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• W4224263722 startingPage "514" @default.
• W4224263722 abstract "Angelman syndrome (AS) is a severe neurodevelopmental disorder featuring ataxia, cognitive impairment, and drug-resistant epilepsy. AS is caused by mutations or deletion of the maternal copy of the paternally imprinted UBE3A gene, with current precision therapy approaches focusing on re-expression of UBE3A. Certain phenotypes, however, are difficult to rescue beyond early development. Notably, a cluster of microRNA binding sites was reported in the untranslated Ube3a1 transcript, including for miR-134, suggesting that AS may be associated with microRNA dysregulation. Here, we report levels of miR-134 and key targets are normal in the hippocampus of mice carrying a maternal deletion of Ube3a (Ube3am-/p+ ). Nevertheless, intracerebroventricular injection of an antimiR oligonucleotide inhibitor of miR-134 (Ant-134) reduced audiogenic seizure severity over multiple trials in 21- and 42-day-old AS mice. Interestingly, Ant-134 also improved distance traveled and center crossings of AS mice in the open-field test. Finally, we show that silencing miR-134 can upregulate targets of miR-134 in neurons differentiated from Angelman patient-derived induced pluripotent stem cells. These findings indicate that silencing miR-134 and possibly other microRNAs could be useful to treat clinically relevant phenotypes with a later developmental window in AS." @default.
• W4224263722 created "2022-04-26" @default.
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• W4224263722 date "2022-06-01" @default.
• W4224263722 modified "2023-10-02" @default.
• W4224263722 title "AntimiR targeting of microRNA-134 reduces seizures in a mouse model of Angelman syndrome" @default.
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• W4224263722 doi "https://doi.org/10.1016/j.omtn.2022.04.009" @default.
• W4224263722 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35592499" @default.
• W4224263722 hasPublicationYear "2022" @default.
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