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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Hepatocyte-specific knockout of Pten and of Pten and Tgfbr2 in mice

ABSTRACT: Gene expression of hepatocyt-specific knockout of Pten and of Pten and Tgfbr2 in mice as a model for human cholangiocarcinoma was determined Affymetrix Mouse 1.0ST chips were used to measure gene expression Gene expression of the following mouse livers were characterized A. WT (n=3). B. Pten-/- (n=4). C. Pten-/- Tgfbr2-/- (n=4).

ORGANISM(S): Mus musculus

SUBMITTER: Robert Schwabe

PROVIDER: E-GEOD-66717 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Epithelial Transforming Growth Factor-β Signaling Does Not Contribute to Liver Fibrosis but Protects Mice From Cholangiocarcinoma.

Mu Xueru X Pradere Jean-Philippe JP Affò Silvia S Dapito Dianne H DH Friedman Richard R Lefkovitch Jay H JH Schwabe Robert F RF

Gastroenterology 20151126 3

<h4>Background & aims</h4>Transforming growth factor-β (TGFβ) exerts key functions in fibrogenic cells, promoting fibrosis development in the liver and other organs. In contrast, the functions of TGFβ in liver epithelial cells are not well understood, despite their high level of responsiveness to TGFβ. We sought to determine the contribution of epithelial TGFβ signaling to hepatic fibrogenesis and carcinogenesis.<h4>Methods</h4>TGFβ signaling in liver epithelial cells was inhibited by albumin-Cr ...[more]

PMID: 26627606

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Sustained axon regeneration induced by a synergy of PTEN and SOCS3 deletion

Project description:A formidable challenge in neural repair in the adult central nervous system (CNS) is the long distances that regenerating axons often need to travel in order to reconnect with their targets. Thus, a sustained capacity for axon regeneration is critical for achieving functional restoration. Although deletion of either Phosphatase and tensin homolog (PTEN), a negative regulator of mammalian target of rapamycin (mTOR), or suppressor of cytokine signaling 3 (SOCS3), a negative regulator of Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, in adult retinal ganglion cells (RGCs) individually promoted significant optic nerve regeneration, such regrowth tapered off around two weeks after the crush injury. Remarkably, we now find that simultaneous deletion of both PTEN and SOCS3 enable robust and sustained axon regeneration. We further show that PTEN and SOCS3 regulate two independent pathways that act synergistically to promote enhanced axon regeneration. Gene expression analyses suggest that double deletion not only result in the induction of many growth-related genes, but also allow RGCs to maintain the expression of a repertoire of genes at the physiological level after injury. Our results reveal concurrent activation of mTOR and STAT3 pathways as a key for sustaining long-distance axon regeneration in adult CNS, a crucial step toward functional recovery. RNAs were extracted from FACS sorted YFP positive mouse retinal cells, and gene-profiled using affymetrix 1.0 ST expression arrays. Three hybridizations were performed for each group (Wild type after crush, PTEN Knockout+crush, SOCS3 Knockout+crush, and PTEN/SOCS3 double knockout+crush) with RNA samples collected from three independent FACS purifications. Data were analyzed using dChIP and SAM.

2011-10-27 | E-GEOD-32309 | biostudies-arrayexpress

Expression data from isogenic Pten WT or KO mouse T-ALLs treated with DBZ or DMSO

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GATA4

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

2013-11-07 | E-GEOD-49132 | biostudies-arrayexpress

Subtle variations in Pten dose determine cancer susceptibility: Gene expression profiling of a Ptenhy/+ mouse model

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2010-02-21 | E-GEOD-20316 | biostudies-arrayexpress

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