Bahari-Javan, Sanaz

[["dc.bibliographiccitation.firstpage","3452"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","3464"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Kranz, Andrea"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Stewart, Adrian Francis"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:47:49Z"],["dc.date.available","2017-09-07T11:47:49Z"],["dc.date.issued","2013"],["dc.description.abstract","The consolidation of long-term memories requires differential gene expression. Recent research has suggested that dynamic changes in chromatin structure play a role in regulating the gene expression program linked to memory formation. The contribution of histone methylation, an important regulatory mechanism of chromatin plasticity that is mediated by the counteracting activity of histone-methyltransferases and histone-demethylases, is, however, not well understood. Here we show that mice lacking the histone-methyltransferase myeloid/lymphoid or mixed-lineage leukemia 2 (mll2/kmt2b) gene in adult forebrain excitatory neurons display impaired hippocampus-dependent memory function. Consistent with the role of KMT2B in gene-activation DNA microarray analysis revealed that 152 genes were downregulated in the hippocampal dentate gyrus region of mice lacking kmt2b. Downregulated plasticity genes showed a specific deficit in histone 3 lysine 4 di-and trimethylation, while histone 3 lysine 4 monomethylation was not affected. Our data demonstrates that KMT2B mediates hippocampal histone 3 lysine 4 di-and trimethylation and is a critical player for memory formation."],["dc.identifier.doi","10.1523/JNEUROSCI.3356-12.2013"],["dc.identifier.gro","3142390"],["dc.identifier.isi","000315195700021"],["dc.identifier.pmid","23426673"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7752"],["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","Histone-Methyltransferase MLL2 (KMT2B) Is Required for Memory Formation 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","49"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Learning & Memory"],["dc.bibliographiccitation.lastpage","57"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Kuczera, Tanja"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Hsia, Hung-En"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Irniger, Stefan"],["dc.contributor.author","Nasmyth, Kim"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:45:07Z"],["dc.date.available","2017-09-07T11:45:07Z"],["dc.date.issued","2011"],["dc.description.abstract","Learning and memory processes critically involve the orchestrated regulation of de novo protein synthesis. On the other hand it has become clear that regulated protein degradation also plays a major role in neuronal plasticity and learning behavior. One of the key pathways mediating protein degradation is proteosomal protein destruction. The anaphase-promoting complex/cyclosome (APC/C) is an E3 ubiquitin ligase that targets proteins for proteosomal degradation by the 26S proteasome. While the APC/C is essential for cell cycle progression it is also expressed in postmitotic neurons where it has been implicated with axonal outgrowth and neuronal survival. In this study we addressed the role of APC/C in learning and memory function by generating mice that lack the essential subunit APC2 from excitatory neurons of the adult forebrain. Those animals are viable but exhibit a severe impairment in the ability to extinct fear memories, a process critical for the treatment of anxiety diseases such as phobia or post-traumatic stress disorder. Since deregulated protein degradation and APC/C activity has been implicated with neurodegeneration we also analyzed the effect of Apc2 deletion in a mouse model for Alzheimer's disease. In our experimental setting loss of APC2 form principle forebrain neurons did not affect the course of pathology in an Alzheimer's disease mouse model. In conclusion, our data provides genetic evidence that APC/C activity in the adult forebrain is required for cognitive function."],["dc.identifier.doi","10.1101/lm.1998411"],["dc.identifier.gro","3142805"],["dc.identifier.isi","000285547500001"],["dc.identifier.pmid","21191042"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/250"],["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","1072-0502"],["dc.title","The anaphase promoting complex is required for memory function 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","1"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","9"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Varbanov, Hristo"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Anderson-Schmidt, Heike"],["dc.contributor.author","Anghelescu, Ion"],["dc.contributor.author","Budde, Monika"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Costa, Joan"],["dc.contributor.author","Medina, Juan"],["dc.contributor.author","Dietrich, Detlef E."],["dc.contributor.author","Figge, Christian"],["dc.contributor.author","Folkerts, Here"],["dc.contributor.author","Gade, Katrin"],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Koller, Manfred"],["dc.contributor.author","Konrad, Carsten"],["dc.contributor.author","Nussbeck, Sara Y."],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Spitzer, Carsten"],["dc.contributor.author","Stierl, Sebastian"],["dc.contributor.author","Stöckel, Judith"],["dc.contributor.author","Thiel, Andreas"],["dc.contributor.author","von Hagen, Martin"],["dc.contributor.author","Zimmermann, Jörg"],["dc.contributor.author","Zitzelsberger, Antje"],["dc.contributor.author","Schulz, Sybille"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Delalle, Ivana"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Dityatev, Alexander"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.date.accessioned","2018-01-09T14:44:03Z"],["dc.date.available","2018-01-09T14:44:03Z"],["dc.date.issued","2017-06-06"],["dc.description.abstract","Schizophrenia is a devastating disease that arises on the background of genetic predisposition and environmental risk factors, such as early life stress (ELS). In this study, we show that ELS-induced schizophrenia-like phenotypes in mice correlate with a widespread increase of histone-deacetylase 1 (Hdac1) expression that is linked to altered DNA methylation. Hdac1 overexpression in neurons of the medial prefrontal cortex, but not in the dorsal or ventral hippocampus, mimics schizophrenia-like phenotypes induced by ELS. Systemic administration of an HDAC inhibitor rescues the detrimental effects of ELS when applied after the manifestation of disease phenotypes. In addition to the hippocampus and prefrontal cortex, mice subjected to ELS exhibit increased Hdac1 expression in blood. Moreover, Hdac1 levels are increased in blood samples from patients with schizophrenia who had encountered ELS, compared with patients without ELS experience. Our data suggest that HDAC1 inhibition should be considered as a therapeutic approach to treat schizophrenia."],["dc.identifier.doi","10.1073/pnas.1613842114"],["dc.identifier.pmid","28533418"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14906"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11605"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1091-6490"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","HDAC1 links early life stress to schizophrenia-like phenotypes"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1912"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","EMBO Journal"],["dc.bibliographiccitation.lastpage","1927"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Roenicke, Raik"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Urbanke, Hendrik"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Barth, Jonas"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Schuetz, Anna L."],["dc.contributor.author","Dyczkowski, Jerzy"],["dc.contributor.author","Martinez-Hernandez, Ana"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Dent, Sharon Y. R."],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Reymann, Klaus G."],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:45:35Z"],["dc.date.available","2017-09-07T11:45:35Z"],["dc.date.issued","2014"],["dc.description.abstract","Neuronal histone acetylation has been linked to memory consolidation, and targeting histone acetylation has emerged as a promising therapeutic strategy for neuropsychiatric diseases. However, the role of histone-modifying enzymes in the adult brain is still far from being understood. Here we use RNA sequencing to screen the levels of all known histone acetyltransferases (HATs) in the hippocampal CA1 region and find that K-acetyltransferase 2a (Kat2a)-a HAT that has not been studied for its role in memory function so far-shows highest expression. Mice that lack Kat2a show impaired hippocampal synaptic plasticity and long-term memory consolidation. We furthermore show that Kat2a regulates a highly interconnected hippocampal gene expression network linked to neuroactive receptor signaling via a mechanism that involves nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B). In conclusion, our data establish Kat2a as a novel and essential regulator of hippocampal memory consolidation."],["dc.identifier.doi","10.15252/embj.201487870"],["dc.identifier.gro","3142062"],["dc.identifier.isi","000341839500009"],["dc.identifier.pmid","25024434"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/4123"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1460-2075"],["dc.relation.issn","0261-4189"],["dc.title","K-Lysine acetyltransferase 2a regulates a hippocampal gene expression network linked to memory formation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4299"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","EMBO Journal"],["dc.bibliographiccitation.lastpage","4308"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Zovoilis, Athanasios"],["dc.contributor.author","Agbemenyah, Hope Yao"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Edbauer, Dieter"],["dc.contributor.author","Rao, Pooja"],["dc.contributor.author","Farinelli, Laurent"],["dc.contributor.author","Delalle, Ivana"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:43:21Z"],["dc.date.available","2017-09-07T11:43:21Z"],["dc.date.issued","2011"],["dc.description.abstract","MicroRNAs are key regulators of transcriptome plasticity and have been implicated with the pathogenesis of brain diseases. Here, we employed massive parallel sequencing and provide, at an unprecedented depth, the complete and quantitative miRNAome of the mouse hippocampus, the prime target of neurodegenerative diseases such as Alzheimer's disease (AD). Using integrative genetics, we identify miR-34c as a negative constraint of memory consolidation and show that miR-34c levels are elevated in the hippocampus of AD patients and corresponding mouse models. In line with this, targeting miR-34 seed rescues learning ability in these mouse models. Our data suggest that miR-34c could be a marker for the onset of cognitive disturbances linked to AD and indicate that targeting miR-34c could be a suitable therapy."],["dc.identifier.doi","10.1038/emboj.2011.327"],["dc.identifier.gro","3142641"],["dc.identifier.isi","000296715800017"],["dc.identifier.pmid","21946562"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/67"],["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","0261-4189"],["dc.title","MicroRNA-34c is a novel target to treat dementias"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]