Options
Sananbenesi, Farahnaz
Loading...
Preferred name
Sananbenesi, Farahnaz
Official Name
Sananbenesi, Farahnaz
Alternative Name
Sananbenesi, F.
Now showing 1 - 1 of 1
2018Journal Article [["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","14"],["dc.contributor.author","Weise, Stefan C."],["dc.contributor.author","Arumugam, Ganeshkumar"],["dc.contributor.author","Villarreal, Alejandro"],["dc.contributor.author","Videm, Pavankumar"],["dc.contributor.author","Heidrich, Stefanie"],["dc.contributor.author","Nebel, Nils"],["dc.contributor.author","Dumit, Verónica I."],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Reimann, Viktoria"],["dc.contributor.author","Craske, Madeline"],["dc.contributor.author","Schilling, Oliver"],["dc.contributor.author","Hess, Wolfgang R."],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Backofen, Rolf"],["dc.contributor.author","Vogel, Tanja"],["dc.date.accessioned","2019-07-09T11:51:06Z"],["dc.date.available","2019-07-09T11:51:06Z"],["dc.date.issued","2018"],["dc.description.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."],["dc.identifier.doi","10.1007/s12035-018-1444-7"],["dc.identifier.pmid","30539330"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16050"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59877"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","FOXG1 Regulates PRKAR2B Transcriptionally and Posttranscriptionally via miR200 in the Adult Hippocampus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC