Kahanovitch, UriCuddapah, Vishnu A.Pacheco, Natasha L.Holt, Leanne M.Murphy, Daniel K.Percy, Alan K.Olsen, Michelle L.2018-11-192018-11-192018http://hdl.handle.net/10919/85877Rett syndrome is a devastating neurodevelopmental disorder that affects 1 in 10,000–25,000 females. Mutations in methyl-CpG-binding protein 2 (MeCP2), a transcriptional regulator, are responsible for >95% of RTT cases. Recent work has shown that astrocytes contribute significantly to the disorder, although their contribution to this disease is not known. Here, we demonstrate that the critical astrocyte K⁺ channel Kir4.1 is a novel molecular target of MeCP2. MeCP2 deficiency leads to decreased Kcnj10/Kir4.1 mRNA levels, protein expression, and currents. These findings provide novel mechanistic insight and begin to elucidate the role of astrocytes in this disorder.en-USCreative Commons Attribution 4.0 InternationalEpigenetic regulationKcnj10MeCP2Rett syndromeArticle - Refereedhttps://doi.org/10.1523/ENEURO.0194-17.201851