@Article{Weise2018,
author="Weise, Stefan C.
and Arumugam, Ganeshkumar
and Villarreal, Alejandro
and Videm, Pavankumar
and Heidrich, Stefanie
and Nebel, Nils
and Dumit, Ver{\'o}nica I.
and Sananbenesi, Farahnaz
and Reimann, Viktoria
and Craske, Madeline
and Schilling, Oliver
and Hess, Wolfgang R.
and Fischer, Andre
and Backofen, Rolf
and Vogel, Tanja",
title="FOXG1 Regulates PRKAR2B Transcriptionally and Posttranscriptionally via miR200 in the Adult Hippocampus",
journal="Molecular Neurobiology",
year="2018",
month="Dec",
day="11",
abstract="Rett syndrome is a complex neurodevelopmental disorder that is mainly caused by mutations in MECP2. However, mutations in FOXG1 cause a less frequent form of atypical Rett syndrome, called FOXG1 syndrome. FOXG1 is a key transcription factor crucial for forebrain development, where it maintains the balance between progenitor proliferation and neuronal differentiation. Using genome-wide small RNA sequencing and quantitative proteomics, we identified that FOXG1 affects the biogenesis of miR200b/a/429 and interacts with the ATP-dependent RNA helicase, DDX5/p68. Both FOXG1 and DDX5 associate with the microprocessor complex, whereby DDX5 recruits FOXG1 to DROSHA. RNA-Seq analyses of Foxg1cre/+ hippocampi and N2a cells overexpressing miR200 family members identified cAMP-dependent protein kinase type II-beta regulatory subunit (PRKAR2B) as a target of miR200 in neural cells. PRKAR2B inhibits postsynaptic functions by attenuating protein kinase A (PKA) activity; thus, increased PRKAR2B levels may contribute to neuronal dysfunctions in FOXG1 syndrome. Our data suggest that FOXG1 regulates PRKAR2B expression both on transcriptional and posttranscriptional levels.",
issn="1559-1182",
doi="10.1007/s12035-018-1444-7",
url="https://doi.org/10.1007/s12035-018-1444-7",
  user =	 {videmp}
}