5hmC-seq in human kidney DNA
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ABSTRACT:
PROVIDER: PRJNA418466 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:DNA IP for 5hmC modified CpGs to determine 5hmC paterns across male human kidney
2018-03-01 | GSE106935 | GEO
Project description:Ten-Elven Translocation (TET) proteins oxidize 5-methylcytosine (5mC) to 5-hydroxymethylcytonsie (5hmC). Our recent work found a decline in global 5hmC level in mouse kidney insulted by ischemia reperfusion (IR). However, the genomic distribution of 5hmC in mouse kidney and its relationship with gene expression remain elusive. Here, we profiled the DNA hydroxymethylome of mouse kidney by hMeDIP-seq and revealed that 5hmC is enriched in genic regions but depleted from intergenic regions. Correlation analyses showed that 5hmC enrichment in gene body is positively associated with gene expression level in mouse kidney. Moreover, IR injury-associated genes (both up- and down-regulated genes during renal IR injury) in mouse kidney exhibit significantly higher 5hmC enrichment in their gene body regions when compared to those un-changed genes. Collectively, our study not only provides the first DNA hydroxmethylome of kidney tissues but also suggests that DNA hyper-hydroxymethylation in gene body may be a novel epigenetic mark of IR injury-associated genes. Eamination of the genome-wide distribution of 5-hydroxymethylcytosine in mouse kidney tissues
2016-04-01 | E-GEOD-79093 | biostudies-arrayexpress
Project description:We developed a novel approach, J-binding protein 1 sequencing (JBP1-seq), that combines the benefits of an improved recombinant JBP1 protein, Nextera-based library construction, and nextgeneration sequencing (NGS) for genome-wide profiling of 5-hydroxymethylcytosine (5hmC). Compared with the original JBP1, this new recombinant JBP1 was biotinylatedin vivo and conjugated to magnetic beads via biotin-streptavidin interactions. These modifications allowed a more efficient and consistent pull-down of β-glucosyl-5-hydroxymethylcytosine (β-glu-5hmC), and sequence-ready libraries can be generated within 4.5 hours from DNA inputs as low as 50 ng. 5hmC enrichment of human brain DNA using the new JBP1 resulted in over 25,000 peaks called, which is significantly higher than the 4,003 peaks enriched using the old JBP1. Comparison of the technical duplicates and validations with other platforms indicated the results are reproducible and reliable. Thus, JBP1-seq provides a fast, efficient, cost-effective method for accurate 5hmC genome-wide profiling. An improvement of JBP1-Seq
2014-11-26 | E-GEOD-61193 | biostudies-arrayexpress
Project description:Ten-Elven Translocation (TET) proteins oxidize 5-methylcytosine (5mC) to 5-hydroxymethylcytonsie (5hmC). Our recent work found a decline in global 5hmC level in mouse kidney insulted by ischemia reperfusion (IR). However, the genomic distribution of 5hmC in mouse kidney and its relationship with gene expression remain elusive. Here, we profiled the DNA hydroxymethylome of mouse kidney by hMeDIP-seq and revealed that 5hmC is enriched in genic regions but depleted from intergenic regions. Correlation analyses showed that 5hmC enrichment in gene body is positively associated with gene expression level in mouse kidney. Moreover, IR injury-associated genes (both up- and down-regulated genes during renal IR injury) in mouse kidney exhibit significantly higher 5hmC enrichment in their gene body regions when compared to those un-changed genes. Collectively, our study not only provides the first DNA hydroxmethylome of kidney tissues but also suggests that DNA hyper-hydroxymethylation in gene body may be a novel epigenetic mark of IR injury-associated genes.
2016-04-01 | GSE79093 | GEO
Project description:EMT is associated with profound epigenetic regualtion. 5hMC is the first product of TET-dependent DNA methylation product. chromatin immunoprecipitation-sequencing (ChIP-seq) provide a tool to define the changes of 5hmC at the genome level. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for 5hMC in HMLE cells.
2023-03-16 | GSE227135 | GEO
Project description:DNA methylation in murine WT ES cells was investigated by MBD domain mediated pull down of methylated DNA followed by chip analysis. For examination of 5hmC, hydroxymethylated DNA was enriched by Click-chemistry mediated pull down. Because of the lower amount of 5hmC, two different approached were adopted. The first approach was based on direct labeling of 5hmC DNA, and in the second method DNA was labeled after amplification with vitro transcription (IVT) . Microarray based hybridization (chip) analysis of epigenetic modifications, namely, 5mC and 5hmC for murine WT ES cells.
2014-10-21 | E-GEOD-51473 | biostudies-arrayexpress
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
Project description:Genomic DNA was prepared, fragmented, and immunoprecipitated with antibodies specific for 5mC or 5hmC prior to standard sequencing. The neurodegenerative disease known as ataxia-telangiectasia (A-T) is caused by the absence of the ATM (A-T mutated) protein. A long-standing mystery surrounding A-T is why cerebellar Purkinje cells (PCs) appear uniquely vulnerable to ATM-deficiency. Here, we present that 5-hydroxymethylcytosine (5hmC), a newly recognized epigenetic marker found at high levels in neurons, is substantially reduced in human A-T and Atm-/- mouse cerebellar PCs. TET1, an enzyme that converts 5mC to 5hmC, responds to DNA damage. Manipulation of TET1 activity directly affects neuronal cell cycle reentry and cell death after the induction of DNA damage. Quantitative, genome-wide analysis of 5hmC of samples from human cerebellum showed that in ATM-deficiency there is a remarkable genome-wide reduction of 5hmC enrichment at both proximal and distal regulatory elements. These results reveal a role of TET1-mediated 5hmC in DNA damage response, and provide insights into the basis of a PC-specific DNA demethylation alteration in ATM-deficiency.
2015-10-30 | GSE61133 | GEO
Project description:scRNA-seq of human fetal kidney tissue
| PRJEB38382 | ENA
Project description:Genomic DNA was prepared, fragmented, and immunoprecipitated with antibodies specific for 5mC or 5hmC prior to standard sequencing. The neurodegenerative disease known as ataxia-telangiectasia (A-T) is caused by the absence of the ATM (A-T mutated) protein. A long-standing mystery surrounding A-T is why cerebellar Purkinje cells (PCs) appear uniquely vulnerable to ATM-deficiency. Here, we present that 5-hydroxymethylcytosine (5hmC), a newly recognized epigenetic marker found at high levels in neurons, is substantially reduced in human A-T and Atm-/- mouse cerebellar PCs. TET1, an enzyme that converts 5mC to 5hmC, responds to DNA damage. Manipulation of TET1 activity directly affects neuronal cell cycle reentry and cell death after the induction of DNA damage. Quantitative, genome-wide analysis of 5hmC of samples from human cerebellum showed that in ATM-deficiency there is a remarkable genome-wide reduction of 5hmC enrichment at both proximal and distal regulatory elements. These results reveal a role of TET1-mediated 5hmC in DNA damage response, and provide insights into the basis of a PC-specific DNA demethylation alteration in ATM-deficiency. There are two groups, A-T and Control. For each group, cerebellar DNA samples were immunoprecipitated with anti-5mC (n=1) or anti-5hmC (n=3). There were also two replicates of input control for each group.
2015-10-30 | E-GEOD-61133 | biostudies-arrayexpress