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Fine-tuning Mybl2 levels are required for proper MET process during somatic reprogramming [RNA-seq]

ABSTRACT: Fine-tuning Mybl2 levels are required for proper MET process during somatic reprogramming [RNA-seq]

PROVIDER: PRJNA420798 | ENA |

REPOSITORIES: ENA

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Fine-tuning Mybl2 levels are required for proper MET process during somatic reprogramming

Project description:Fine-tuning Mybl2 levels are required for proper MET process during somatic reprogramming

| PRJNA420731 | ENA

Fine-tuning Mybl2 levels are required for proper MET process during somatic reprogramming [ChIP-Seq]

Project description:Fine-tuning Mybl2 levels are required for proper MET process during somatic reprogramming [ChIP-Seq]

| PRJNA432408 | ENA

Fine-tuning Mybl2 levels are required for proper MET process during somatic reprogramming [ATAC-Seq]

Project description:Fine-tuning Mybl2 levels are required for proper MET process during somatic reprogramming [ATAC-Seq]

| PRJNA420796 | ENA

Fine-tuning Mybl2 levels are required for proper MET process during somatic reprogramming [ChIP-Seq]

Project description:Genome wide data investigating the role of Mybl2 in reprogramming

2020-11-29 | GSE109952 | GEO

Fine-tuning Mybl2 levels are required for proper MET process during somatic reprogramming [RNA-seq]

Project description:Genome wide data investigating the role of Mybl2 in reprogramming

2018-07-17 | GSE107578 | GEO

Fine-tuning Mybl2 levels are required for proper MET process during somatic reprogramming [ATAC-Seq]

Project description:Genome wide data investigating the role of Mybl2 in reprogramming

2018-07-17 | GSE107577 | GEO

Fine-tuning Mybl2 levels are required for proper MET process during somatic reprogramming

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

2018-07-17 | GSE107579 | GEO

Fine-Tuning Mybl2 Is Required for Proper Mesenchymal-to-Epithelial Transition during Somatic Reprogramming.

Project description:During somatic reprogramming, Yamanaka's pioneer factors regulate a complex sequence of molecular events leading to the activation of a network of pluripotency factors, ultimately resulting in the acquisition and maintenance of a pluripotent state. Here, we show that, contrary to the pluripotency factors studied so far, overexpression of Mybl2 inhibits somatic reprogramming. Our results demonstrate that Mybl2 levels are crucial to the dynamics of the reprogramming process. Mybl2 overexpression changes chromatin conformation, affecting the accessibility of pioneer factors to the chromatin and promoting accessibility for early immediate response genes known to be reprogramming blockers. These changes in the chromatin landscape ultimately lead to a deregulation of key genes that are important for the mesenchymal-to-epithelial transition. This work defines Mybl2 level as a gatekeeper for the initiation of reprogramming, providing further insights into the tight regulation and required coordination of molecular events that are necessary for changes in cell fate identity during the reprogramming process.

| S-EPMC6092268 | biostudies-literature

Global binding profiles of MYBL2 and FOXM1 in lung adenocarcinoma reveal that MYBL2 regulates FOXM1 to control cell-cycle genes including CENPA [ChIP-seq]

Project description:MYBL2 is a transcription factor that has either pro-survival or anti-survival functions in a cell-type specific manner. Overexpression of MYBL2 is associated with worse survival of lung adenocarcinoma, but the mechanism by which it regulates transcription has not yet been elucidated. In this study, we found that MYBL2 mainly binds to the promoters of highly expressed genes in lung adenocarcinoma cells using ChIP-seq. Using knock-down and RNA-seq approach, we identified over a thousand of genes deregulated by MYBL2. By integrating ChIP-seq and RNA-seq data, we identified target genes of MYBL2. We revealed that FOXM1 is regulated by MYBL2 in lung adenocarcinoma cells, and FOXM1 binding sites are largely shared with MYBL2 binding sites. We treated lung adenocarcinoma cells with FDI-6, a known FOXM1 inhibitor and investigated the effect of FDI-6 in transcriptional regulation of MYBL2 and FOXM1. We found that CENPA is one of the key genes regulated by MYBL2 and FOXM1, and that it can be inhibited by FDI-6. Our signaling pathway analysis results revealed that MYBL2 and FOXM1 activate cell-cycle genes, suggesting that MYBL2 and FOXM1 act as oncogenic transcription factors in lung adenocarcinoma cells and FDI-6 could be a potential treatment of the disease.

2022-11-02 | GSE201271 | GEO

Global binding profiles of MYBL2 and FOXM1 in lung adenocarcinoma reveal that MYBL2 regulates FOXM1 to control cell-cycle genes including CENPA [RNA-seq]

2022-11-02 | GSE201270 | GEO

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