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. 2015 Jan 29;7(1):9. doi: 10.1186/s13073-015-0134-6

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© Scourzic et al.; licensee BioMed Central. 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Regulation of DNA methylation and demethylation. DNA demethylation can occur spontaneously via the DNMT enzymes that methylated the nucleotide cytosine (5-methylcytosine, 5-mC) originally. A passive replication-dependent mechanism of DNA methylation is also possible. Several active demethylation pathways have been postulated. TET family proteins catalyze the oxidation of 5-mC into 5-hydroxymethylcytosine (5-hmC) and can further oxidize 5-hmC to 5-formylcytosine (5-fC) and 5-carboxycytosine (5-caC). 5-hmC recognition and transformation into 5-hydroxymethyluracyl (5-hmU) by activation-induced deaminase (AID) to facilitate repair by DNA glycosylase and the base-excision repair (BER) pathway is still controversial. These latter activities are also thought to process 5-fC and 5-caC into unmodified cytosine . The decarboxylases involved in this process are still to be identified. APOBEC, apolipoprotein B mRNA editing enzyme; DNMT, DNA methyltransferase; T, thymine; TDG, thymine DNA glycosylase; TET, ten-eleven translocation.