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Genome wide analysis of gene expression of rat ES cells, rat embryonic fibroblast cells and mouse ES cells

ABSTRACT: Rat ES cells were derived using 3I medium from E4.5 blastocysts. Rat embryonic fibroblast cells were derived form E14.5 embryos. To analyze the mechanism under the selfrenewal of rat ES cells, microarrays were used for the genome wide analysis of gene expressoin profiles in rat ES cells. Rat embryonic fibroblast cells and mouse ES cells were tested at same time as control. Our results from clustering analysis demonstrated that the gene expression profile of rat ES cells resembles mouse ES cells, but not REFs. Keyword: 3I medium; rat embryonic stem cells; mouse ES cells; rat embryonic fibroblast cells

ORGANISM(S): Mus musculus Rattus norvegicus

PROVIDER: GSE13681 | GEO | 2008/11/25

SECONDARY ACCESSION(S): PRJNA110431

REPOSITORIES: GEO

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Genome wide analysis of gene expression of rat ES cells, rat embryonic fibroblast cells and mouse ES cells

Project description:Rat ES cells were derived using 3I medium from E4.5 blastocysts. Rat embryonic fibroblast cells were derived form E14.5 embryos. To analyze the mechanism under the selfrenewal of rat ES cells, microarrays were used for the genome wide analysis of gene expressoin profiles in rat ES cells. Rat embryonic fibroblast cells and mouse ES cells were tested at same time as control. Our results from clustering analysis demonstrated that the gene expression profile of rat ES cells resembles mouse ES cells, but not REFs. Keyword: 3I medium; rat embryonic stem cells; mouse ES cells; rat embryonic fibroblast cells Rat ES cells were cultured in 3I medium; rat embryonic fibroblast cells were derived and cultured GMEM/10% FBS; mouse ES cells (C57/BL6)were cultured in GMEM/10% FBS added LIF and feeder cells were removed before RNA extraction. Three replicates each.

2010-05-15 | E-GEOD-13681 | biostudies-arrayexpress

Genome wide analysis of gene expression of rat ES cells, rat embryonic fibroblast cells and mouse ES cells

Project description:Genome wide analysis of gene expression of rat ES cells, rat embryonic fibroblast cells and mouse ES cells

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Expression profile of Sall4-null ES cells and Sall4 heterozygous ES cells

Project description:Sall4 is a mouse homolog of a causative gene of the autosomal dominant disorder known as Okihiro syndrome. We previously showed that Sall4 absence leads to lethality during peri-implantation and that Sall4-null embryonic stem (ES) cells proliferate poorly with intact pluripotency when cultured on feeder cells. However, a subsequent report indicated that shRNA-mediated Sall4 inhibition in ES cells led to a severe reduction in Oct3/4 and a secondary increase in Cdx2, which resulted in complete differentiation into the trophectoderm when cultured in the feeder-free condition. So we profiled gene expression changes when Sall4 is deleted in ES cells in the presence or absence of feeder cells. key word: embryonic stem (ES) cell, Sall4, feeder ES cells were cultured with or without mouse embryonic fibroblast (MEF) feeder cells in LIF-supplemented medium as described. To maintain the expression of Oct3/4, all ES cells were cultured in the presence of Blasticidin. Four samples were analyzed. GSM356329, GSM356330 : cultured in the absence of feeders GSM356331, GSM356332 : cultured on the feeders

2009-04-01 | E-GEOD-14219 | biostudies-arrayexpress

Expression data from mouse ES and iPS cells

Project description:Induced pluripotent stem (iPS) cells were produced from reprogramming of somatic cells, and they are shown to possess pluripotent properties similar to embryonic stem (ES) cells. Here we used microarrays to detail the global expression pattern among the ES cells and iPS cells, as well as the original mouse embryo fibroblast (MEF), to identify important players involved in the reprogramming process.

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Expression data from mouse ES and iPS cells

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Metabolic enhancement of developmental pausing (ES dataset)

Project description:Embryonic stem (ES) cells and embryos reversibly pause via chemical mTOR inhibition. In this study, we investigate the tissue-specific response to mTORi-induced pausing in ES and trophoblast stem (TS) cells. To resolve the sequential rewiring of the proteome, we conducted a time-series proteomics experiment at 1, 3, 6, 12, 24, and 48 hours upon induction of pausing, and at 1, 3, 6, 12, 24, and 48 hours upon release of pausing in ES and TS cells. We find that ES, but not TS cells pause reversibly. To optimise developmental pausing conditions, we reasoned that by understanding the difference in pausing response of ES and TS cells, we could identify which pathways are essential for pausing. We found that KEGG pathways related to amino acid degradation, fatty acid degradation, and DNA repair are upregulated in ES cells, but downregulated in TS cells during entry into pausing. Moreover, by targeted metabolomics, we found a depletion of short chain carnitines in the paused ES cells. To extend the length of developmental pausing, we supplemented paused embryos with L-carnitine. The L-carnitine supplementation facilitates lipid usage and prolongs the pausing length by 19 days through the establishment of a more dormant state.

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Expression data from rat androgenetic embryonic stem cells

Project description:The rat androgenetic embryonic stem cells (RahES cells) have only 21 chromosomes. However, they express pluripotency markers, differentiate into three germ layer cells as well as contribute to the germline as the normal diploid rat ES cells. Moreover, the RahES cells can produce fertile rats after intracytoplasmic injection into oocytes, thus are capable to transmit genetic modifications to offspring. We used microarrays to detail the global gene expression profile of RahES cells and identified distinct classes of up-regulated and down-regulated genes compared with the expression of normal diploid rat ES cells.

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Protein expression profile of miR-33b overexpressing ES-2 cells upon OCM treatment

Project description:Omentum conditioned medium (OCM) is known to enhance ovarian cancer oncogenesis. In this study, miR-33b exerts tumor suppressive effects on ovarian cancer cells in response to omentum conditioned medium (OCM) treatment. To identify the molecular mechanism and main biological pathways involved in the tumor inhibiting activity by miR-33b in the ovarian cancer metastasis. To achieve this, miR-33b was stably overexpressed in ovarian cancer cell line ES-2, and the protein expression profile of miR-33b overexpressing ES-2 cells upon OCM treatment was determined.

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