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FOR AUTHORS General Physiology and Biophysics 2017 General Physiology and Biophysics Vol.36, No.5, p.513–520, 2017
FOR AUTHORS General Physiology and Biophysics 2017 General Physiology and Biophysics Vol.36, No.5, p.513–520, 2017
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General Physiology and Biophysics Vol.36, No.5, p.513–520, 2017 |
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| Title: Role of S-adenosylmethionine cycle in carcinogenesis | ||
| Author: Radovan Murín, Eva Vidomanová, Bhavani S. Kowtharapu, Jozef Hatok, Dušan Dobrota | ||
| Abstract: Alterations in enzymatic activities underlying the cellular capacity to maintain functional S-adenosylmethionine (SAM) cycle are associated with modified levels of its constituents. Since SAM is the most prominent donor of methyl group for sustaining the methylation pattern of macromolecules by methyltransferases, its availability is an essential prerequisite for sustaining the methylation pattern of nucleic acids and proteins. In addition, increased intracellular concentrations of S-adenosylhomocysteine and homocysteine, another two constituents of SAM cycle, exerts an inhibitory effect on the enzymatic activity of methyltranferases. While methylation pattern of DNA and histones is considered as an important regulatory hallmark in epigenetically regulated gene expression, amended methylation of several cellular proteins, including transcription factors, affects their activity and stability. Indeed, varied DNA methylome is a common consequence of disturbed SAM cycle and is linked with molecular changes underlying the transformation of the cells that may underlay the carcinogenesis. Here we summarize the recent evidences about the impact of disturbed SAM cycle on carcinogenesis. |
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| Keywords: S-adenosylmethionine — DNA methylation — Cancer — Epigenetic regulation— Metabolism | ||
| Published online: 17-Nov-2017 | ||
| Year: 2017, Volume: 36, Issue: 5 | Page From: 513, Page To: 520 | |
| doi:10.4149/gpb_2017031 |
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