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http://purl.uniprot.org/citations/33898448http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/33898448http://www.w3.org/2000/01/rdf-schema#comment"Congenital heart defects are the most common birth defect and have a clear genetic component, yet genomic structural variations or gene mutations account for only a third of the cases. Epigenomic dynamics during human heart organogenesis thus may play a critical role in regulating heart development. However, it is unclear how histone mark H3K36me3 acts on heart development. Here we report that histone-lysine N-methyltransferase SETD2, an H3K36me3 methyltransferase, is a crucial regulator of the mouse heart epigenome. Setd2 is highly expressed in embryonic stages and accounts for a predominate role of H3K36me3 in the heart. Loss of Setd2 in cardiac progenitors results in obvious coronary vascular defects and ventricular non-compaction, leading to fetus lethality in mid-gestation, without affecting peripheral blood vessel, yolk sac, and placenta formation. Furthermore, deletion of Setd2 dramatically decreased H3K36me3 level and impacted the transcriptional landscape of key cardiac-related genes, including Rspo3 and Flrt2. Taken together, our results strongly suggest that SETD2 plays a primary role in H3K36me3 and is critical for coronary vascular formation and heart development in mice."xsd:string
http://purl.uniprot.org/citations/33898448http://purl.org/dc/terms/identifier"doi:10.3389/fcell.2021.651655"xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/author"Chen F."xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/author"Chen J."xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/author"Huang L."xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/author"Li L."xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/author"Liu J."xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/author"Wang S."xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/author"Tang H."xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/author"Wang X."xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/author"Wang H."xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/author"Han Z."xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/author"Fang X."xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/author"Ouyang K."xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/date"2021"xsd:gYear
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/name"Front Cell Dev Biol"xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/pages"651655"xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/title"Histone Lysine Methyltransferase SETD2 Regulates Coronary Vascular Development in Embryonic Mouse Hearts."xsd:string
http://purl.uniprot.org/citations/33898448http://purl.uniprot.org/core/volume"9"xsd:string
http://purl.uniprot.org/citations/33898448http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/33898448
http://purl.uniprot.org/citations/33898448http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/33898448
http://purl.uniprot.org/uniprot/#_A0A0G2JDY1-mappedCitation-33898448http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/33898448
http://purl.uniprot.org/uniprot/#_A0A0G2JDZ6-mappedCitation-33898448http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/33898448
http://purl.uniprot.org/uniprot/#_A0A0A6YWN6-mappedCitation-33898448http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/33898448