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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. 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.

ORGANISM(S): Mus musculus

SUBMITTER: Combiz Khozoie

PROVIDER: E-GEOD-32498 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2012-04-12 | GSE32498 | GEO

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

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Human epidermal keratinocytes treated with retinoic acid or thyroid hormone

Project description:Targets of Retinoic Acid (RA) were identified in primary human epidermal keratinocytes grown in the presence or absence of all-trans retinoic acid for 1, 4, 24, 48 and 72 hours. Targets of Thyroid Hormone (T3) were identified in primary human epidermal keratinocytes grown in the presence or absence of the hormone; same controls as for RA. Time course, 1, 4, 24, 48 and 72 hours

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Expression profiling of pancreatic beta-cells harboring a pancreatic-specific deletion of PPAR-beta

Project description:Peroxisome proliferator-activated receptor beta/delta protects against obesity by reducing dyslipidemia and insulin resistance via effects in various organs, including muscle, adipose tissue, liver, and heart. However, nothing is known about the function of PPAR-beta in pancreas, a prime organ in the control of glucose metabolism. To gain insight into so far hypothetical functions of this PPAR isotype in insulin production, we specifically ablated Ppar-beta in pancreas. The mutated mice developed a chronic hyperinsulinemia, due to an increase in both beta-cell mass and insulin secretion. Gene expression profiling indicated a broad repressive function of PPAR-beta impacting the vesicular compartment, actin cytoskeleton, and metabolism of glucose and fatty acids. Analyses of insulin release from the islets revealed an increased second-phase glucose-stimulated insulin secretion. Higher levels of PKD, PKC-delta and diacyglycerol in mutated animals lead to an enhanced formation of trans-Golgi network (TGN)-to-plasma-membrane transport carriers in concert with F-actin disassembly, which resulted in increased insulin secretion and its associated systemic effects. Taken together, these results provide evidence for PPAR-beta playing a repressive role on beta-cell growth and insulin exocytosis, which shed new light on its anti-obesity action. Pancreas-specific knock-out animals were generated by breeding mice harbouring a floxed Ppar-beta (PPARbetafl/fl) to mice expressing the Cre transgene under the control of the Pdx1 promoter (Pdx1Cre). Islets from 3 different animals from the knock-out group Pdx1Cre;PPARbetafl/fl and the control littermates group PPARbetafl/fl were compared.

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Expression profiling of pancreatic beta-cells harboring a pancreatic-specific deletion of PPAR-beta

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TRANSCRIPTIONAL EFFECTS OF INHIBITING EGFR IN KERATINOCYTES

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2012-10-19 | E-GEOD-41680 | biostudies-arrayexpress

Expression profile of proliferating and differentiating primary human keratinocytes in vitro

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2010-08-01 | E-GEOD-21413 | biostudies-arrayexpress

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2014-05-06 | E-GEOD-57314 | biostudies-arrayexpress

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