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http://purl.uniprot.org/citations/24368734http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24368734http://www.w3.org/2000/01/rdf-schema#comment"Enhancers play a central role in cell-type-specific gene expression and are marked by H3K4me1/2. Active enhancers are further marked by H3K27ac. However, the methyltransferases responsible for H3K4me1/2 on enhancers remain elusive. Furthermore, how these enzymes function on enhancers to regulate cell-type-specific gene expression is unclear. In this study, we identify MLL4 (KMT2D) as a major mammalian H3K4 mono- and di-methyltransferase with partial functional redundancy with MLL3 (KMT2C). Using adipogenesis and myogenesis as model systems, we show that MLL4 exhibits cell-type- and differentiation-stage-specific genomic binding and is predominantly localized on enhancers. MLL4 co-localizes with lineage-determining transcription factors (TFs) on active enhancers during differentiation. Deletion of Mll4 markedly decreases H3K4me1/2, H3K27ac, Mediator and Polymerase II levels on enhancers and leads to severe defects in cell-type-specific gene expression and cell differentiation. Together, these findings identify MLL4 as a major mammalian H3K4 mono- and di-methyltransferase essential for enhancer activation during cell differentiation. DOI: http://dx.doi.org/10.7554/eLife.01503.001."xsd:string
http://purl.uniprot.org/citations/24368734http://purl.org/dc/terms/identifier"doi:10.7554/elife.01503"xsd:string
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/author"Feng X."xsd:string
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/author"Peng W."xsd:string
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/author"Wang C."xsd:string
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/author"Wang L."xsd:string
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/author"Zhuang L."xsd:string
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/author"Xu S."xsd:string
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/author"Sartorelli V."xsd:string
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/author"Lee J.E."xsd:string
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/author"Cho Y.W."xsd:string
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/author"Ge K."xsd:string
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/author"Baldridge A."xsd:string
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/name"Elife"xsd:string
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/pages"e01503"xsd:string
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/title"H3K4 mono- and di-methyltransferase MLL4 is required for enhancer activation during cell differentiation."xsd:string
http://purl.uniprot.org/citations/24368734http://purl.uniprot.org/core/volume"2"xsd:string
http://purl.uniprot.org/citations/24368734http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24368734
http://purl.uniprot.org/citations/24368734http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/24368734
http://purl.uniprot.org/uniprot/#_A0A0G2JE02-mappedCitation-24368734http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24368734
http://purl.uniprot.org/uniprot/#_A0A0A6YY77-mappedCitation-24368734http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24368734
http://purl.uniprot.org/uniprot/#_A0A087WRV7-mappedCitation-24368734http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24368734
http://purl.uniprot.org/uniprot/#_A0A0A0MQ73-mappedCitation-24368734http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24368734