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Mus musculus

ABSTRACT: Reversing SKI–SMAD4-mediated suppression is essential for TH17 cell differentiation [ChIP-seq]

OTHER RELATED OMICS DATASETS IN: PXD007172

PROVIDER: PRJNA394907 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5838320_1.fastq.gz	Fastqsanger.gz
	SRR5838320_2.fastq.gz	Fastqsanger.gz
	SRR5838321_1.fastq.gz	Fastqsanger.gz
	SRR5838321_2.fastq.gz	Fastqsanger.gz
	SRR5838322_1.fastq.gz	Fastqsanger.gz

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Mus musculus

Project description:Reversing SKI–SMAD4-mediated suppression is essential for TH17 cell differentiation

| PRJNA394763 | ENA

Reversing SKI–SMAD4-mediated suppression is essential for TH17 cell differentiation [ChIP-seq]

Project description:Disruption of Ski/Smad4 license Th17 differentiation. TGF-b-Ski-Smad4-RORgt-Th17 axis

2017-10-25 | GSE101593 | GEO

Reversing SKI–SMAD4-mediated suppression is essential for TH17 cell differentiation

Project description:Disruption of Ski/Smad4 license Th17 differentiation. TGF-b-Ski-Smad4-RORgt-Th17 axis

2017-10-25 | GSE101527 | GEO

Genome binding/occupancy profiling of Smad4 in Th17 cells cultured at 37°C and 39.5°C after 24 hours.

Project description:Smad4 was required for febrile temperature enhanced Th17 differentiation. In order to further understand the mechanisms whereby Smad4 enhance Th17 differentiation, we conducted ChIP-seq analysis of Smad4 in Th17 cells cutured 37°C and 39.5°C after 24 hours.

2020-06-26 | GSE125263 | GEO

Elucindating the role of the transcription factor IRF4 in Th17 and Treg cells

Project description:- transcription factor interferon regulatory factor 4 (IRF4) = crucial transcription factor for different immune cells, incl pro-inflammatory Th17 and anti-inflammatory Treg cells - IRF4 is essential for the cell differentiation and fate determination - however molecular mechanisms of IRF4-mediated gene expression in fully differentiated Th17/Treg cells are still not fully understood - integration of data derived from affinity-purification and full mass spectrometry-based proteome analysis with chromatin immune precipitation sequencing (ChIP-Seq) - characterization of proteins generally involved in the T cell development as well as subtype-specific differentiation and identification of novel, yet uncharted IRF4 interactors

2024-08-02 | PXD044298 | JPOST Repository

SKI-dependent TGFb signaling dictates CD103 expression in CD8+ T cells (ChIP-seq)

Project description:Initially identified as a functional marker for resident-memory (Trm) CD8+ T cells, CD103 (encoded by ITGAE gene) has broad roles in immunity and diseases. Elucidating the function and regulation of CD103 is thus of importance. This study revealed that the CD103 expression by CD8 T cells under steady state contributes to the clearance of acute viral infection. More importantly, it discovered TGF-SKI-Smad4 a critical signaling axis in restricting CD103 expression in CD8+ T cells for their function. Mechanistically, by ChIP-Seq and ChIP analysis, SKI associated with Smad4 was found to directly and epigenetically suppress CD103 transcription. This study therefore reveals a novel TGF-SKI-Smad4 pathway to specifically enable CD103 expression in CD8+ T cells for protective immunity.

2020-07-28 | GSE135533 | GEO

Global gene expression profile of wild type and Smad4-deficient Th17 cells cultured at 37°C and 39.5°C

Project description:Febrile temperature enhanced Th17 differentiation in Smad4 SUMOylation-dependent manner. Smad4-deficiency impaired the febrile temperature-enhanced Th17 differentiation. In order to understand how febrile temperature and Smad4 contribute to Th17 pathogenicity, we conducted transcriptional analysis of wild type and Smad4-deficient Th17 cells cultured at 37°C and 39.5°C (Day 3).

2020-03-01 | GSE125264 | GEO

Transcription profiling timecourse of induced DACH1 expression in a human breast cancer cell line

Project description:The vertebrate homologues of Drosophila dachsund, DACH1 and DACH2, have been implicated as important regulatory genes in development. DACH1 plays a role in retinal and pituitary precursor cell proliferation and DACH2 plays a specific role in myogenesis. DACH proteins contain a domain (DS-domain) that is conserved with the proto-oncogenes Ski and Sno. Since the Ski/Sno proto-oncogenes repress AP-1 and SMAD signaling, we hypothesized that DACH1 might play a similar cellular function. Herein, DACH1 was found to be expressed in breast cancer cell lines and to inhibit TGF-beta induced apoptosis. DACH1 repressed TGF-beta induction of AP-1 and Smad signaling in gene reporter assays and repressed endogenous TGF-beta responsive genes by microarray analyses. DACH1 bound to endogenous NCoR and Smad4 in cultured cells and DACH1 co-localized with NCoR in nuclear dot-like structures. NCoR enhanced DACH1 repression and the repression of TGF-beta-induced AP-1 or Smad-signaling by DACH1 required the DACH1 DS domain. The DS-domain of DACH was sufficient for NCoR-binding at a Smad4-binding site. Smad4 was required for DACH1 repression of Smad signaling. In Smad4 null HTB-134 cells, DACH1 inhibited the activation of SBE-4 reporter activity induced by Smad2 or Smad3 only in the presence of Smad4. DACH1 participates in the negative regulation of TGF-beta signaling by interacting with NCoR and Smad4.

2007-07-19 | E-GEOD-685 | biostudies-arrayexpress

Cistrome analysis of SKI and RUNX1 in HL60

Project description:SKI is a transcriptional co-regulator and overexpressed in various human tumors, for example in acute myeloid leukemia (AML). SKI contributes to the origin and maintenance of the leukemic phenotype. Here we use ChIP-seq and RNA-seq to identify the epigenetic alterations induced by SKI overexpression in AML cells. We show that approximately two thirds of differentially expressed genes are up-regulated upon SKI deletion, of which nearly 50% harbour SKI binding sites in their proximity, primarily in enhancer regions. Gene ontology analysis reveals that many of the differentially expressed genes are annotated to hematopoietic cell differentiation and inflammatory response, corroborating our finding that SKI deletion causes a release of the myeloid differentiation block in HL60 cells. We find that SKI peaks are enriched for RUNX1 consensus motifs, particularly in up-regulated SKI targets. RUNX1 ChIP-seq demonstrates that nearly 70% of RUNX1 binding sites overlap with SKI peaks, mainly at enhancer regions. SKI and RUNX1 co-occupy the same genomic sites and cooperate in gene silencing. Our work demonstrates for the first time on a genome-wide scale the predominant co-repressive function of SKI in AML cells and uncovers the transcription factor RUNX1 as an important mediator of SKI-dependent transcriptional repression.

2018-02-07 | GSE107553 | GEO

DACH1 inhibits TGF-beta signaling through binding Smad4

2003-10-15 | GSE685 | GEO