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Gene expression of wild-type and Ppar-beta null primary keratinocytes, with and without infection with an activated Hras retrovirus, with and without the Ppar-beta specific ligand GW0742

ABSTRACT: Differential gene expression profiles were observed in response to Hras in either wild-type or Ppar-beta null primary keratinocytes and differentail gene edxpression profiles by GW0742 were only found in wild-type keratinocytes.

ORGANISM(S): Mus musculus

PROVIDER: GSE32498 | GEO | 2012/04/12

SECONDARY ACCESSION(S): PRJNA147771

REPOSITORIES: GEO

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Gene expression of wild-type and Ppar-beta null primary keratinocytes, with and without infection with an activated Hras retrovirus, with and without the Ppar-beta specific ligand GW0742

Project description:Differential gene expression profiles were observed in response to Hras in either wild-type or Ppar-beta null primary keratinocytes and differentail gene edxpression profiles by GW0742 were only found in wild-type keratinocytes. Primary keratinocytes from wild-type and Ppar-beta null mice were either mock infected or infected with an Hras encoding retrovirus and treated with or without 1 uM GW0742 for 24 hours.

2012-04-11 | E-GEOD-32498 | biostudies-arrayexpress

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MicroRNA-203 represses selection and expansion of oncogenic HRas transformed tumor initiating cells [seq]

Project description:In many mouse models of skin cancer, only a few tumors typically form although many cells competent for tumorigenesis receive the same oncogenic mutations. These observations suggest a selection process for defining tumor initiating cells. Here we use quantitative mRNA- and miR-Seq to determine the impact of HRasG12V on the transcriptome of keratinocytes. We discover that microRNA-203 is downregulated by HRasG12V. Using a knockout mouse model, we demonstrate that loss of microRNA-203 promotes selection and expansion of tumor-initiating cells. Conversely, restoration of microRNA-203 with an inducible model potently inhibits proliferation of these cells. We comprehensively identify microRNA-203 targets required for HRas-initiated tumorigenesis. These targets include important effectors of the Ras pathway and essential genes required for cell division. Together, this study establishes a role for the loss of microRNA-203 in promoting selection and expansion of HRas mutated cells and identifies a mechanism through which microRNA-203 antagonizes HRas-mediated tumorigenesis. Identifying mRNA and microRNA networks regulated by oncogenic HRasG12V in primary keratinocytes through the use of 3Seq and small-RNA-Sequencing. Additionally we utilize ribosome-profiling, 3Seq, Microarray and Ago2-HITS-CLIP approaches to identify novel miR-203 target genes.

2015-07-23 | E-GEOD-66054 | biostudies-arrayexpress

MicroRNA-203 represses selection and expansion of oncogenic HRas transformed tumor initiating cells [array]

2015-07-23 | E-GEOD-66055 | biostudies-arrayexpress

Normal mouse skin lacking Hras

2015-03-01 | GSE60769 | GEO

Normal mouse skin lacking Hras

Project description:Oncogenic activating mutations in Ras genes are among the most common drivers of human disease. Treating mouse skin with the chemical carcinogen DMBA induces a characteristic mutation in Hras at codon 61. To understand how skin responds to a constitutive lack of Hras, we generated a cohort of Hras knockout mice. A backcross was generated using male Mus spretus and female FVB/N Hras-/- mice; female F1 hybrids were mated with male FVB/N Hras -/- or Hras -/+ mice to generate a backcross population. This series contains mice that were Hras -/-. Mice were aged to 8 weeks and a tail skin sample was snap frozen.

2015-03-01 | E-GEOD-60769 | biostudies-arrayexpress

MicroRNA-203 represses selection and expansion of oncogenic HRas transformed tumor initiating cells [array]

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MicroRNA-203 represses selection and expansion of oncogenic HRas transformed tumor initiating cells [seq]

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Functional robustness of spermatogonial stem cells after induction of hyperactive Hras

Project description:We report on gene expression in stem cell-enriched, undifferentiated spermatogonia isolated from the adult mouse testis, in which one group are wild type and the other group contain a heterozygous Hras G12V mutation.

2019-04-18 | GSE129493 | GEO

An integrated global analysis of compartmentalized HRAS signaling - Phosphoproteomics

Project description:Modern omics technologies allow us obtaining global information on different types of biological networks. However, integrating these different types of analyzes into a coherent framework for a comprehensive biological interpretation remains challenging. Here, we present a conceptual framework that integrates protein interaction, phosphoproteomics and transcriptomics data. Applying this method to analyze HRAS signaling from different subcellular compartments shows that spatially-defined networks contribute specific functions to HRAS signaling. Changes in HRAS protein interactions at different sites lead to different kinase activation patterns that differentially regulate gene transcription. HRAS mediated signaling is the strongest from the plasma membrane, but it regulates the largest number of genes from the endoplasmic reticulum. The integrated networks provide a topologically and functionally resolved view of HRAS signaling. They reveal new HRAS functions including the control of cell migration from the endoplasmic reticulum and p53 dependent cell survival when signaling from the Golgi apparatus.

2019-03-08 | PXD012506 | Pride

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