Sananbenesi, Farahnaz

[["dc.bibliographiccitation.firstpage","1145"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Biological Chemistry"],["dc.bibliographiccitation.lastpage","1153"],["dc.bibliographiccitation.volume","390"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:46:46Z"],["dc.date.available","2017-09-07T11:46:46Z"],["dc.date.issued","2009"],["dc.description.abstract","The orchestrated expression of genes is essential for the development and survival of every organism. In addition to the role of transcription factors, the availability of genes for transcription is controlled by a series of proteins that regulate epigenetic chromatin remodeling. The two most studied epigenetic phenomena are DNA methylation and histone-tail modifications. Although a large body of literature implicates the deregulation of histone acetylation and DNA methylation with the pathogenesis of cancer, recently epigenetic mechanisms have also gained much attention in the neuroscientific community. In fact, a new field of research is rapidly emerging and there is now accumulating evidence that the molecular machinery that regulates histone acetylation and DNA methylation is intimately involved in synaptic plasticity and is essential for learning and memory. Importantly, dysfunction of epigenetic gene expression in the brain might be involved in neurodegenerative and psychiatric diseases. In particular, it was found that inhibition of histone deacetylases attenuates synaptic and neuronal loss in animal models for various neurodegenerative diseases and improves cognitive function. In this article, we will summarize recent data in the novel field of neuroepigenetics and discuss the question why epigenetic strategies are suitable therapeutic approaches for the treatment of brain diseases."],["dc.identifier.doi","10.1515/BC.2009.131"],["dc.identifier.gro","3143028"],["dc.identifier.isi","000270513600009"],["dc.identifier.pmid","19747081"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/497"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: European Science Foundation"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1431-6730"],["dc.title","The epigenetic bottleneck of neurodegenerative and psychiatric diseases"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","825"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","838"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Pang, Petti"],["dc.contributor.author","Lu, Bai"],["dc.contributor.author","Tsai, Li-Huei"],["dc.date.accessioned","2017-09-07T11:53:39Z"],["dc.date.available","2017-09-07T11:53:39Z"],["dc.date.issued","2005"],["dc.description.abstract","While deregulation of cyclin-dependent kinase 5 (Cdk5) has been implicated in neurodegenerative diseases, its precise role in synaptic plasticity and memory remains elusive. Proteolytic cleavage of p35, a regulatory subunit of Cdk5, by calpain results in the generation of the truncated p25 protein, which causes hyperactivation of Cdk5. Using region-specific and inducible transgenic mice, we show that transiently increased p25 expression in the hippocampus enhanced long-term potentiation (LTP) and facilitated hippocampus-dependent memory. Moreover, p25 expression increased the number of dendritic spines and synapses. Importantly, enhanced memory achieved by a transient expression of p25 followed by its repression did not cause neurodegeneration. In contrast, prolonged p25 production caused severe cognitive deficits, which were accompanied by synaptic and neuronal loss and impaired LTP. Our data suggest a role for p25 in synaptic plasticity, synaptogenesis, learning, and memory and provide a model whereby deregulation of a plasticity factor can contribute to neurodegeneration."],["dc.identifier.doi","10.1016/j.neuron.2005.10.033"],["dc.identifier.gro","3143777"],["dc.identifier.isi","000233927300020"],["dc.identifier.pmid","16337919"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1328"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Intramural NIH HHS; NINDS NIH HHS [NS051874]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0896-6273"],["dc.title","Opposing roles of transient and prolonged expression of p25 in synaptic plasticity and hippocampus-dependent memory"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2815"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","The EMBO journal"],["dc.bibliographiccitation.lastpage","2828"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Pinheiro, Paulo S."],["dc.contributor.author","Rebola, Nelson"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Gertig, Michael"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Delalle, Ivana"],["dc.contributor.author","Jatzko, Alexander"],["dc.contributor.author","Dettenhofer, Markus"],["dc.contributor.author","Zunszain, Patricia A"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Pape, Julius C"],["dc.contributor.author","Binder, Elisabeth B."],["dc.contributor.author","Mulle, Christophe"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.date.accessioned","2018-01-09T14:50:41Z"],["dc.date.available","2018-01-09T14:50:41Z"],["dc.date.issued","2017"],["dc.description.abstract","Age-associated memory decline is due to variable combinations of genetic and environmental risk factors. How these risk factors interact to drive disease onset is currently unknown. Here we begin to elucidate the mechanisms by which post-traumatic stress disorder (PTSD) at a young age contributes to an increased risk to develop dementia at old age. We show that the actin nucleator Formin 2 (Fmn2) is deregulated in PTSD and in Alzheimer's disease (AD) patients. Young mice lacking the Fmn2 gene exhibit PTSD-like phenotypes and corresponding impairments of synaptic plasticity, while the consolidation of new memories is unaffected. However, Fmn2 mutant mice develop accelerated age-associated memory decline that is further increased in the presence of additional risk factors and is mechanistically linked to a loss of transcriptional homeostasis. In conclusion, our data present a new approach to explore the connection between AD risk factors across life span and provide mechanistic insight to the processes by which neuropsychiatric diseases at a young age affect the risk for developing dementia."],["dc.identifier.doi","10.15252/embj.201796821"],["dc.identifier.pmid","28768717"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14923"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11608"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1460-2075"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Formin 2 links neuropsychiatric phenotypes at young age to an increased risk for dementia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","463"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Molecular and Cellular Neuroscience"],["dc.bibliographiccitation.lastpage","476"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Schrick, Christina"],["dc.contributor.author","Spiess, Joachim"],["dc.contributor.author","Radulovic, Jelena"],["dc.date.accessioned","2017-09-07T11:45:13Z"],["dc.date.available","2017-09-07T11:45:13Z"],["dc.date.issued","2002"],["dc.description.abstract","The phosphorylation of proteins involved in the MAP kinase signal transduction pathway was investigated during associative learning of C57BL/6J mice. Context-dependent fear conditioning, consisting of a single exposure of mice to a context followed by foot shock, was employed as a learning paradigm. Control groups consisted of mice exposed to context only or an immediate shock in the context. Coincident up-regulation of phosphorylated Erk-1/2 and Elk-1 was observed in the CA3 hippocampal subfield and dentate gyrus 30 min after fear conditioning but not after the control paradigms. Phosphorylated Erk-1/2 and Elk-1 were associated and predominantly colocalized in the mossy fibers. In vitro kinase assays showed that hippocampal Erk-1/2 phosphorylates Elk-1. Notably, Elk-1 in turn enhances the phosphorylation of Erk-1/2 and its downstream target p90Rsk-1. Increased phosphorylation and nuclear translocation of p90Rsk-1 was also demonstrated in the CA3 hippocampal area in vivo during contextual fear conditioning. The observed interactions between hippocampal Elk-1 and Erk-1/2 proteins may affect the consolidation of contextual memories through activation of the downstream nuclear targets of Erk-1/2, such as p90Rsk-1, without requiring nuclear translocation of Elk-1 and Erk-1/2."],["dc.identifier.doi","10.1006/mcne.2002.1188"],["dc.identifier.gro","3144158"],["dc.identifier.isi","000180054800008"],["dc.identifier.pmid","12498787"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1751"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1044-7431"],["dc.title","Phosphorylation of hippocampal Erk-1/2, Elk-1, and p90-Rsk-1 during contextual fear conditioning: Interactions between Erk-1/2 and Elk-1"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1962"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","1966"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Schrick, Christina"],["dc.contributor.author","Spiess, Joachim"],["dc.contributor.author","Radulovic, Jelena"],["dc.date.accessioned","2017-09-07T11:43:59Z"],["dc.date.available","2017-09-07T11:43:59Z"],["dc.date.issued","2004"],["dc.description.abstract","It is believed that de novo protein synthesis is fundamentally linked to synaptic changes in neuronal circuits involved in acquisition and extinction of conditioned responses. Recent studies show that neuronal plasticity may be also altered by cytoskeletal rearrangement independently of protein synthesis. We investigated the role of these processes in the hippocampus during acquisition and extinction of context-dependent conditioned fear in mice. Intrahippocampal injections of the protein synthesis inhibitors anisomycin and puromycin, or of the actin rearrangement inhibitors cytochalasin D and latrunculin A, prevented the acquisition of context-dependent fear. Unexpectedly, anisomycin and puromycin enhanced extinction without erasing the fear memory. In contrast, cytochalasin D and latrunculin A prevented extinction of context-dependent freezing. On the basis of these findings, it is suggested that certain hippocampal mechanisms mediating extinction of conditioned contextual fear are inhibited by protein synthesis and involve actin rearrangement. Such mechanisms might predominantly elicit modifications of hippocampal circuits that store the conditioning memory."],["dc.identifier.doi","10.1523/JNEUROSCI.5112-03.2004"],["dc.identifier.gro","3144009"],["dc.identifier.isi","000189210300020"],["dc.identifier.pmid","14985438"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1586"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0270-6474"],["dc.title","Distinct roles of hippocampal de novo protein synthesis and actin rearrangement in extinction of contextual fear"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1565"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","1579"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Kastner, Anne"],["dc.contributor.author","Poggi, Giulia"],["dc.contributor.author","Mitjans, Marina"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Hartmann, Annette M."],["dc.contributor.author","Van der Auwera, Sandra"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Krueger-Burg, Dilja"],["dc.contributor.author","Matuszko, Gabriela"],["dc.contributor.author","Brosi, Cornelia"],["dc.contributor.author","Homuth, Georg"],["dc.contributor.author","Völzke, H."],["dc.contributor.author","Benseler, Fritz"],["dc.contributor.author","Bagni, Claudia"],["dc.contributor.author","Fischer, Utz"],["dc.contributor.author","Dityatev, Alexander"],["dc.contributor.author","Grabe, Hans-Jörgen"],["dc.contributor.author","Rujescu, Dan"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:54:49Z"],["dc.date.available","2017-09-07T11:54:49Z"],["dc.date.issued","2015"],["dc.description.abstract","Fragile X syndrome (FXS) is mostly caused by a CGG triplet expansion in the fragile X mental retardation 1 gene (FMR1). Up to 60% of affected males fulfill criteria for autism spectrum disorder (ASD), making FXS the most frequent monogenetic cause of syndromic ASD. It is unknown, however, whether normal variants (independent of mutations) in the fragile X gene family (FMR1, FXR1, FXR2) and in FMR2 modulate autistic features. Here, we report an accumulation model of 8 SNPs in these genes, associated with autistic traits in a discovery sample of male patients with schizophrenia (N = 692) and three independent replicate samples: patients with schizophrenia (N = 626), patients with other psychiatric diagnoses (N = 111) and a general population sample (N = 2005). For first mechanistic insight, we contrasted microRNA expression in peripheral blood mononuclear cells of selected extreme group subjects with high-versus low-risk constellation regarding the accumulation model. Thereby, the brain-expressed miR-181 species emerged as potential \"umbrella regulator\", with several seed matches across the fragile X gene family and FMR2. To conclude, normal variation in these genes contributes to the continuum of autistic phenotypes."],["dc.identifier.doi","10.15252/emmm.201505696"],["dc.identifier.gro","3141771"],["dc.identifier.isi","000368135400005"],["dc.identifier.pmid","26612855"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12871"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/890"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1757-4684"],["dc.relation.issn","1757-4676"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Accumulated common variants in the broader fragile X gene family modulate autistic phenotypes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","753"],["dc.bibliographiccitation.issue","5979"],["dc.bibliographiccitation.journal","Science"],["dc.bibliographiccitation.lastpage","756"],["dc.bibliographiccitation.volume","328"],["dc.contributor.author","Peleg, Shahaf"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Zovoilis, Athanasios"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Cota, Perla"],["dc.contributor.author","Wittnam, Jessica"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Dettenhofer, Markus"],["dc.contributor.author","Kang, Hui"],["dc.contributor.author","Farinelli, Laurent"],["dc.contributor.author","Chen, Wei"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Doering, Aaron"],["dc.date.accessioned","2017-09-07T11:46:04Z"],["dc.date.available","2017-09-07T11:46:04Z"],["dc.date.issued","2010"],["dc.description.abstract","As the human life span increases, the number of people suffering from cognitive decline is rising dramatically. The mechanisms underlying age-associated memory impairment are, however, not understood. Here we show that memory disturbances in the aging brain of the mouse are associated with altered hippocampal chromatin plasticity. During learning, aged mice display a specific deregulation of histone H4 lysine 12 (H4K12) acetylation and fail to initiate a hippocampal gene expression program associated with memory consolidation. Restoration of physiological H4K12 acetylation reinstates the expression of learning-induced genes and leads to the recovery of cognitive abilities. Our data suggest that deregulated H4K12 acetylation may represent an early biomarker of an impaired genome-environment interaction in the aging mouse brain."],["dc.identifier.doi","10.1126/science.1186088"],["dc.identifier.gro","3142928"],["dc.identifier.isi","000277357100040"],["dc.identifier.pmid","20448184"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/386"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0036-8075"],["dc.title","Altered Histone Acetylation Is Associated with Age-Dependent Memory Impairment in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3700"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","3707"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Schrick, Christina"],["dc.contributor.author","Spiess, Joachim"],["dc.contributor.author","Radulovic, Jelena"],["dc.date.accessioned","2017-09-07T11:45:54Z"],["dc.date.available","2017-09-07T11:45:54Z"],["dc.date.issued","2002"],["dc.description.abstract","Transient stressful experiences may persistently facilitate associative and nonassociative learning, possibly through alterations of gene expression. Here we identify, by subtractive hybridization, differential expression of the Cdk5 gene in response to stress. The Cdk5 protein is selectively induced in the fibers of septohippocampal cholinergic neurons but not in other regions of prominent Cdk5 production. This upregulation is accompanied by increased Cdk5 kinase activity, which is blocked completely by the Cdk5 inhibitor butyrolactone I. Microinjection of butyrolactone I into the lateral septum and hippocampus prevents the acquisition of conditioned context-dependent fear as well as its stress-induced facilitation. By demonstrating that a transient increase of Cdk5 activity within the septohippocampal system is required for associative learning, an important novel role of Cdk5 has been identified."],["dc.identifier.doi","10.1523/JNEUROSCI.22-09-03700.2002"],["dc.identifier.gro","3144203"],["dc.identifier.isi","000175296200047"],["dc.identifier.pmid","11978846"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1802"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0270-6474"],["dc.title","Cyclin-dependent kinase 5 is required for associative learning"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Islam, Md Rezaul"],["dc.contributor.author","Lbik, Dawid"],["dc.contributor.author","Sakib, M Sadman"],["dc.contributor.author","Maximilian Hofmann, Raoul"],["dc.contributor.author","Berulava, Tea"],["dc.contributor.author","Jiménez Mausbach, Martí"],["dc.contributor.author","Cha, Julia"],["dc.contributor.author","Goldberg, Maria"],["dc.contributor.author","Vakhtang, Elerdashvili"],["dc.contributor.author","Schiffmann, Christian"],["dc.contributor.author","Zieseniss, Anke"],["dc.contributor.author","Katschinski, Dörthe Magdalena"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2021-04-14T08:29:54Z"],["dc.date.available","2021-04-14T08:29:54Z"],["dc.date.issued","2021"],["dc.description.abstract","n current clinical practice, care of diseased patients is often restricted to separated disciplines. However, such an organ-centered approach is not always suitable. For example, cognitive dysfunction is a severe burden in heart failure patients. Moreover, these patients have an increased risk for age-associated dementias. The underlying molecular mechanisms are presently unknown, and thus, corresponding therapeutic strategies to improve cognition in heart failure patients are missing. Using mice as model organisms, we show that heart failure leads to specific changes in hippocampal gene expression, a brain region intimately linked to cognition. These changes reflect increased cellular stress pathways which eventually lead to loss of neuronal euchromatin and reduced expression of a hippocampal gene cluster essential for cognition. Consequently, mice suffering from heart failure exhibit impaired memory function. These pathological changes are ameliorated via the administration of a drug that promotes neuronal euchromatin formation. Our study provides first insight to the molecular processes by which heart failure contributes to neuronal dysfunction and point to novel therapeutic avenues to treat cognitive defects in heart failure patients."],["dc.identifier.doi","10.15252/emmm.201911900"],["dc.identifier.pmid","33471428"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83025"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/117"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/378"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D04: Bedeutung der Methylierung von RNA (m6A) und des Histons H3 (H3K4) in der Herzinsuffizienz"],["dc.relation.eissn","1757-4684"],["dc.relation.issn","1757-4676"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY 4.0"],["dc.title","Epigenetic gene expression links heart failure to memory impairment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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"]]