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@ARTICLE{Weise:140922,
      author       = {Weise, Stefan C and Arumugam, Ganeshkumar and Villarreal,
                      Alejandro and Videm, Pavankumar and Heidrich, Stefanie and
                      Nebel, Nils and Dumit, Verónica 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        = {{FOXG}1 {R}egulates {PRKAR}2{B} {T}ranscriptionally and
                      {P}osttranscriptionally via mi{R}200 in the {A}dult
                      {H}ippocampus.},
      journal      = {Molecular neurobiology},
      volume       = {56},
      number       = {7},
      issn         = {0893-7648},
      address      = {Totowa, NJ},
      publisher    = {Humana Press},
      reportid     = {DZNE-2020-07244},
      pages        = {5188-5201},
      year         = {2019},
      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.},
      keywords     = {Age Factors / Animals / Cyclic AMP-Dependent Protein Kinase
                      RIIbeta Subunit: genetics / Cyclic AMP-Dependent Protein
                      Kinase RIIbeta Subunit: metabolism / Forkhead Transcription
                      Factors: genetics / Forkhead Transcription Factors:
                      metabolism / Hippocampus: growth $\&$ development /
                      Hippocampus: metabolism / Mice / Mice, Inbred C57BL / Mice,
                      Transgenic / MicroRNAs: genetics / MicroRNAs: metabolism /
                      Nerve Tissue Proteins: genetics / Nerve Tissue Proteins:
                      metabolism / Transcription, Genetic: physiology / Cyclic
                      AMP-Dependent Protein Kinase RIIbeta Subunit (NLM Chemicals)
                      / Forkhead Transcription Factors (NLM Chemicals) / Foxg1
                      protein, mouse (NLM Chemicals) / MicroRNAs (NLM Chemicals) /
                      Mirn200 microRNA, mouse (NLM Chemicals) / Nerve Tissue
                      Proteins (NLM Chemicals) / PRKAR2B protein, human (NLM
                      Chemicals)},
      cin          = {AG Bonn 2 / AG Fischer 1},
      ddc          = {570},
      cid          = {I:(DE-2719)1440012 / I:(DE-2719)1410002},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30539330},
      pmc          = {pmc:PMC6647430},
      doi          = {10.1007/s12035-018-1444-7},
      url          = {https://pub.dzne.de/record/140922},
}