<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>8(1)</volume><submitter>Ariumi Y</submitter><pubmed_abstract>Long interspersed element-1 (LINE-1, L1) is a mobile genetic element comprising about 17% of the human genome. L1 utilizes an endonuclease to insert L1 cDNA into the target genomic DNA, which induces double-strand DNA breaks in the human genome and activates the DNA damage signaling pathway, resulting in the recruitment of DNA-repair proteins. This may facilitate or protect L1 integration into the human genome. Therefore, the host DNA repair machinery has pivotal roles in L1 mobility. In this study, we have, for the first time, demonstrated that the DNA repair protein, Rad18, restricts L1 mobility. Notably, overexpression of Rad18 strongly suppressed L1 retrotransposition as well as L1-mediated Alu retrotransposition. In contrast, L1 retrotransposition was enhanced in Rad18-deficient or kn</pubmed_abstract><journal>Scientific reports</journal><pagination>15894</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6203705</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>DNA repair protein Rad18 restricts LINE-1 mobility.</pubmed_title><pmcid>PMC6203705</pmcid><pubmed_authors>Ariumi Y</pubmed_authors><pubmed_authors>Kawano K</pubmed_authors><pubmed_authors>Yasuda-Inoue M</pubmed_authors><pubmed_authors>Siddiqui R</pubmed_authors><pubmed_authors>Turelli P</pubmed_authors><pubmed_authors>Kuroki M</pubmed_authors><pubmed_authors>Tateishi S</pubmed_authors><pubmed_authors>Fukuda H</pubmed_authors></additional><is_claimable>false</is_claimable><name>DNA repair protein Rad18 restricts LINE-1 mobility.</name><description>Long interspersed element-1 (LINE-1, L1) is a mobile genetic element comprising about 17% of the human genome. L1 utilizes an endonuclease to insert L1 cDNA into the target genomic DNA, which induces double-strand DNA breaks in the human genome and activates the DNA damage signaling pathway, resulting in the recruitment of DNA-repair proteins. This may facilitate or protect L1 integration into the human genome. Therefore, the host DNA repair machinery has pivotal roles in L1 mobility. In this study, we have, for the first time, demonstrated that the DNA repair protein, Rad18, restricts L1 mobility. Notably, overexpression of Rad18 strongly suppressed L1 retrotransposition as well as L1-mediated Alu retrotransposition. In contrast, L1 retrotransposition was enhanced in Rad18-deficient or kn</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Oct</publication><modification>2026-05-05T23:28:58.731Z</modification><creation>2026-04-07T22:06:33.365Z</creation></dates><accession>S-EPMC6203705</accession><cross_references><pubmed>30367120</pubmed><doi>10.1038/s41598-018-34288-9</doi></cross_references></HashMap>