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Battle against RNA oxidation: molecular mechanisms for reducing oxidized RNA to protect cells

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Oxidation is probably the most common type of damage that occurs in cellular RNA. Oxidized RNA may be dysfunctional and is implicated in the pathogenesis of age‐related human diseases. Cellular mechanisms controlling oxidized RNA have begun to be revealed. Currently, a number of ribonucleases and RNA‐binding proteins have been shown to reduce oxidized RNA and to protect cells under oxidative stress. Although information about how these factors work is still very limited, we suggest several mechanisms that can be used to minimize oxidized RNA in various organisms. This article is categorized under: RNA Turnover and Surveillance > Turnover/Surveillance Mechanisms RNA in Disease and Development > RNA in Disease

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Molecular mechanisms for reducing oxidized RNA in cells. RNA may become nonfunctional once it is oxidized. At the early stage after oxidation modification, the RNA may possibly be reverted to normal, functional RNA by repair activities. Oxidized RNA is also subjected to degradation, which is responsible to irreversibly eliminate probably the majority of oxidized RNA. The oxidized nucleotides resulted from degradation are blocked from transcription, reducing the formation of oxidized RNA by synthesis. RNA molecules are shown as blue lines. Oxidized residues in RNA are marked by a red ‘X’.
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Recognition and sequestration target oxidized RNA for elimination. In the recognition step, oxidized RNA molecules can be marked by proteins that specifically bind them. After being recognized, oxidized RNA may be separated from normal RNA either physically or functionally in the sequestration step. Recognition and sequestration may help recruiting repair/degradation activities that will eventually eliminate oxidized RNA. RNA molecules are shown as blue lines. Oxidized residues in RNA are marked by a red ‘X’. Oxidized RNA‐binding proteins are shown as light blue ovals.
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Predicted action of apurinic/apyrimidinic endonuclease 1 (APE1) on oxidized RNA, which is activated by oxidative stress. Under normal conditions, APE1 interacts with NPM1 and RNA and accumulates in the nucleolus. APE1 activity on damaged RNA is inhibited by binding NPM1. Oxidative stress induces acetylation of lysine residues (marked by *) at the N‐terminus of APE1, resulting in the dissociation of APE1 and NPM1 and activation of APE1 on oxidized RNA. RNA and DNA molecules are shown as blue lines. Oxidized residues are marked by a red ‘X’.
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RNA Turnover and Surveillance > Turnover/Surveillance Mechanisms
RNA in Disease and Development > RNA in Disease

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