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Mus musculus

ABSTRACT: A general transcription co-factor, Smad3, potentiates master transcription factor mediated cell identity conversions [ChIP-seq]

PROVIDER: PRJNA336441 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3997990.fastq.gz	Fastqsanger.gz
	SRR3997991.fastq.gz	Fastqsanger.gz
	SRR3997992.fastq.gz	Fastqsanger.gz
	SRR3997993.fastq.gz	Fastqsanger.gz
	SRR3997994.fastq.gz	Fastqsanger.gz

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A general transcription co-factor, Smad3, potentiates master transcription factor mediated cell identity conversions

Project description:A general transcription co-factor, Smad3, potentiates master transcription factor mediated cell identity conversions

| PRJNA336438 | ENA

Mus musculus

Project description:A general transcription co-factor, Smad3, potentiates master transcription factor mediated cell identity conversions [ATAC-seq]

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SMAD2/3 potentiate cell identity conversions with master transcription factors

Project description:The exogenous expression of master transcription factors (TFs) is a powerful and exciting approach to convert cellular identity. Yet, the generation of desired cell types is often plagued by inefficiency, slow kinetics and inability to produce mature cell types. Through investigations of the molecular mechanisms of induced plurpipotent stem cell generation, we discovered that expression of constitutively active Smad2/3 (Smad2CA/3CA), together with the Yamanaka factors, could dramatically improve the efficiency and kinetics of reprogramming. Mechanistically, SMAD3 interacted with both co-activators and reprogramming factors, bridging their interaction during reprogramming. Fascinatingly, SMAD2/3 interact with a multitude of master TFs in different cell types, and conversions of B cells to macrophages, myoblasts to adipocytes, and human fibroblasts to neurons were also markedly enhanced when their master TFs were co-expressed with Smad3CA. These results revealed the existence of shared molecular mechanisms underlying diverse TF-mediated cellular conversions, and demonstrated SMAD2/3 as a widely applicable booster.

2017-11-03 | GSE72596 | GEO

Mus musculus

Project description:SMAD2/3 potentiate cell identity conversions with master transcription factors

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Cell-Type-Specific TGF-beta Signaling is Targeted to Genes that Control Cell Identity: ChIP-Seq

Project description:Smad3 co-occupies DNA binding sites with master transcription factors. Pu.1, MyoD, Oct4, IgG, Smad3, and Smad2/3 ChIP-Seq.

2011-08-24 | E-GEOD-21614 | biostudies-arrayexpress

Cell-Type-Specific TGF-beta Signaling is Targeted to Genes that Control Cell Identity: Gene Expression

Project description:Smad3 co-occupies DNA binding sites with master transcription factors. Treated (Cy5) vs. untreated (Cy3).

2011-08-23 | E-GEOD-21608 | biostudies-arrayexpress

Cell-Type-Specific TGF-beta Signaling is Targeted to Genes that Control Cell Identity: ChIP-Seq

Project description:Smad3 co-occupies DNA binding sites with master transcription factors.

2011-08-24 | GSE21614 | GEO

Cell-Type-Specific TGF-beta Signaling is Targeted to Genes that Control Cell Identity: Gene Expression

Project description:Smad3 co-occupies DNA binding sites with master transcription factors.

2011-08-24 | GSE21608 | GEO

A master cistromic circuit governing hepatic fibrogenesis [ChIP-seq]

Project description:Liver fibrosis is a reversible wound-healing response to liver injury and hepatic stellate cells (HSCs) are central cellular players that mediate hepatic fibrogenesis. However, the molecular mechanisms that govern this process remain unclear. Here, we reveal a novel cistromic circuit in HSCs comprising the vitamin D receptor (VDR) and SMAD transcription factors that restrains the intensity of hepatic fibrogenesis. Ligand-activated VDR suppresses TGFβ1-induced pro-fibrotic gene expression in HSCs. Administration of a vitamin D analogue, calcipotriol, diminishes the fibrotic response in a mouse model of liver fibrosis, while VDR knockout mice spontaneous develop extensive hepatic fibrosis by age 6 months. Using ChIP-Seq, we find that the anti-fibrotic properties of VDR are due to crosstalk with SMAD, mediated by their co-occupancy of DNA-binding sites on pro-fibrotic genes. Specifically, SMAD binding potentiates local chromatin accessibility to enhance VDR recruitment at the same cis-regulatory elements, which reciprocally antagonizes the interaction between SMAD3 and chromatin and limits the assembly of transcriptional activation complexes at fibrotic genes, a process that is enhanced by the presence of VDR agonists. These results not only establish this coordinated VDR/SMAD cistromic circuit as a master regulator of hepatic fibrogenesis, but also support VDR as a potential drug target to ameliorate liver fibrosis. Identification of VDR, SMAD3 and H3 binding sites in human stellate LX2 cells that were pre-treated with calcipotriol (100nM) for 16 hrs (where calcipotriol treatment is indicated) followed by incubation of calcipotriol (100nM) or TGFβ1 (1ng/ml) for another 4 hours (where indicated).

2013-04-29 | E-GEOD-38103 | biostudies-arrayexpress

A general transcription co-factor, Smad3, potentiates master transcription factor mediated cell identity conversions [ChIP-seq]

Project description:We have identified that expression of constitutive active Smad3 (Smad3CA) significantly enhanced reprogramming by Oct4, Sox2, Klf4, c-Myc. Smad3 is known to interact with several master transcription factors and boost their activity during development. Therefore, we hypothesized that Smad3CA is recruited to Oct4 binding sites during reprogramming. To test this hypothesis, we investigated genome-wide Smad3 binding sites in the presence and absence of reprogramming factor expression.

2017-11-03 | GSE85177 | GEO

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