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http://purl.uniprot.org/citations/11479595http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11479595http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11479595http://www.w3.org/2000/01/rdf-schema#comment"In mammals, dosage compensation of X-linked genes is achieved by the transcriptional silencing of one X chromosome in the female (reviewed in ref. 1). This process, called X inactivation, is usually random in the embryo proper. In marsupials and the extra-embryonic region of the mouse, however, X inactivation is imprinted: the paternal X chromosome is preferentially inactivated whereas the maternal X is always active. Having more than one active X chromosome is deleterious to extra-embryonic development in the mouse. Here we show that the gene eed (embryonic ectoderm development), a member of the mouse Polycomb group (Pc-G) of genes, is required for primary and secondary trophoblast giant cell development in female embryos. Results from mice carrying a paternally inherited X-linked green fluorescent protein (GFP) transgene implicate eed in the stable maintenance of imprinted X inactivation in extra-embryonic tissues. Based on the recent finding that the Eed protein interacts with histone deacetylases, we suggest that this maintenance activity involves hypoacetylation of the inactivated paternal X chromosome in the extra-embryonic tissues."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.org/dc/terms/identifier"doi:10.1038/ng574"xsd:string
http://purl.uniprot.org/citations/11479595http://purl.org/dc/terms/identifier"doi:10.1038/ng574"xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/author"Chen Y."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/author"Chen Y."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/author"Magnuson T."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/author"Magnuson T."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/author"Schneider E."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/author"Schneider E."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/author"Nagy A."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/author"Nagy A."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/author"Cross J.C."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/author"Cross J.C."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/author"Mager J."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/author"Mager J."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/date"2001"xsd:gYear
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/date"2001"xsd:gYear
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/name"Nat. Genet."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/name"Nat. Genet."xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/pages"371-375"xsd:string
http://purl.uniprot.org/citations/11479595http://purl.uniprot.org/core/pages"371-375"xsd:string