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. 2018 May 1;32(9-10):658–669. doi: 10.1101/gad.313460.118

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© 2018 Ahmed and Lingner; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 6. — Model for telomerase inhibition in MTH1 knockout and PRDX1/MTH1 double-knockout cells. ROS increase the concentration of 8-oxo dGTP. In MTH1 knockout cells, 8-oxo dGTP is not hydrolyzed to 8-oxo dGMP. Telomerase incorporates 8-oxo G, leading to premature chain termination. Loss of PRDX1 further enhances telomerase inhibition. PRDX1 loss increases ROS, promoting oxidation of dGTP to 8-oxo dGTP. PRDX1 loss may also enhance direct ROS-mediated damage of telomeres at the chromosome 3′ end, leading to inhibition of telomerase.