MeCP2 Deficiency Leads to Loss of Glial Kir4.1

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dc.contributor.authorKahanovitch, Urien
dc.contributor.authorCuddapah, Vishnu A.en
dc.contributor.authorPacheco, Natasha L.en
dc.contributor.authorHolt, Leanne M.en
dc.contributor.authorMurphy, Daniel K.en
dc.contributor.authorPercy, Alan K.en
dc.contributor.authorOlsen, Michelle L.en
dc.contributor.departmentSchool of Neuroscienceen
dc.date.accessioned2018-11-19T18:31:58Zen
dc.date.available2018-11-19T18:31:58Zen
dc.date.issued2018en
dc.description.abstractRett 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
dc.identifier.doihttps://doi.org/10.1523/ENEURO.0194-17.2018en
dc.identifier.issue1en
dc.identifier.urihttp://hdl.handle.net/10919/85877en
dc.identifier.volume5en
dc.language.isoen_USen
dc.publisherSociety for Neuroscienceen
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectEpigenetic regulationen
dc.subjectKcnj10en
dc.subjectMeCP2en
dc.subjectRett syndromeen
dc.titleMeCP2 Deficiency Leads to Loss of Glial Kir4.1en
dc.title.serialeNeuroen
dc.typeArticle - Refereeden
dc.type.dcmitypetexten

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