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[Research progress of Rett syndrome causing gene MECP2--the structure, function and modulation of MECP2].
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HAGLR promotes neuron differentiation through the miR-130a-3p-MeCP2 axis.
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MeCP2 prevents age-associated cognitive decline via restoring synaptic plasticity in a senescence-accelerated mouse model.
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Role of Virus-Induced Host Cell Epigenetic Changes in Cancer.
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An RNA interference screen identifies druggable regulators of MeCP2 stability.
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MeCP2 and histone deacetylases 1 and 2 in dorsal striatum collectively suppress repetitive behaviors.
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MeCP2 regulates activity-dependent transcriptional responses in olfactory sensory neurons.
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Global transcriptional and translational repression in human-embryonic-stem-cell-derived Rett syndrome neurons.
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The impact of MeCP2 loss- or gain-of-function on synaptic plasticity.
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Neuronal MeCP2 is expressed at near histone-octamer levels and globally alters the chromatin state.
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Mouse models of MeCP2 disorders share gene expression changes in the cerebellum and hypothalamus.
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MeCP2, a key contributor to neurological disease, activates and represses transcription.
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Transcriptional profiling of a mouse model for Rett syndrome reveals subtle transcriptional changes in the brain.
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Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl-CpG-binding protein 2.
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