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Title: The role of DNA methylation in aging, rejuvenation, and age-related disease
Authors: Johnson, Adiv A.
Akman, Kemal
Calimport, Stuart R.G.
Wuttke, Daniel
Stolzing, Alexandra
De Magalhaes, Joao Pedro
Issue Date: 2012
Publisher: © Mary Ann Liebert, Inc.
Citation: JOHNSON, A.A. ... et al., 2012. The role of DNA methylation in aging, rejuvenation, and age-related disease. Rejuvenation Research, 15 (5), pp. 483 - 494.
Abstract: DNA methylation is a major control program that modulates gene expression in a plethora of organisms. Gene silencing through methylation occurs through the activity of DNA methyltransferases, enzymes that transfer a methyl group from S-adenosyl-l-methionine to the carbon 5 position of cytosine. DNA methylation patterns are established by the de novo DNA methyltransferases (DNMTs) DNMT3A and DNMT3B and are subsequently maintained by DNMT1. Aging and age-related diseases include defined changes in 5-methylcytosine content and are generally characterized by genome-wide hypomethylation and promoter-specific hypermethylation. These changes in the epigenetic landscape represent potential disease biomarkers and are thought to contribute to age-related pathologies, such as cancer, osteoarthritis, and neurodegeneration. Some diseases, such as a hereditary form of sensory neuropathy accompanied by dementia, are directly caused by methylomic changes. Epigenetic modifications, however, are reversible and are therefore a prime target for therapeutic intervention. Numerous drugs that specifically target DNMTs are being tested in ongoing clinical trials for a variety of cancers, and data from finished trials demonstrate that some, such as 5-azacytidine, may even be superior to standard care. DNMTs, demethylases, and associated partners are dynamically shaping the methylome and demonstrate great promise with regard to rejuvenation. © Copyright 2012, Mary Ann Liebert, Inc. 2012.
Description: Closed access. Final publication is available from Mary Ann Liebert, Inc., publishers http://dx.doi.org/10.1089/rej.2012.1324
Sponsor: The authors thank Daniel Kimbel and Bryan Vukorepa for collaborative interactions and helpful discussions. J.P.M. is grateful to the BBSRC, the Wellcome Trust, the Ellison Medical Foundation, and a Marie Curie International Reintegration Grant within EC-FP7 for supporting work in his laboratory.
Version: Published
DOI: 10.1089/rej.2012.1324
URI: https://dspace.lboro.ac.uk/2134/16821
Publisher Link: http://dx.doi.org/10.1089/rej.2012.1324
ISSN: 1549-1684
Appears in Collections:Closed Access (Mechanical, Electrical and Manufacturing Engineering)

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