Losing Dnmt3a dependent methylation in inhibitory neurons impairs neural function by a mechanism impacting Rett syndrome

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Exclusive expression of MeCP2 in the nervous system distinguishes between brain and peripheral Rett syndrome-like phenotypes

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Manipulations of MeCP2 in glutamatergic neurons highlight their contributions to Rett and other neurological disorders

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MeCP2 in the Rostral Striatum Maintains Local Dopamine Content Critical for Psychomotor Control

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Disruption of DNA-methylation-dependent long gene repression in Rett syndrome

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DNA methyltransferase 3a regulates osteoclast differentiation by coupling to an S-adenosylmethionine–producing metabolic pathway

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Loss of MeCP2 in Parvalbumin-and Somatostatin-Expressing Neurons in Mice Leads to Distinct Rett Syndrome-like Phenotypes

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MeCP2 binds to non-CG methylated DNA as neurons mature, influencing transcription and the timing of onset for Rett syndrome

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Loss of MeCP2 From Forebrain Excitatory Neurons Leads to Cortical Hyperexcitation and Seizures

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Dnmt3a in Sim1 Neurons Is Necessary for Normal Energy Homeostasis

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Mutations in the DNA methyltransferase gene DNMT3A cause an overgrowth syndrome with intellectual disability

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Cellular origins of auditory event-related potential deficits in Rett syndrome

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Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows

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MeCP2 Is Critical within HoxB1-Derived Tissues of Mice for Normal Lifespan

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Dnmt3a-Dependent Nonpromoter DNA Methylation Facilitates Transcription of Neurogenic Genes

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MeCP2-Mediated Transcription Repression in the Basolateral Amygdala May Underlie Heightened Anxiety in a Mouse Model of Rett Syndrome

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Loss of MeCP2 in aminergic neurons causes cell-autonomous defects in neurotransmitter synthesis and specific behavioral abnormalities

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Deletion of Mecp2 in Sim1-Expressing Neurons Reveals a Critical Role for MeCP2 in Feeding Behavior, Aggression, and the Response to Stress

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