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Myc and YAP roles in the control of the cell cycle [Liver ChIP-seq]

ABSTRACT: ChIPseq analysis was performed on liver of tet-YAP and tet-Myc transgenic mice induced for 2 days (R26-mice)

ORGANISM(S): Mus musculus

PROVIDER: GSE83863 | GEO | 2017/11/22

SECONDARY ACCESSION(S): PRJNA327244

REPOSITORIES: GEO

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Myc and YAP roles in the control of the cell cycle [Liver RNA-seq]

Project description:RNAseq analysis was performed on liver of tet-YAP and tet-Myc transgenic mice induced for 2 days (R26-mice) or 4 weeks (laptTA-mice) or in liver tumor noduli.

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Myc and YAP roles in the control of the cell cycle [3T9 ChIP-seq]

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Myc and YAP roles in the control of the cell cycle [3T9 RNA-seq pharmacological treatment]

Project description:RNAseq analysis of YAP and Myc induced in quiescent and confluent 3T9 fibroblasts treated with Y27632 and Verteporfin

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Myc and YAP roles in the control of the cell cycle

Project description:Myc and YAP roles in the control of the cell cycle

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ChIP-sequencing analysis of Myc binding sites 4 hours after Myc activation in liver and heart tissue, from wild type and R26CAG-c-MycERT2 mice

Project description:Aim: To determine Myc binding sites in mouse heart and liver, 4 hours post MycER activation. c-Myc ChIP sequencing performed on chromatin isolated from hearts and livers harvested from wild-type (R26+/+) and R26CAG-c-MycERT2/+ mice 4 hours post administration of (Z)-4-hydroxytamoxifen.

2020-02-24 | E-MTAB-7592 | biostudies-arrayexpress

Identification of Myc-regulated microRNAs in human P493 cells

Project description:We previously described the use of a spotted oligonucleotide array to identify the mir-17 cluster as a direct transcriptional target of Myc. In order to determine whether Myc regulates additional miRNAs, we produced custom microarrays with an expanded set of probes capable of assaying the expression of 313 human miRNAs and 233 mouse miRNAs. P493-6 cells which are Epstein-Barr virus-immortalized human B cells that harbor a tetracycline (tet)-repressible allele of Myc were studied. These cells are tumorigenic in immunocompromised mice and represent a model of human B cell lymphoma. miRNA expression profiles were examined in the high Myc (-tet) and low Myc (+tet) state. Keywords: Dose response P493 cells with high Myc (-tet) and low Myc (+tet) were compared.

2007-12-05 | E-GEOD-9070 | biostudies-arrayexpress

Myc and YAP roles in the control of the cell cycle [MEF RNA-seq pharmacological treatment]

Project description:Myc and YAP roles in the control of the cell cycle [MEF RNA-seq pharmacological treatment]

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YAP/TAZ initiates gastric tumorigenesis via upregulation of MYC

Project description:YAP/TAZ initiates gastric tumorigenesis via upregulation of MYC

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Pi3kcb links Hippo-YAP and PI3K-AKT signaling pathways to promote cardiomyocyte proliferation and survival [ChIPseq]

Project description:Background—YAP, the nuclear effector of Hippo signaling, regulates cellular growth and survival in multiple organs, including the heart, by interacting with TEAD sequence specific DNA-binding proteins. Recent studies showed that YAP stimulates cardiomyocyte proliferation and survival. However, the direct transcriptional targets through which YAP exerts its effects are poorly defined. Methods and Results—To identify genes directly regulated by YAP in cardiomyocytes, we combined differential gene expression analysis in YAP gain- and loss-of-function with genome-wide identification of YAP bound loci using chromatin immunoprecipitation and high throughput sequencing. This screen identified Pik3cb, encoding p110β, a catalytic subunit of phosphoinositol-3-kinase (PI3K), as a candidate YAP effector that promotes cardiomyocyte proliferation and survival. We validated YAP and TEAD occupancy of a conserved enhancer within the first intron of Pik3cb, and show that this enhancer drives YAP-dependent reporter gene expression. Yap gain- and loss-of-function studies indicated that YAP is necessary and sufficient to activate the PI3K-Akt pathway. Like Yap, Pik3cb gain-of-function stimulated cardiomyocyte proliferation, and Pik3cb knockdown dampened the YAP mitogenic activity. Reciprocally, Yap loss-of-function impaired heart function and reduced cardiomyocyte proliferation and survival, all of which were significantly rescued by AAV-mediated Pik3cb expression. Conclusion—Pik3cb is a crucial direct target of YAP, through which the YAP activates PI3K-AKT pathway and regulates cardiomyocyte proliferation and survival. Yap wild type ChIPseq and input

2015-02-20 | E-GEOD-57717 | biostudies-arrayexpress

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