<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gu W</submitter><funding>Japan Agency for Medical Research and Development</funding><funding>Ministry of Education, Culture, Sports, Science and Technology</funding><pagination>bio032318</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5829515</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>7(1)</volume><pubmed_abstract>Spontaneous testicular teratoma develops from primordial germ cells (PGCs) in embryos; however, the molecular mechanisms underlying teratoma formation are not fully understood. Mutation of the dead-end 1 (&lt;i>Dnd1&lt;/i>) gene, which encodes an RNA-binding protein, drastically enhances teratoma formation in the 129/Sv mouse strain. To elucidate the mechanism of &lt;i>Dnd1&lt;/i> mutation-induced teratoma formation, we focused on histone H3 lysine 27 (H3K27) trimethylation (me3), and found that the levels of H3K27me3 and its responsible methyltransferase, enhancer of zeste homolog 2 (Ezh2), were decreased in the teratoma-forming cells of &lt;i>Dnd1&lt;/i> mutant embryos. We also showed that Dnd1 suppressed miR-26a-mediated inhibition of Ezh2 expression, and that Dnd1 deficiency resulted in decreased H3K27m</pubmed_abstract><journal>Biology open</journal><pubmed_title>Dnd1-mediated epigenetic control of teratoma formation in mouse.</pubmed_title><pmcid>PMC5829515</pmcid><funding_grant_id>JP17gm0510017h</funding_grant_id><funding_grant_id>25114003</funding_grant_id><pubmed_authors>Matsui Y</pubmed_authors><pubmed_authors>Mochizuki K</pubmed_authors><pubmed_authors>Gu W</pubmed_authors><pubmed_authors>Otsuka K</pubmed_authors><pubmed_authors>Hamada R</pubmed_authors><pubmed_authors>Takehara A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Dnd1-mediated epigenetic control of teratoma formation in mouse.</name><description>Spontaneous testicular teratoma develops from primordial germ cells (PGCs) in embryos; however, the molecular mechanisms underlying teratoma formation are not fully understood. Mutation of the dead-end 1 (&lt;i>Dnd1&lt;/i>) gene, which encodes an RNA-binding protein, drastically enhances teratoma formation in the 129/Sv mouse strain. To elucidate the mechanism of &lt;i>Dnd1&lt;/i> mutation-induced teratoma formation, we focused on histone H3 lysine 27 (H3K27) trimethylation (me3), and found that the levels of H3K27me3 and its responsible methyltransferase, enhancer of zeste homolog 2 (Ezh2), were decreased in the teratoma-forming cells of &lt;i>Dnd1&lt;/i> mutant embryos. We also showed that Dnd1 suppressed miR-26a-mediated inhibition of Ezh2 expression, and that Dnd1 deficiency resulted in decreased H3K27m</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Jan</publication><modification>2026-06-18T04:53:19.15Z</modification><creation>2019-03-26T23:04:28Z</creation></dates><accession>S-EPMC5829515</accession><cross_references><pubmed>29378702</pubmed><doi>10.1242/bio.032318</doi></cross_references></HashMap>