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• W2756784367 abstract "Genomic imprinting is an allelic gene expression phenomenon primarily controlled by allele-specific DNA methylation at the imprinting control region (ICR), but the underlying mechanism remains largely unclear. N-α-acetyltransferase 10 protein (Naa10p) catalyzes N-α-acetylation of nascent proteins, and mutation of human Naa10p is linked to severe developmental delays. Here we report that Naa10-null mice display partial embryonic lethality, growth retardation, brain disorders, and maternal effect lethality, phenotypes commonly observed in defective genomic imprinting. Genome-wide analyses further revealed global DNA hypomethylation and enriched dysregulation of imprinted genes in Naa10p-knockout embryos and embryonic stem cells. Mechanistically, Naa10p facilitates binding of DNA methyltransferase 1 (Dnmt1) to DNA substrates, including the ICRs of the imprinted allele during S phase. Moreover, the lethal Ogden syndrome-associated mutation of human Naa10p disrupts its binding to the ICR of H19 and Dnmt1 recruitment. Our study thus links Naa10p mutation-associated Ogden syndrome to defective DNA methylation and genomic imprinting." @default.
• W2756784367 created "2017-10-06" @default.
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• W2756784367 date "2017-10-01" @default.
• W2756784367 modified "2023-10-17" @default.
• W2756784367 title "The Role of N-α-acetyltransferase 10 Protein in DNA Methylation and Genomic Imprinting" @default.
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• W2756784367 doi "https://doi.org/10.1016/j.molcel.2017.08.025" @default.
• W2756784367 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6322414" @default.
• W2756784367 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28943313" @default.
• W2756784367 hasPublicationYear "2017" @default.
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