ArticleFEBS open bio2018
Inhibition of DNA methyltransferase leads to increased genomic 5-hydroxymethylcytosine levels in hematopoietic cells.
Article in FEBS open bio, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Mass Spectrometry Quantification of Epigenetic Changes: A Scoping Review for Cancer and Beyond.International journal of molecular sciences · 2025Article
- Global DNA-methylation in quantitative epigenetics: orbitrap mass spectrometry.Frontiers in molecular biosciences · 2025Article
- Cytosine methylase and hydroxymethylase activity in mammalian mitochondria.Frontiers in cell and developmental biology · 2025Article
- Methods for Detection and Mapping of Methylated and Hydroxymethylated Cytosine in DNA.Biomolecules · 2024Review
- Improve-RRBS: a novel tool to correct the 3' trimming of reduced representation sequencing reads.Bioinformatics advances · 2024Article
- Article
- Review
- Cytosine Methylation Studies in Patients with Diabetic Kidney Disease.Current diabetes reports · 2019Review
- Decreased Nuclear Ascorbate Accumulation Accompanied with Altered Genomic Methylation Pattern in Fibroblasts from Arterial Tortuosity Syndrome Patients.Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
5-Hydroxymethylcytosine (5hmC) is produced from 5-methylcytosine (5mC) by Ten-eleven translocation (TET) dioxygenases. The epigenetic modification 5hmC has crucial roles in both cellular development and differentiation. The 5hmC level is particularly high in the brain. While 5mC is generally associated with gene silencing/reduced expression, 5hmC is a more permissive epigenetic mark. To understand its physiological function, an easy and accurate quantification method is required. Here, we have developed a novel LC-MS/MS-based approach to quantify both genomic 5mC and 5hmC contents. The method is based on the liberation of nucleobases by formic acid. Applying this method, we characterized the levels of DNA methylation and hydroxymethylation in mouse brain and liver, primary hepatocytes, and various cell lines. Using this approach, we confirm that the treatment of different cell lines with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine leads to a decrease in 5mC content. This decrease was accompanied by an increase in 5hmC levels in cell lines of hematopoietic origin. Finally, we showed that ascorbate elevates the levels of 5hmC and augments the effect of 5-aza-2'-deoxycytidine without significantly influencing 5mC levels.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.