Abstract
Both increases and decreases in methyl CpG-binding protein 2 (MeCP2) levels cause neurodevelopmental defects. We found that MeCP2 translation is regulated by microRNA 132 (miR132). Block of miR132-mediated repression increased MeCP2 and brain-derived neurotrophic factor (BDNF) levels in cultured rat neurons and the loss of MeCP2 reduced BDNF and miR132 levels in vivo. This feedback loop may provide a mechanism for homeostatic control of MeCP2 expression.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Animals, Newborn
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Brain-Derived Neurotrophic Factor / pharmacology
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CREB-Binding Protein / physiology*
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Cells, Cultured
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Cerebral Cortex / cytology
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Colforsin / pharmacology
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Drug Interactions
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Embryo, Mammalian
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Gene Expression Regulation, Developmental / drug effects*
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Green Fluorescent Proteins / biosynthesis
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Green Fluorescent Proteins / genetics
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Methyl-CpG-Binding Protein 2 / deficiency
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Methyl-CpG-Binding Protein 2 / metabolism*
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Mice
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Mice, Knockout
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MicroRNAs / antagonists & inhibitors
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MicroRNAs / pharmacology*
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Neurons / drug effects
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Oligonucleotides, Antisense / pharmacology
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RNA, Small Interfering / pharmacology
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Regulatory Elements, Transcriptional / genetics
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Thionucleotides / pharmacology
Substances
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Brain-Derived Neurotrophic Factor
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Mecp2 protein, mouse
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Methyl-CpG-Binding Protein 2
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MicroRNAs
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Oligonucleotides, Antisense
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RNA, Small Interfering
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Thionucleotides
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Green Fluorescent Proteins
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Colforsin
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CREB-Binding Protein