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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Conversion of Mouse Fibroblasts to Sphere Cells with Differentiation Potential Induced by AlbuMAXI-containing Medium

ABSTRACT: Analysis of gene expression levels during Fibroblast to sphere cell conversion induced by albumax I containing medium. Murine embryonic fibroblasts (MEF) can be converted to sphere cells in the presence of arachidonic acid and pluronic - F 68. The converted cells exhibit stem cell like properties and and have the potential to differentiate into all the three embryonic germ layers. Our results provide important information on genes that are up- or down-regulated during the reprogramming/conversion process. Total RNA was isolated from murine embryonic fibroblasts, normal mouse embryonic stem (MES) cells and converted sphere cells. MES cells were taken as a control/reference population. Three replicated were included for each sample.

ORGANISM(S): Mus musculus

SUBMITTER: yiling hong

PROVIDER: E-GEOD-29277 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Conversion of Mouse Fibroblasts to Sphere Cells with Differentiation Potential Induced by AlbuMAXI-containing Medium

Project description:Analysis of gene expression levels during Fibroblast to sphere cell conversion induced by albumax I containing medium. Murine embryonic fibroblasts (MEF) can be converted to sphere cells in the presence of arachidonic acid and pluronic - F 68. The converted cells exhibit stem cell like properties and and have the potential to differentiate into all the three embryonic germ layers. Our results provide important information on genes that are up- or down-regulated during the reprogramming/conversion process.

2011-05-13 | GSE29277 | GEO

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2011-07-29 | E-GEOD-31031 | biostudies-arrayexpress

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Systems biology approach to identify transcriptional reprogramming and microRNA targets during the progression of Polycystic Kidney Disease

Project description:Autosomal dominant polycystic kidney disease (ADPKD) is characterized by cyst formation throughout the kidney parenchyma. It is caused by mutations in either of two genes, PKD1 and PKD2. Mice that lack functional Pkd1 (Pkd1null/null), develop rapidly progressive cystic disease during embryogenesis, and serve as a model to study human ADPKD. We examined the molecular pathways that modulate renal cyst growth in the Pkd1null/null model by performing global gene-expression proﬁling in embryonic kidneys at day 14 and 17. Gene Ontology and gene set enrichment analysis were used to identify overrepresented signaling pathways in Pkd1null/null kidneys. We found dysregulation of developmental, metabolic, and signaling pathways (e.g. Wnt, calcium, TGF-b and MAPK) in Pkd1null/null kidneys. Total RNA were obtained from kidneys of wild-type and Pkd1null/null animals at embryonic ages 14.5 and 17.5.

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2012-04-05 | E-GEOD-34921 | biostudies-arrayexpress

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