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DNA IP for 5hmC modified CpGs in DNA of ESC derived hepatocyte like cells exposed to high energy substrates.

ABSTRACT: DNA IP for 5hmC modified CpGs in DNA of ESC derived hepatocyte like cells exposed to high energy substrates.

PROVIDER: PRJNA429758 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6467780.fastq.gz	Fastqsanger.gz
	SRR6467781.fastq.gz	Fastqsanger.gz
	SRR6467782.fastq.gz	Fastqsanger.gz
	SRR6467783.fastq.gz	Fastqsanger.gz
	SRR6467774.fastq.gz	Fastqsanger.gz

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5hmC-seq in human kidney DNA

Project description:DNA IP for 5hmC modified CpGs to determine 5hmC paterns across male human kidney

2018-03-01 | GSE106935 | GEO

DNA IP for 5hmC modified CpGs in the liver of control and HFD fed mouse liver.

Project description:DNA IP for 5hmC modified CpGs in the liver of control and HFD fed mouse liver.

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DNA IP for 5hmC modified CpGs in DNA of ESC derived hepatocyte like cells exposed to high energy substrates.

Project description:We report the application of antibody affinity DNA immunoprecipitation followed by proton sequencing to map 5'hydroxymethylcytosine profiles in DNA of ESC derived hepatocyte like cells exposed to high energy substrates.

2019-01-12 | GSE109139 | GEO

DNA IP for 5hmC modified CpGs in the liver of control and HFD fed mouse liver.

Project description:We carry out 5-hydroxymethylation DNA immunoprecipitation (hmeDIP) prior to sequencing Ion Proton P1 to report on the genome-wide 5hmC patterns of hepatic in murine hepatic steatosis.

2019-01-12 | GSE109138 | GEO

DNA IP for 5hmC modified CpGs in the liver of control mice and a Tet1 -/- mouse liver [hmeDIP-seq]

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. We carry out 5-hydroxymethylation DNA immunoprecipitation (hmeDIP) prior to sequencing Ion Proton P1 to report on the genome-wide 5hmC patterns. Heterozygote pairs of Tet1 B6;129S4-Tet1tm1.1Jae/J mice were bought from The Jackson Laboratory (Maine USA). Heterozygotes were interbred to produce homozygous knock out males with colony mate wild type controls. Genome-wide 5hmC patterns were generated by hydroxymethyl-DNA immuoprecipitation (hmeDIP) followed by genome wide sequencing on the Ion Proton P1 sequencer.

2016-05-17 | E-GEOD-77730 | biostudies-arrayexpress

DNA IP for 5hmC modified CpGs in the liver of control mice and a Tet1 -/- mouse liver [hmeDIP-seq]

2016-05-17 | GSE77730 | GEO

5hmC-seq in human kidney DNA

Project description:5hmC-seq in human kidney DNA

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Detection of 5mC and 5hmC in DNA templates generated by PCR using modified dCTPs by linear PCR using KTq DNA polymerase variant RIV A8

Project description:We have engineered the thermostable KlenTaq DNA polymerase variant called RIV A8 that produces error signatures specific for 5-methylcytosine (5mC) and 5-hydroxycytosine (5hmC) without prior chemical treatment of the DNA samples. These signatures are amplified during DNA amplicon library preparation and are detected by NGS. This method was applied to distinguish C from 5mC and C from 5hmC in DNA templates generated by PCR using modified dCTPs (unmodified by using dCTP, methylated by using d5mCTP, hydroxymethylated by using d5hmCTP).

2024-09-09 | GSE270850 | GEO

Role of Tet1 and 5-hydroxymethylcytosine in cocaine action (5hmC-Seq and ChIP-Seq)

Project description:Here we show that Tet1 is down-regulated in mouse nucleus accumbens (NAc), a key brain reward structure, by repeated cocaine administration which enhances behavioral responses to cocaine. Through genome-wide 5hmC profiling, we identified 5hmC changes selectively clustered in both enhancer and coding regions of genes with several annotated neural functions. By coupling with mRNA sequencing, we found cocaine-induced alterations in 5hmC correlate positively with alternative splicing. We also demonstrated that 5hmC alteration at certain genes lasts up to a month after cocaine exposure. DNA Nac samples were collected at various time points after 7 daily cocaoine ip administration for 5hmC and transcriptome analysis

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Sequencing analysis for 5hmC pull-down DNA

Project description:The gene body regions of cardiomyocyte-specific genes in cardiomyocytes are hypomethylated. We confirmed that the DNA methylation in gene body regions were demethylated during development. We speculated that the demethylation of gene body regions in cardiomyocyte-specific genes might be associated with active demethylation by Tet oxidation.To explore 5hmC distribution in cells and tissues, we performed 5hmC-specific chemical labeling-mediated pull-down DNA sequencing (hMe-Seal)(Song 2011 Nat genet, PMID:21151123). We found that the 5hmC in gene body regions are associated with demethylation, but not exclusively, and also with transcriptional activity. We concluded that gene body DNA hypomethylation in cardiomyocyte specific genes were mediated by oxidative demethylation.

2016-09-22 | GSE87165 | GEO

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