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Unknown,Transcriptomics,Genomics,Proteomics

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RSpondin1 treatment of control and Yap cKO mice

ABSTRACT: RSpondin1 adenovirus was administered to mice and intestine was isolated for expression analysis 1 week later. Yap control and cKO mice were given Rspondin virus and sacrificed 1 week later.

ORGANISM(S): Mus musculus

SUBMITTER: Fernando Camargo

PROVIDER: E-GEOD-41507 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Restriction of intestinal stem cell expansion and the regenerative response by YAP.

Barry Evan R ER Morikawa Teppei T Butler Brian L BL Shrestha Kriti K de la Rosa Rosemarie R Yan Kelley S KS Fuchs Charles S CS Magness Scott T ST Smits Ron R Ogino Shuji S Kuo Calvin J CJ Camargo Fernando D FD

Nature 20121125 7430

A remarkable feature of regenerative processes is their ability to halt proliferation once an organ's structure has been restored. The Wnt signalling pathway is the major driving force for homeostatic self-renewal and regeneration in the mammalian intestine. However, the mechanisms that counterbalance Wnt-driven proliferation are poorly understood. Here we demonstrate in mice and humans that yes-associated protein 1 (YAP; also known as YAP1)--a protein known for its powerful growth-inducing and ...[more]

PMID: 23178811

Similar Datasets

RSpondin1 treatment of control and Yap cKO mice

Project description:RSpondin1 adenovirus was administered to mice and intestine was isolated for expression analysis 1 week later.

2012-11-29 | GSE41507 | GEO

Expression data from YAP-S127D DLD1 Xenografts

Project description:We overexpressed YAP-S127D in DLD1 colorectal cancer cells for 21 days after sub-cutaneous (SubQ) injection into the flanks of nude mice. Mice were given dox for 21 days, sacrificed, and tumors were isolated for RNA extraction and analyzed by Affymetrix microarrays.

2012-11-29 | E-GEOD-41508 | biostudies-arrayexpress

Next Generation Sequencing Identifies Hoxa1 and Hoxc13 as Downstream Targets of Yap in Mouse Epithelial Tissues

Project description:The goals of this study are to identify in vivo downstream targets of Yap through NGS-derived tooth germ transcriptome profiling. The mRNA profiles of wild-type, Yap conditional knockout (CKO) and YAP transgenic (Tg) mouse tooth germs at embryonic day 14.5 were generated by deep sequencing using Illumina Hiseq2000. The sequence reads that passed quality filters were analyzed at the transcript isoform level via DNAnexus. The validation was performed through qRT–PCR and in situ hybrydization. A set of Hox genes were differentially expression in Yap CKO and YAP Tg mouse tooth germs, demonstating concurrent expression changes with Yap transcripts. This study provides a platform to systematically identify in vivo downstream targets of genes of interest. The mRNA profiles of wild type, Yap CKO and YAP Tg mouse tooth germs at embryonic day 14.5 were generated by deep sequencing using Illumina Hiseq.

2015-02-21 | E-GEOD-65524 | biostudies-arrayexpress

Expression data from YAP-S127A Villin-rtTA crypts

Project description:We overexpressed YAP in the intestinal epithelium by adding doxycycline to the drinking water of experimental mice. Mice were given dox for 2 days, and referred to as Tg (transgenic). Mice were given dox for 2 days, sacrificed, and crypts were isolated for RNA extraction and analyzed by Affymetrix microarrays.

2012-11-29 | E-GEOD-41506 | biostudies-arrayexpress

Effect of YAP-S127A overexpression on gene expression profile

Project description:To investigate the mechanism by which YAP regulates methionine metabolism, seven-week-old C57 mice were injected with AAV8-TBG-control or AAV8-TBG-YAP-S127A through tail vein. 8 weeks later, the primary hepatocytes from two groups were isolated for RNA sequence analysis.

2024-05-04 | GSE263889 | GEO

Yap role in intestine

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2012-11-29 | E-GEOD-41509 | biostudies-arrayexpress

Uveitic glaucoma-like features in Yap conditional knockout mice

Project description:Glaucoma is a multifactorial neurodegenerative disease characterized by the progressive and irreversible degeneration of the optic nerve and retinal ganglion cells. Despite medical advances aiming at slowing degeneration down, around 40% of treated glaucomatous patients will undergo vision loss. It is thus of utmost importance to have a better understanding of the disease and to investigate more deeply its early causes. The transcriptional coactivator YAP, an important regulator of eye homeostasis, has recently drawn attention in the glaucoma research field. Here we show that Yap conditional knockout mice (Yap cKO), in which the deletion of Yap is induced in both Müller glia (i.e. the only retinal YAP-expressing cells) and the non-pigmented epithelial cells of the ciliary body, exhibit a breakdown of the aqueous-blood barrier, accompanied by a progressive collapse of the ciliary body. A similar phenotype is observed in human samples that we obtained from patients presenting with uveitis. In addition, aged Yap cKO mice harbor glaucoma-like features, including deregulation of key homeostatic Müller-derived proteins, retinal vascular defects, optic nerve degeneration and retinal ganglion cell death. Finally, transcriptomic analysis of Yap cKO retinas pointed to early-deregulated genes involved in extracellular matrix organization potentially underlying the onset and/or progression of the observed phenotype. Together, our findings reveal the essential role of YAP in preserving the integrity of the ciliary body and retinal ganglion cells, thereby preventing the onset of uveitic glaucoma-like features.

2024-01-01 | GSE251685 | GEO

Next Generation Sequencing Identifies Hoxa1 and Hoxc13 as Downstream Targets of Yap in Mouse Epithelial Tissues

2015-02-21 | GSE65524 | GEO

Discovery of immediate YAP target genes with inducible form of YAP

Project description:Microarray analyses with cells/tissues overexpressing YAP have revealed many transcription targets of YAP (Dong et al, 2007; Zhao et al, 2008). However, as YAP induces transformation of non-cancerous cells, we thought many of known targets of YAP may be indirect consequence of transforming property of YAP. To identify the immediate transcription targets for YAP, we utilized immortalized mammary epithelial MCF-10A cells expressing a tamoxifen inducible, hyperactive (S127/381A) YAP mutant (MCF-10A ERT2-YAP 2SA). MCF-10A ERT2 and MCF-10A ERT2-YAP 2SA are generated. Each cell line was treated with 0.1% of ethanol (solvent) or 1uM of 4-hydroxytamoxifen for 2 or 6 hours. This makes 6 samples per set. The experiments were done in duplicate. The expression data from MCF-10A ERT2 and MCF-10A ERT2-YAP 2SA before tamoxifen treatment can serve as control.

2015-11-23 | E-GEOD-60579 | biostudies-arrayexpress

Genome-wide transcriptional profiling of YAP target genes in human endothelial cells

Project description:Endothelial cell is the major cell type that senses and transduces mechanosignal generated by shear stress. We have recently shown that Hippo/YAP pathway is a mechanosensitive pathway that is critical for maintaining endothelial cell homeostasis. However, the transcritpional targets and biological functions of YAP in endothelial cells remain largely unknown. To evaluate YAP-dependent gene expression in endothelial cells, we performed RNA-sequencing in YAP depleted (by transfection with by YAP siRNA) and overexpressed (by infection with YAP-S127A catalytically active adenovirus) human endothelial cells. We observed that YAP critically regulates endothelial function by modulating multiple atherosclerosis-related genes. Our study provides mechanistic insights into the question how YAP regulates endothelial function and atherosclerosis by modulating endothelial transcriptional profile.

2017-10-03 | GSE87554 | GEO

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