{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gu W"],"funding":["Japan Agency for Medical Research and Development","Ministry of Education, Culture, Sports, Science and Technology"],"pagination":["bio032318"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5829515"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(1)"],"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 (<i>Dnd1</i>) gene, which encodes an RNA-binding protein, drastically enhances teratoma formation in the 129/Sv mouse strain. To elucidate the mechanism of <i>Dnd1</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 <i>Dnd1</i> mutant embryos. We also showed that Dnd1 suppressed miR-26a-mediated inhibition of Ezh2 expression, and that Dnd1 deficiency resulted in decreased H3K27m"],"journal":["Biology open"],"pubmed_title":["Dnd1-mediated epigenetic control of teratoma formation in mouse."],"pmcid":["PMC5829515"],"funding_grant_id":["JP17gm0510017h","25114003"],"pubmed_authors":["Matsui Y","Mochizuki K","Gu W","Otsuka K","Hamada R","Takehara A"],"additional_accession":[]},"is_claimable":false,"name":"Dnd1-mediated epigenetic control of teratoma formation in mouse.","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 (<i>Dnd1</i>) gene, which encodes an RNA-binding protein, drastically enhances teratoma formation in the 129/Sv mouse strain. To elucidate the mechanism of <i>Dnd1</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 <i>Dnd1</i> mutant embryos. We also showed that Dnd1 suppressed miR-26a-mediated inhibition of Ezh2 expression, and that Dnd1 deficiency resulted in decreased H3K27m","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Jan","modification":"2026-06-18T04:53:19.15Z","creation":"2019-03-26T23:04:28Z"},"accession":"S-EPMC5829515","cross_references":{"pubmed":["29378702"],"doi":["10.1242/bio.032318"]}}