-35975 | biostudies-arrayexpress

Gene expression profiles of SOX17 overexpression in the KYSE170 luciferase cell

2014-02-12 | GSE35975 | GEO

E2F1 mediates SOX17 Deficiency-Induced Pulmonary Hypertension

Project description:SRY-Box Transcription Factor 17 (SOX17) enhancers variants and mutations are found in patients with pulmonary arterial hypertension (PAH). In human PAH pulmonary microvascular endothelial cells (HPMVEC), there is a significant downregulation of SOX17 expression. We hypothesized that SOX17 deficiency contributes to the pathogenesis of PAH and found that mice with endothelial specific disruption (ecKO Sox17) developed spontaneous pulmonary hypertension (PH) and exacerbated hypoxia-induced PH. Loss of SOX17 in lung ECs induces cell cycle programming, proliferative and anti-apoptotic phenotypes, a process mediated by the activation of E2F Transcription Factor 1 (E2F1) signaling. Pharmacological inhibition of E2F1 in ecKO Sox17 mice attenuated PH and cell cycle programming. Our study demonstrated that endothelial SOX17 deficiency induces PH and targeting E2F1 signaling represents a promising approach in PAH patients.

2023-03-15 | GSE192649 | GEO

E2F1 mediates SOX17 Deficiency-Induced Pulmonary Hypertension [scRNA-seq]

Project description:SRY-Box Transcription Factor 17 (SOX17) enhancers variants and mutations are found in patients with pulmonary arterial hypertension (PAH). In human PAH pulmonary endothelial cells, there is a significant downregulation of SOX17 expression. We hypothesized that SOX17 deficiency contributes to the pathogenesis of PAH and found that mice with endothelial specific disruption (ecKO Sox17) developed spontaneous pulmonary hypertension (PH) and exacerbated hypoxia-induced PH. Loss of SOX17 in lung ECs induced endothelial dysfunctions including upregulation of cell cycle programming and paracrine effect, proliferative and anti-apoptotic phenotypes, impaired cellular junction and BMP signaling. E2F Transcription Factor 1 (E2F1) signaling was showed to mediate the SOX17 deficiency-induced EC dysfunction. Pharmacological inhibition of E2F1 in ecKO Sox17 mice attenuated PH and cell cycle programming. Our study demonstrated that endothelial SOX17 deficiency induces PH through E2F1 and targeting E2F1 signaling represents a promising approach in PAH patients.

2023-06-27 | GSE218398 | GEO

Effects of the Sox17 ∆50 mutation on SOX17 function in mouse embryonic liver development

Project description:To determine the role of specific cis-regulatory elements within the Sox17 endoderm-preferential TSS2 promoter, we generated Sox17∆50 mutant animals and surveyed how this mutation altered Sox17 expression. Livers were isolated from E12.5 Sox17∆50/∆50 and Sox17+/+ embryos (n = 4 of each genotype), RNA isolated, and bulk RNA-Seq performed.

2024-10-31 | E-MTAB-13982 | biostudies-arrayexpress

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