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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.

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Smad2/3-mediated TGFβ signaling modulates neural crest developmental plasticity

Project description:The neural crest is a highly plastic stem cell population that represents a notable exception to the germ layer theory. Despite being of ectodermal origin, these cells can differentiate into skeletal derivatives like cartilage and bone, tissues that are typically formed by mesoderm. The inductive program that endows the neural crest with these unique properties is still poorly understood. Here, we report that Smad2/3-mediated TGFβ signaling endows cranial neural crest cells with enhanced developmental potential. Our results show that TGFβ signaling modulates neural crest axial identity and directly activates the gene circuits that support skeletal differentiation. Cooperation between TGFβ and low levels of WNT-signaling in the embryonic head activates cranial-specific cis-regulatory elements of anterior genes. Activation of the TGFβ pathway allowed reprogramming of trunk neural crest cells to adopt an anterior identity and led to the development of an improved protocol for the generation of human cranial neural crest cells. Our findings indicate TGFβ signaling is required for the specification of cranial neural crest cells, endowing them with the potential to give rise to the craniofacial skeleton.

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Smad2/3-mediated TGFβ signaling modulates neural crest developmental plasticity [RNA-seq]

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Smad2/3-mediated TGFβ signaling modulates neural crest developmental plasticity [ATAC-seq]

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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.

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