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SMAD2/3 are redirected to novel sites in MCF10A MII after prolonged TGFβ stimulation

ABSTRACT: SMAD2/3 are redirected to novel sites in MCF10A MII after prolonged TGFβ stimulation

PROVIDER: PRJNA326978 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3723530.fastq.gz	Fastqsanger.gz
	SRR3723540_1.fastq.gz	Fastqsanger.gz
	SRR3723540_2.fastq.gz	Fastqsanger.gz
	SRR3723531.fastq.gz	Fastqsanger.gz
	SRR3723541_1.fastq.gz	Fastqsanger.gz

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JUNB is a critical AP1 component for SMAD2/3 binding after TGFβ stimulation [RNA-seq]

Project description:We performed SMAD2/3 ChIP-seq analysis in MCF10A MII cells. To validate whether the changes in SMAD2/3 binding to the genome indeed resulted in changes in target gene expression, we performed RNA-seq transcriptome analysis after short and long periods of TGFβ stimulation (0, 1.5h and 16h) in MII cells. In addition, we revealed that JUNB is a critical AP1 component for SMAD2/3 binding after TGFβ stimulation. To assess the significance of JUNB for TGFβ-SMAD-target genes on a genome-wide scale, we also performed RNA-seq transcriptome analysis in JUNB-knock-downed MII cells.

2017-11-15 | GSE83786 | GEO

SMAD2/3 binding pattern in a breast epithelial cell line, MCF10A MII [ChIP-seq]

Project description:We report that SMAD2/3 are redirected to novel binding sites on the genome after prolonged TGFβ stimulation.

2017-11-15 | GSE83787 | GEO

SMAD2/3 are redirected to novel sites in MCF10A MII after prolonged TGFβ stimulation

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

2017-11-15 | GSE83788 | GEO

Fibroblast-specific genetic dissection of TGFβ-Smad2/3 signaling in cardiac fibrosis

Project description:Overall goal: To elucidate fibroblast-specific role of TGFβ-Smad2/3 signaling in fibroblast activation and their differentiation to myofibroblasts. Purpose of analysis: To generate transcriptional profile of Smad2/3 and TGFβreceptors1/2-deficient fibroblasts in the context of pathological cardiac fibrosis.

2017-10-25 | GSE101772 | GEO

SNON and Arkadia (RNF111) regulate TGFβ-SMAD2/3 dose-dependent responses

Project description:SNON and Arkadia (RNF111) regulate TGFβ-SMAD2/3 dose-dependent responses

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Smad2 and Smad3 have differential sensitivity in relaying TGF b signaling and inversely regulate early lineage specification

Project description:The transforming growth factor beta (TGFβ) related signaling is one of the most important signaling pathways regulating early developmental events. Smad2 and Smad3 are structurally similar and it is mostly considered that they are equally important in mediating TGFβ signals. Here, we show that Smad3 is an insensitive TGFβ transducer as compared with Smad2. Smad3 preferentially localizes within the nucleus and is thus sequestered from membrane signaling. The ability of Smad3 in oligomerization with Smad4 upon agonist stimulation is also impaired given its unique linker region. Smad2 mediated TGFβ signaling plays a crucial role in epiblast development and patterning of three germ layers. However, signaling unrelated nuclear localized Smad3 is dispensable for TGFβ signaling-mediated epiblast specification, but important for early neural development, an event blocked by TGFβ/Smad2 signaling. Both Smad2 and Smad3 bind to the conserved Smads binding element (SBE), but they show nonoverlapped target gene binding specificity. We conclude that Smad2 and Smad3 possess differential sensitivities in relaying TGFβ signaling and have distinct roles in regulating early developmental events.

2016-03-01 | GSE76557 | GEO

Genome-wide maps of SMAD2-chromatin binding state in TGFbeta-treated vascular smooth muscle cells

Project description:To further explore the role of these two factors in SMC reprogramming, we treated human aortic smooth muscle (HASMCs) in vitro with TGFβ and mapped binding of Smad2/3, which reflects TGFβ activity, and Pol2-Ser2p, which reflects transcriptional activity, by ChIP-seq analysis. Smad2/3 bound to numerous regulatory regions in the genome differentially regulating expression of numerous genes as demonstrate by alterations in Pol2-Serp2 binding profile and analysis of bulk RNA sequencing. Examination of the top 20 transcription factors identified by sequencing of Smad2/3 binding regulatory regions identified KLF4 gene as one of the most prominently regulated genes. Further analysis showed Smad2/3 binding to multiple KLF4 gene regulatory elements that increased following TGFβ treatment, indicating that KLF4 is a direct target of Smad2/3. At the same time, the amount of bound Pol2-Ser2p decreased, pointing to reduced transcriptional activity. In contrast, Smad2/3 did not bind to KLF2 or KLF5 regulatory elements, demonstrating that these genes are not directly regulated by TGFβ.

2018-03-27 | GSE112326 | GEO

SMAD2/3 chromatin immunoprecipitation sequencing (ChIP-seq) in human naïve and primed human pluripotent stem cells

Project description:The aim of this experiment was to investigate the role of TGFβ signalling pathway in human pluripotency, through ChIP-seq analysis of its main downstream effector SMAD2/3 in naïve and primed human pluripotent stem cells (hPSCs).

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Transforming growth factor β (TGFβ) and BMP7 regulate glioblastoma stem cells differentiation status

Project description:Glioblastoma stem cells (GSCs) fate is controlled by environmental cues, among which cytokines play a crucial role. The transforming growth factor β (TGFβ) family signaling pathways controls GSCs. On one hand, TGFβ promotes cell proliferation in GBM, it induces the expression of platelet-derived growth factor-B (PDGFB). Moreover, TGFβ, via its signaling mediators Smad2/3, induces the expression of the cytokine leukemia inhibitory factor (LIF) and Sox4, which in turn enhances the expression of the stem cell transcription factor Sox2; this increases the self-renewal capacity of the GSCs and their stemness characteristics, and enhances the GSC tumor-initiating potential. On the other hand, Bone morphogenic proteins (BMPs) are known to promote GSC differentiation towards the astrocytic phenotype. To further understand which genes are regulated by TGFβ and BMP7 in GSCs we performed a microarray in the Affymetrix HTA2 platform in three different glioblastoma cell line, U2987, and two patient-derived glioblastoma stem cells, U3031MG and U3034MG, in the presence or absence of 5 ng/ml of TGFβ or 30 ng/ml BMP7 for 24 h, three biological replicates per condition.

2020-09-01 | E-MTAB-9076 | biostudies-arrayexpress

DNMT3b mediates TGFβ-Smad2/3 action to maintain Epiblast homeostasis upon Smad4 Loss

Project description:DNMT3b mediates TGFβ-Smad2/3 action to maintain Epiblast homeostasis upon Smad4 Loss

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