期刊
REDOX BIOLOGY
卷 5, 期 -, 页码 275-289出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.redox.2015.05.008
关键词
Oxidative stress; Redox signaling; Gene regulation; Epigenetics; DNA repair
资金
- Johannes Gutenberg-University Mainz
- University Medical Center Mainz
- Science Foundation Ireland
- German Research Foundation [DFG GO709/4-5]
- European Cooperation in Science and Technology (COST Action) [BM1203/EU-ROS]
- International PhD Program on the Dynamics of Gene Regulation, Epigenetics and DNA Damage Response from the Institute of Molecular Biology gGmbH, (Mainz, Germany) - Boehringer Ingelheim Foundation
Reactive oxygen and nitrogen species (e.g. H2O2, nitric oxide) confer redox regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. In addition, classical regulation of gene expression or activity, including gene transcription to RNA followed by translation to the protein level, by transcription factors (e.g. NF-kappa B, HIF-1 alpha) and mRNA binding proteins (e.g. GAPDH, HuR) is subject to redox regulation. This review will give an update of recent discoveries in this field, and specifically highlight the impact of reactive oxygen and nitrogen species on DNA repair systems that contribute to genomic stability. Emphasis will be placed on the emerging role of redox mechanisms regulating epigenetic pathways (e.g. miRNA, DNA methylation and histone modifications). By providing clinical correlations we discuss how oxidative stress can impact on gene regulation/activity and vise versa, how epigenetic processes, other gene regulatory mechanisms and DNA repair can influence the cellular redox state and contribute or prevent development or progression of disease. (C) 2015 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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