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

ABSTRACT: We have identified that expression of constitutive active Smad3 (Smad3CA) significantly enhanced reprogramming by Oct4, Sox2, Klf4, c-Myc. To investigate how Smad3CA expression impacts on chromatin opening, we performed ATAC-seq on day 3 of reprogramming in the presence or absence of Smad3CA expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE85175 | GEO | 2017/11/03

SECONDARY ACCESSION(S): PRJNA336447

REPOSITORIES: GEO

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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

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

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

2017-11-02 | GSE85178 | GEO

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

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

ChIPseq Smad3-JMJD3

Project description:ChIPseq Smad3-JMJD3

| PRJEB2739 | ENA

ChIPseq Smad3-JMJD3

Project description:ChIP seq of endogenous Smad3 and JMJD3 proteins in mouse embryonic neural stem cells treated with TGFbeta during 30 minutes. Neural stem cells were treated with TGFbeta during 30 minutes, and then chromatin immunoprecipitation was carried out with specific JMJD3 or Smad3 antibodies. Positive and negative controls for each immunoprecipitation were checked before sequencing. Input was used to normalized the sequencing results.

2011-12-30 | E-MTAB-825 | biostudies-arrayexpress

Endothelial OTUD1 promotes Ang II-induced vascular remodeling by deubiquitinating SMAD3

Project description:Understanding the molecular mechanisms of pathological vascular remodeling is important for treating cardiovascular diseases and complications. Recent studies have highlighted a role of deubiquitinases in vascular pathophysiology. In this study, we investigated the role of a deubiquitinase, OTUD1, in angiotensin II (Ang II)-induced vascular remodeling. We identified upregulated OTUD1 in the vascular endothelium of Ang II-challenged mice and showed OTUD1 deletion attenuated vascular remodeling, collagen deposition, and EndMT. Conversely, OTUD1 overexpression aggravated these pathological changes both in vivo and in vitro. Mechanistically, SMAD3 was identified as a substrate of OTUD1 using co-immunoprecipitation followed with LC-MS/MS. We found OTUD1 stabilizes SMAD3 and facilitates SMAD3/SMAD4 complex formation and subsequent nuclear translocation through both K48- and K63-linked deubiquitination. OTUD1-mediated SMAD3 activation regulate the transcription of genes involved in vascular EndMT and remodeling in HUVECs. Finally, SMAD3 inhibition reversed OTUD1-promoted vascular remodeling. Our findings demonstrate endothelial OTUD1 promoted Ang II-induced vascular remodeling by deubiquitinating SMAD3. This study identified SMAD3 as a target of OTUD1 and indicates OTUD1 as a potential therapeutic target for the diseases related to vascular remodeling.

2022-12-24 | PXD037926 | Pride

Smad3 regulates the miR-200 family in gastric cancer

Project description:To find potential microRNA links between Smad3 and E-cadherin, we characterized the microRNA profiles of two gastric cancer cell lines: SNU484-LPCX, which does not express Smad3, and SNU484-Smad3, in which Smad3 is overexpressed. We found that miR-200 families, among other differentially expressed miRNAs, are overexpressed in SNU484-Smad3. Through subsequent studies, including silencing of Smad3 in SNU484-Smad3 and expression profiling of epithelial-mesenchymal markers and ZEB1/2, known repressors of E-cadherin, we found that Smad3 regulates miR-200 families at the transcriptional level, which regulate ZEB 1/2, known transcriptional repressors of E-cadherin, at the post-transcriptional level. This represents an important link between the TGF-beta signaling pathway and post-transcriptional regulation by miRNAs. Examination of small RNA expression in 2 different cell lines (SNU484-LPCX, SNU484-Smad3).

2011-09-14 | E-GEOD-27977 | biostudies-arrayexpress

Gene expression profiling of six MEF cell genotypes (wild type, β2SP+/-, β2SP-/-, SMAD3+/-, SMAD3-/-, and β2SP+/-; SMAD3+/-)

Project description:Gene expression profiling was carried out in six (wild type, β2SP+/-, β2SP-/-, SMAD3+/-, SMAD3-/- and β2SP+/-/ SMAD3+/-) different mouse knockout embryonic fibroblast (MEF) cells. Beta-2-spectrin (β2SP) is a dynamic intracellular non-pleckstrin homology (PH)-domain protein that belongs to a family of polypeptides that have been implicated in conferring cell polarity. Spectrins have been linked to multiple signaling pathways, including cell cycle regulation, DNA repair and TGFβ signaling. In this study, we report a major role of the TGFβ/Smad3 adaptor β2-Spectrin in conserving genomic integrity from alcohol-induced DNA damage and describe a novel pathway that protects genomes from genotoxic stresses. To determine the mechanism for the oncogenic switch, and whether it is related to the role of β2SP in TGF-β signaling transduction or secondary to its cytoskeletal functions, we analyzed disruption of two elements of the TGF-β pathway by generating double heterozygous Sptbn1+/−/Smad3+/− mice.

2016-04-30 | GSE69750 | GEO

Genes regulated by SMAD3 in HCC cells

Project description:To identify genes regulated by SMAD3, we have employed whole transcriptome microarray expression profiling to identify genes downstream of SMAD3. Total RNAs from SMAD3-overexpression (7721-SMAD3 vs 7721-VEC) or SMAD3-knockdown (LM3-shSMAD3 vs LM3-CON) cell lines were measured.

2022-06-10 | GSE132518 | GEO

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