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Mus musculus

ABSTRACT: Gene expression changes following demethylation by 5-aza-2'-deoxycytidine in primary mouse dermal fibroblasts

OTHER RELATED OMICS DATASETS IN: E-GEOD-4695E-MEXP-701E-MEXP-700

PROVIDER: PRJNA96745 | ENA |

REPOSITORIES: ENA

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Transcription profiling of primary mouse dermal fibroblasts, chondrocytes and osteoblasts treated with 5-aza-2?-deoxycytidine for 96/72h to identify key developmental regulator genes whose expression in terminally differentiated cells may be inhibited by DNA methylation

Project description:DNA methylation can contribute to the stable transcriptional silencing of mammalian genes. Oftentimes, these genes are important developmental regulators, and their silencing in cell types where they are not supposed to be active is important for the phenotypic stability of the cells. To identify key developmental regulator genes whose expression in terminally differentiated cells may be inhibited by DNA methylation, mouse dermal fibroblasts were demethylated with 5-aza-2-deoxycytidine, and changes in gene expression monitored by microarray analysis. Three biological replicates for both control and 5-aza-2'-deoxycytidine treatment were derived. Cells were primary mouse dermal fibroblasts, primary mouse chondrocytes, and primary mouse osteoblasts derived separately for each biological replicate. Treated cells were exposed to 5uM 5-aza-2'-deoxycytidine for 96 hours with recovery in normal medium for 24 hours. Control cells were untreated.

2007-11-23 | E-GEOD-4768 | biostudies-arrayexpress

Transcription profiling of mouse primary dermal fibroblasts treated with the de-methylating agent 5-aza-2?-deoxycytidine vs untreated to investigate methylation related changes in gene expression

Project description:DNA methylation can contribute to the stable transcriptional silencing of mammalian genes. Oftentimes, these genes are important developmental regulators, and their silencing in cell types where they are not supposed to be active is important for the phenotypic stability of the cells. To identify key developmental regulator genes whose expression in terminally differentiated cells may be inhibited by DNA methylation, mouse dermal fibroblasts were demethylated with 5-aza-2-deoxycytidine, and changes in gene expression monitored by microarray analysis. Three biological replicates for both control and 5-aza-2'-deoxycytidine treatment were derived. Cells were primary mouse dermal fibroblasts derived by explant procedure separately for each biological replicate. Treated cells were exposed to 5uM 5-aza-2'-deoxycytidine for 96 hours with recovery in normal medium for 24 hours. Control cells were untreated.

2007-11-23 | E-GEOD-4696 | biostudies-arrayexpress

Gene expression changes following demethylation by 5-aza-2'-deoxycytidine in primary mouse dermal fibroblasts

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Global analysis of transcriptional changes following genomic demethylation in chondrocytes, osteoblasts, and fibroblasts

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Transcription profiling of mouse primary dermal fibroblasts treated with DNA demethylating agent 5-aza-2-deoxycytidine and sorted by X-chromosome-linked GFP expression

Project description:Primary mouse dermal fibroblasts from heterozygous female X chromosome-linked GFP mice were sorted through FACS for GFP non-expressing cells (~50% of cells due to X-inactivation). The GFP- cells were treated with 4uM 5-aza-2'-deoxycytidine (5A2dC) for 48 hours with recovery in normal medium for 24 hours. Following the treatment, cells were again sorted by FACS into GFP-activated and GFP-nonexpressing cells. These populations, along with a control untreated population were assayed for transcriptional changes by microarray.

2005-01-01 | E-MEXP-704 | biostudies-arrayexpress

Transcription profiling of mouse primary dermal fibroblasts treated with DNA demethylating agent 5-aza-2-deoxycytidine

Project description:Mouse primary dermal fibroblasts were treated with DNA demethylating agent 5-aza-2'-deoxycytidine. The exposure was 5um 5A2dC for 96 hours followed by recovery in normal medium for 24 hours. Three biological replicates were created for both the control and treated populations. Each biological replicate represents a separate derivation of dermal fibroblasts from genetically identical mouse pups aged 0-3 days. Cells reached passage 4 before initiating drug exposure.

2005-01-01 | E-MEXP-701 | biostudies-arrayexpress

Improved DNA methylation analysis via enrichment of demethylated cells expressing an X-inactivated GFP transgene

Project description:The demethylating drug 5-aza-2’-deoxycytidine (5-aza-2dC) is frequently used to investigate the effect of global DNA demethylation on gene expression in cultured mammalian cells. Here, we utilize a novel method that uses the reactivation of an X-inactivated GFP transgene as a marker to enrich for cells that have undergone drug-induced demethylation. By combining it with microarray gene expression profiling, we demonstrate the method’s utility in identifying genes activated by global DNA demethylation. Keywords: 5-aza-2'-deoxycytidine; methylation; dermal fibroblast; X-linked GFP

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Mus musculus

Project description:Gene expression changes following demethylation by 5-aza-2'-deoxycytidine（decitabine, DAC）in mouse T cell lymphoma EL4 cells

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MCF7 cells gene expression change by inducing CpG demethylation using 5-Aza-2'-deoxycytidine (Aza)

Project description:Promoter methylation is able to induce downregulation of gene expression. 5-Aza-2'-deoxycytidine(Aza), methytransferase inhibitor, induce CpG demethylation. Here, 5-Aza-2'-deoxycytidine(Aza) is treated in a human breast cancer cell, MCF7, for detection of gene expression change.

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Transcription profiling of mouse dermal fibroblasts from X linked GFP transgenics - improved dna methylation analysis via enrichment of demethylated cells expressing an X-inactivated GFP transgene

Project description:The demethylating drug 5-aza-2â-deoxycytidine (5-aza-2dC) is frequently used to investigate the; effect of global DNA demethylation on gene expression in cultured mammalian cells. Here, we utilize a novel method that uses the reactivation of an X-inactivated GFP transgene as a marker to enrich for cells that have undergone drug-induced demethylation. By combining it with microarray gene expression profiling, we demonstrate the methodâs utility in identifying genes activated by global DNA demethylation. Experiment Overall Design: Mice used have an X-linked GFP transgene driven by the chicken Î²-actin promoter and CMV Experiment Overall Design: intermediate early enhancer in a 129/ICR mixed genetic background obtained from The Jackson Experiment Overall Design: Laboratory. Male transgenic animals were bred to wildtype BL6 female mice to obtain females that were heterozygous for the transgene. Dermal fibroblasts were obtained from explant cultures of neonatal female mice from these crosses. The cells were then sorted using FACS to obtain only GFP-nonexpressing cells. These cells represent the population with the GFP transgene on the inactive X chromosome. The GFP-silent cells were treated with the demethylating drug 5-aza-2'-deoxycytidine. This drug does not affect all cells and uses a passive form of demethylation that results in a heterogenous population of unaffected and demethylated cells. A portion of the cells affected by demethylation activate the inactive GFP transgene by demethylating the inactive X chromosome. The GFP-active and GFP-inactive cells were sorted by FACS and assayed by microarray to determine what genes were affected by demethylation. Also the microarray results indicated if sorting for GFP-active cells enriches for cells affected by the drug.

2008-06-13 | E-GEOD-4718 | biostudies-arrayexpress

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