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E-GEOD-53225

ABSTRACT: Expression data from miR-92 over-expressing R26MER/MER mouse embryonic fibroblast (MEFs)

OTHER RELATED OMICS DATASETS IN: PRJNA231168

PROVIDER: E-GEOD-53225 | ExpressionAtlas | 2015-07-31

REPOSITORIES: ExpressionAtlas

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Dataset's files

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			Action	DRS
	E-GEOD-53225-analysis-methods.tsv	Tabular
	E-GEOD-53225-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-53225-configuration.xml	Xml
	E-GEOD-53225-percentile-ranks.tsv	Tabular
	E-GEOD-53225.condensed-sdrf.tsv	Tabular

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Project description:Expression data from miR-92 over-expressing R26MER/MER mouse embryonic fibroblast (MEFs)

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Expression data from miR-92 over-expressing R26MER/MER mouse embryonic fibroblast (MEFs)

Project description:miR-92 enhances c-Myc induced apoptosis. In the R26MER/MER mouse embryonic fibroblasts (MEFs), a switchable variant of Myc, MycERT2, was knocked into the genomic region downstream of the constitutive Rosa26 promoter, allowing acute activation of c-Myc by 4-OHT-induced nuclear translocation. This in vitro system nicely recapitulates c-Myc-induced apoptosis, as activated MycERT2 induces strong p53-dependent apoptosis in response to serum starvation. Enforced miR-92 expression in three independent R26MER/MER MEF lines significantly enhanced Myc-induced apoptosis. We used microarrays to investigate the molecular mechanism underlying miR-92 functions. Three independent R26MER/MER MEF lines were infected by MSCV vector alone or by MSCV vector encoding miR-92. These MEFs were serum starved and 4-OHT treated to trigger strong Myc-induced apoptosis.

2013-12-11 | E-GEOD-53225 | biostudies-arrayexpress

Expression data from miR-92 over-expressing R26MER/MER mouse embryonic fibroblast (MEFs)

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miR-17-92/106b regulate beta cell mitotic checkpoint and insulin secretion

Project description:Adult beta cells in the pancreas are the sole source of insulin in our body. Beta cell loss or increased demand for insulin, impose metabolic challenges because adult beta cells are generally quiescent and infrequently re-enter the cell division cycle. miR-17-92/106b is a family of proto-oncogene microRNAs, that regulate proliferation in normal tissues and in cancer. Here, we employ mouse genetics to demonstrate a critical role for miR-17-92/106b in glucose homeostasis and in controlling insulin secretion. Mass spectrometry analysis was performed on miR-17-92LoxP/LoxP;106-25-/- MEF lysate, without or with CRE-Adenovirus. miR-17-92LoxP/LoxP;106-25+/+ MEFs with GFP-Adenovirus served as controls. We demonstrate that miR-17-92/106b regulate the adult beta cell mitotic checkpoint and that miR-17-92/106b deficiency results in reduction in beta cell mass in-vivo. Furthermore, protein kinase A (PKA) is a new relevant molecular pathway downstream of miR-17-92/106b in control of adult beta cell division and glucose homeostasis. Therefore, contributes to the understanding of proto-oncogene miRNAs in the normal, untransformed endocrine pancreas, and illustrates new genetic means for regulation of beta cell mitosis and function by non-coding RNAs.

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49a825c3-18bb-44ea-a4bc-f1afcc86c4ad - samples

Project description:Organoid cultures derived from colorectal adenomas were transduced with a miR-17-92 expressing vector. RNA from miR17-92-overexpressing organoids and respective non-transduced organoids (controls) was isolated for expression analysis.

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Project description:miR-17-92 mediates the MYC oncogene addiction in a conditional mouse lymphoma model. To identify targets of miR-17-92 in this model, miR-17-92 was expressed in the conditional lymphoma cell lines using MSCV-puro. Both control and miR-17-92-expressing conditional lymphoma cell lines were treated with doxycycline (DOX) (20ng/ml) for 48 hours to shut off MYC expression.

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