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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Hydroxymethyl DNA-IP of genomic DNA for many different normal human tissues

ABSTRACT: 5-hmC is a novel epigenetic mark derived from oxidation of methylcytosine. We profile this mark in several normal human tissues 5-hmC patterns are highly tissue specific and enriched in the body of transcribed genes 5-hmC patterns are highly tissue specific and enriched in the body of transcribed genes comparison of six normal human tissue types

ORGANISM(S): Homo sapiens

SUBMITTER: Colm Nestor

PROVIDER: E-GEOD-33219 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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IP of 5-methylcytosine (5-hmC) enriched DNA fragments from control and PB treated mouse livers (1 day)

Project description:5-hmC is an epigenetic modification of the DNA base cytosine with roles in gene silencing events, imprinting and X inactivation. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5hmC in both control mouse livers as well as in the livers of 1 day PB treated mice. 5hmC is largely found to reside in the bodies of active genes and promoter levels are perturbed upon PB induced gene activation events. 5-hmC is assocated with promoters fo silent genes. Upon PB exposire a handfull of genes are induced which reveal decreases in promoter 5hmC levels comparison of 5-hmC profiles in 5 control and 5 PB exposed mouse livers (dose: 1day PB)

2012-11-10 | E-GEOD-41395 | biostudies-arrayexpress

IP of 5-methylcytosine (5-hmC) enriched DNA fragments from control and PB treated mouse livers (91 day)

Project description:5-hmC is an epigenetic modification of the DNA base cytosine with roles in gene silencing events, imprinting and X inactivation. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5hmC in both control mouse livers as well as in the livers of 91 day PB treated mice. 5hmC is largely found to reside in the bodies of active genes and promoter levels are perturbed upon PB induced gene activation events. 5-hmC is assocated with promoters fo silent genes. Upon PB exposire a handfull of genes are induced which reveal decreases in promoter 5hmC levels comparison of 5-hmC profiles in 5 control and 5 PB exposed mouse livers (dose: 91day PB)

2012-11-10 | E-GEOD-41397 | biostudies-arrayexpress

IP of 5-methylcytosine (5-hmC) enriched DNA fragments from control and PB treated mouse livers (7 day)

Project description:5-hmC is an epigenetic modification of the DNA base cytosine with roles in gene silencing events, imprinting and X inactivation. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5hmC in both control mouse livers as well as in the livers of 7 day PB treated mice. 5hmC is largely found to reside in the bodies of active genes and promoter levels are perturbed upon PB induced gene activation events. 5-hmC is assocated with promoters fo silent genes. Upon PB exposire a handfull of genes are induced which reveal decreases in promoter 5hmC levels comparison of 5-hmC profiles in 5 control and 5 PB exposed mouse livers (dose: 7day PB)

2012-11-10 | E-GEOD-41392 | biostudies-arrayexpress

Rapid reprogramming of epigenetic and transcriptional profiles in mammalian culture systems

Project description:5-hmC profiling of mouse embryonic fibroblasts before and during adaptation to cell culture conditions using hMeDIP-chip

2014-12-17 | E-MTAB-3177 | biostudies-arrayexpress

IP of 5-hydroxymethylcytosine (5-hmC) enriched DNA fragments from control and PB treated mouse livers

Project description:5-hmC is a novel epigenetic mark derived from oxidation of methylcytosine. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5hmC in both control mouse livers as well as in the livers of 28 day PB treated mice. 5hmC is largely found to reside in the bodies of active genes and promoter levels are perturbed upon PB induced gene activation events. 5-hmC is enriched in the bodies of active genes as well as a subset of TSS regions associated with transcriptional silencing. Upon PB exposire a handfull of genes are induced which reveal increases in promoter 5hmC levels comparison of 5hmC profiles in 5 control and 5 PB exposed mouse livers

2012-09-12 | E-GEOD-40537 | biostudies-arrayexpress

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Project description:Through the analysis of mouse liver tumours promoted by distinct routes (DEN exposure alone, DEN exposure plus non-genotoxic insult with phenobarbital and non-alcoholic fatty liver disease); we report that the cancer associated hyper-methylated CGI events in mice are also predicated by silent promoters that are enriched for both the DNA modification 5-hydroxymethylcytosine (5hmC) and the histone modification H3K27me3 in normal liver. During cancer progression these CGIs undergo hypo-hydroxymethylation, prior to subsequent hyper-methylation; whilst retaining H3K27me3. A similar loss of promoter-core 5hmC is observed in Tet1 deficient mouse livers indicating that reduced Tet1 binding at CGIs may be responsible for the epigenetic dysregulation observed during hepatocarcinogenesis. Consistent with this reduced Tet1 protein levels are observed in mouse liver tumour lesions. As in human, DNA methylation changes at CGIs do not appear to be direct drivers of hepatocellular carcinoma progression in mice. Instead dynamic changes in H3K27me3 promoter deposition are strongly associated with tumour-specific activation and repression of transcription. Our data suggests that loss of promoter associated 5hmC in diverse liver tumours licences DNA methylation reprogramming at silent CGIs during cancer progression. 5-hmC is a novel epigenetic mark derived from oxidation of methylcytosine. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5hmC in both control mouse livers as well as in the livers of 12 week PB treated mice. We also profile 5hmC in liver tumours arising in the presence of long term PB exposure (35 week: resulting in Ctnnb1 mutated tumours) to a Ha-Ras liver tumour which arose without PB. Samples: 5hmC profiles in 2 control and 2 PB exposed mouse livers, 3 liver tumours resulting from long term PB exposrue and 1 liver tumour arising without PB

2016-05-17 | E-GEOD-77726 | biostudies-arrayexpress

IP of 5-hydroxymethylcytosine (5-hmC) and 5-methylcytosine (5-mC) enriched DNA fragments from control and PB treated mouse livers

Project description:This SuperSeries is composed of the following subset Series: GSE40537: IP of 5-hydroxymethylcytosine (5-hmC) enriched DNA fragments from control and PB treated mouse livers GSE40538: IP of 5-methylcytosine (5-mC) enriched DNA fragments from control and PB treated mouse livers GSE40773: Dynamic changes in liver 5M-bM-^@M-^P hydroxymethylcytosine profiles upon nonM-bM-^@M-^P genotoxic carcinogen exposure Refer to individual Series

2012-09-12 | E-GEOD-40540 | biostudies-arrayexpress

Rapid reprogramming of epigenetic and transcriptional profiles in mammalian culture systems

Project description:Comparison of the methylation profile of mouse embryonic fibroblasts (MEFs) before and during adaptation to cell culture conditions. Matched expression data is deposited under accession: E-MTAB-3172

2014-12-17 | E-MTAB-3176 | biostudies-arrayexpress

Profiling of epigenetic and transcriptomic landscapes in normal mouse liver, phenobarbital exposed mouse livers and mouse liver tumours

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-05-17 | E-GEOD-77731 | biostudies-arrayexpress

IP of 5-methylcytosine (5-mc) enriched DNA fragments from control and mice with non-acoholic steatohepatitis (NASH) related hepatocellular carcinoma (HCC)

Project description:Through the analysis of mouse liver tumours promoted by distinct routes (DEN exposure alone, DEN exposure plus non-genotoxic insult with phenobarbital and non-alcoholic fatty liver disease); we report that the cancer associated hyper-methylated CGI events in mice are also predicated by silent promoters that are enriched for both the DNA modification 5-hydroxymethylcytosine (5hmC) and the histone modification H3K27me3 in normal liver. During cancer progression these CGIs undergo hypo-hydroxymethylation, prior to subsequent hyper-methylation; whilst retaining H3K27me3. A similar loss of promoter-core 5hmC is observed in Tet1 deficient mouse livers indicating that reduced Tet1 binding at CGIs may be responsible for the epigenetic dysregulation observed during hepatocarcinogenesis. Consistent with this reduced Tet1 protein levels are observed in mouse liver tumour lesions. As in human, DNA methylation changes at CGIs do not appear to be direct drivers of hepatocellular carcinoma progression in mice. Instead dynamic changes in H3K27me3 promoter deposition are strongly associated with tumour-specific activation and repression of transcription. Our data suggests that loss of promoter associated 5hmC in diverse liver tumours licences DNA methylation reprogramming at silent CGIs during cancer progression. 5-mc is a well establisehd epigenetic mark typically related to gene silencing events. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5mC in both control mouse livers as well as in liver tumours of high fat diet exposed mice who have progressed through NASH. Samples: 5mC profiles in livers of 2 control and 2 NASH driven HCC samples

2016-05-17 | E-GEOD-77725 | biostudies-arrayexpress

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