Kerimoglu, Cemil

[["dc.bibliographiccitation.journal","Frontiers in Cell and Developmental Biology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Abbas, Eman"],["dc.contributor.author","Hassan, Mohamed A."],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Kiszka, Kamila"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Nguyen, Huu Phuc"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2021-09-01T06:38:19Z"],["dc.date.available","2021-09-01T06:38:19Z"],["dc.date.issued","2021"],["dc.description.abstract","Oligodendrocytes are responsible for axon myelination in the brain and spinal cord. Generation of oligodendrocytes entails highly regulated multistage neurodevelopmental events, including proliferation, differentiation and maturation. The chromatin remodeling BAF (mSWI/SNF) complex is a notable regulator of neural development. In our previous studies, we determined the indispensability of the BAF complex scaffolding subunits BAF155 and BAF170 for neurogenesis, whereas their role in gliogenesis is unknown. Here, we show that the expression of BAF155 and BAF170 is essential for the genesis of oligodendrocytes during brain development. We report that the ablation of BAF155 and BAF170 in the dorsal telencephalic (dTel) neural progenitors or in oligodendrocyte-producing progenitors in the ventral telencephalon (vTel) in double-conditional knockout (dcKO) mouse mutants, perturbed the process of oligodendrogenesis. Molecular marker and cell cycle analyses revealed impairment of oligodendrocyte precursor specification and proliferation, as well as overt depletion of oligodendrocytes pool in dcKO mutants. Our findings unveil a central role of BAF155 and BAF170 in oligodendrogenesis, and thus substantiate the involvement of the BAF complex in the production of oligodendrocytes in the forebrain."],["dc.description.abstract","Oligodendrocytes are responsible for axon myelination in the brain and spinal cord. Generation of oligodendrocytes entails highly regulated multistage neurodevelopmental events, including proliferation, differentiation and maturation. The chromatin remodeling BAF (mSWI/SNF) complex is a notable regulator of neural development. In our previous studies, we determined the indispensability of the BAF complex scaffolding subunits BAF155 and BAF170 for neurogenesis, whereas their role in gliogenesis is unknown. Here, we show that the expression of BAF155 and BAF170 is essential for the genesis of oligodendrocytes during brain development. We report that the ablation of BAF155 and BAF170 in the dorsal telencephalic (dTel) neural progenitors or in oligodendrocyte-producing progenitors in the ventral telencephalon (vTel) in double-conditional knockout (dcKO) mouse mutants, perturbed the process of oligodendrogenesis. Molecular marker and cell cycle analyses revealed impairment of oligodendrocyte precursor specification and proliferation, as well as overt depletion of oligodendrocytes pool in dcKO mutants. Our findings unveil a central role of BAF155 and BAF170 in oligodendrogenesis, and thus substantiate the involvement of the BAF complex in the production of oligodendrocytes in the forebrain."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3389/fcell.2021.619538"],["dc.identifier.pmid","34336815"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88908"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/409"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/151"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-455"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B06: Die Rolle von RNA in Synapsenphysiologie und Neurodegeneration"],["dc.relation.eissn","2296-634X"],["dc.relation.orgunit","Institut für Neuroanatomie"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.rights","CC BY 4.0"],["dc.title","Conditional Loss of BAF (mSWI/SNF) Scaffolding Subunits Affects Specification and Proliferation of Oligodendrocyte Precursors in Developing Mouse Forebrain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","The EMBO Journal"],["dc.contributor.author","Michurina, Alexandra"],["dc.contributor.author","Sakib, M Sadman"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Krüger, Dennis Manfred"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Islam, Md Rezaul"],["dc.contributor.author","Joshi, Parth Devesh"],["dc.contributor.author","Schröder, Sophie"],["dc.contributor.author","Centeno, Tonatiuh Pena"],["dc.contributor.author","Zhou, Jiayin"],["dc.contributor.author","Fischer, André"],["dc.date.accessioned","2021-12-01T09:22:33Z"],["dc.date.available","2021-12-01T09:22:33Z"],["dc.date.issued","2021"],["dc.description.abstract","In mammals, histone 3 lysine 4 methylation (H3K4me) is mediated by six different lysine methyltransferases. Among these enzymes, SETD1B (SET domain containing 1b) has been linked to syndromic intellectual disability in human subjects, but its role in the mammalian postnatal brain has not been studied yet. Here, we employ mice deficient for Setd1b in excitatory neurons of the postnatal forebrain, and combine neuron-specific ChIP-seq and RNA-seq approaches to elucidate its role in neuronal gene expression. We observe that Setd1b controls the expression of a set of genes with a broad H3K4me3 peak at their promoters, enriched for neuron-specific genes linked to learning and memory function. Comparative analyses in mice with conditional deletion of Kmt2a and Kmt2b histone methyltransferases show that SETD1B plays a more pronounced and potent role in regulating such genes. Moreover, postnatal loss of Setd1b leads to severe learning impairment, suggesting that SETD1B-dependent regulation of H3K4me levels in postnatal neurons is critical for cognitive function."],["dc.identifier.doi","10.15252/embj.2020106459"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94429"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/367"],["dc.identifier.url","https://publications.goettingen-research-online.de/handle/2/94429"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B06: Die Rolle von RNA in Synapsenphysiologie und Neurodegeneration"],["dc.relation.eissn","1460-2075"],["dc.relation.issn","0261-4189"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by-nc-nd/4.0/"],["dc.title","Postnatal expression of the lysine methyltransferase SETD1B is essential for learning and the regulation of neuron‐enriched genes"],["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","35"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Alzheimer's Disease"],["dc.bibliographiccitation.lastpage","44"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Pavelka, Zsuzsa"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:48:20Z"],["dc.date.available","2017-09-07T11:48:20Z"],["dc.date.issued","2013"],["dc.description.abstract","Epigenetic mechanisms such as histone-acetylation have been implicated with learning and memory and are believed to contribute to the pathogenesis of neurodegenerative diseases such as Alzheimer's disease (AD). Histone-deacetylase (HDAC) inhibitors were shown to exhibit neuroprotective and neurodegenerative properties in AD animal models, and targeting HDACs appears to be a promising therapeutic strategy for brain diseases. The role of the distinct HDAC proteins in the adult brain is, however, not well understood and so far only pan-HDAC inhibitors have been tested in preclinical settings. Understanding the role of individual HDACs in cognition and AD pathogenesis is therefore vital to develop more selective HDAC inhibitors for the treatment of AD. In this study we investigated the role of HDAC5 in memory function and AD pathogenesis. We show that loss of HDAC5 impairs memory function but has little impact on pathogenesis in a mouse model for amyloid pathology. Our data reveals a novel role of HDAC5 in memory consolidation and shows that future approaches to develop more selective HDAC inhibitors for the treatment of AD should avoid targeting HDAC5."],["dc.identifier.doi","10.3233/JAD-2012-121009"],["dc.identifier.gro","3142422"],["dc.identifier.isi","000312154400006"],["dc.identifier.pmid","22914591"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8107"],["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","1387-2877"],["dc.title","Loss of HDAC5 Impairs Memory Function: Implications for Alzheimer's Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","332"],["dc.bibliographiccitation.issue","7701"],["dc.bibliographiccitation.journal","Nature"],["dc.bibliographiccitation.lastpage","338"],["dc.bibliographiccitation.volume","556"],["dc.contributor.author","Wendeln, Ann-Christin"],["dc.contributor.author","Degenhardt, Karoline"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Gertig, Michael"],["dc.contributor.author","Ulas, Thomas"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Wagner, Jessica"],["dc.contributor.author","Häsler, Lisa M."],["dc.contributor.author","Wild, Katleen"],["dc.contributor.author","Skodras, Angelos"],["dc.contributor.author","Blank, Thomas"],["dc.contributor.author","Staszewski, Ori"],["dc.contributor.author","Datta, Moumita"],["dc.contributor.author","Centeno, Tonatiuh Pena"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Islam, Md. Rezaul"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Staufenbiel, Matthias"],["dc.contributor.author","Schultze, Joachim L."],["dc.contributor.author","Beyer, Marc"],["dc.contributor.author","Prinz, Marco"],["dc.contributor.author","Jucker, Mathias"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Neher, Jonas J."],["dc.date.accessioned","2020-12-10T18:09:59Z"],["dc.date.available","2020-12-10T18:09:59Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1038/s41586-018-0023-4"],["dc.identifier.eissn","1476-4687"],["dc.identifier.issn","0028-0836"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73816"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Innate immune memory in the brain shapes neurological disease hallmarks"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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.contributor.author","Fischer, André"],["dc.contributor.author","Sakib, M Sadman"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Schütz, Anna-Lena"],["dc.contributor.author","Irniger, Stefan"],["dc.contributor.author","Capece, Vincenzo"],["dc.date.accessioned","2018-04-11T16:20:54Z"],["dc.date.available","2018-04-11T16:20:54Z"],["dc.date.issued","2016"],["dc.description.abstract","Although histone modifications and DNA methylation have been meticulously studied in the context of learning & memory formation, very few studies have demonstrated non-canonical histone variants as potential regulators of memory formation. Compared to canonical histones, these histone variants are expressed independently of DNA replication and are important for many physiological events as they confer altered chromatin structures, thereby regulating transcription. Recently, H2A.Z (variant of canonical histone, H2A) has been reported as a novel epigenetic regulator in memory formation (Zovkic et. al. 2014), which raised the question, whether differential binding of H2A.Z or its modification (e.g acetylation) across the whole genome could be a stable modulator for life-long memory acquisition and cognition. Here, we investigated genomic regions bound by H2A.Z and its acetylated variant (H2A.Zac) using chromatin immunoprecipitation followed by sequencing (ChIP-seq) in FACS-sorted neuronal and nonneuronal nuclei from hippocampal CA1 region. Initially, mRNA levels of H2afz (gene of H2A.Z) were assessed in CA1 region of aged (16 months old) and Alzheimer’s model mice (5XFAD) comparing them to young (3 months old) and wild type mice respectively. Furthermore, ChIP protocols for H2A.Z and H2A.Zac were optimized, as it has not been done before in this context. As a model of enhanced cognition, hippocampal CA1 regions from mice subjected to 4 months enriched environment (EE) were used for ChIP-seq against H2A.Z and H2A.Zac, comparing to home caged animals as controls. ChIP-seq analysis showed decreased binding of H2A.Z and its de-acetylation at specific promoter regions in CA1 neurons upon environmental enrichment. Promoters with decreased binding or decreased acetylation were found to be involved in genes functionally associated with neurogenesis, synaptic plasticity and several biosynthetic pathways. Further study is needed to prove their effect on transcription of those genes."],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13225"],["dc.language.iso","en"],["dc.notes.preprint","yes"],["dc.notes.status","final"],["dc.relation.eventend","4"],["dc.relation.eventlocation","Obergurgl, Austria"],["dc.relation.eventstart","28"],["dc.relation.iserratumof","yes"],["dc.title","Differential binding of non-canonical histone variant H2A.Z & its de-acetylation is evident in enhanced cognitive function"],["dc.type","conference_paper"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["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","109"],["dc.bibliographiccitation.journal","iScience"],["dc.bibliographiccitation.lastpage","126"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Narayanan, Ramanathan"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Castro Hernandez, Ricardo"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Ulmke, Pauline Antonie"],["dc.contributor.author","Kiszka, Kamila A."],["dc.contributor.author","Tonchev, Anton B."],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Seong, Rho H."],["dc.contributor.author","Teichmann, Ulrike"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Stoykova, Anastassia"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2020-12-10T14:24:42Z"],["dc.date.available","2020-12-10T14:24:42Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.isci.2018.05.014"],["dc.identifier.issn","2589-0042"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72326"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Chromatin Remodeling BAF155 Subunit Regulates the Genesis of Basal Progenitors in Developing Cortex"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5062"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","5073"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Maddalena, Andrea"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Wittnam, Jessica"],["dc.contributor.author","Held, Torsten"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Delalle, Ivanna"],["dc.contributor.author","Kügler, Sebastian"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.date.accessioned","2017-09-07T11:48:54Z"],["dc.date.available","2017-09-07T11:48:54Z"],["dc.date.issued","2012"],["dc.description.abstract","Histone acetylation has been implicated with the pathogenesis of neuropsychiatric disorders and targeting histone deacetylases (HDACs) using HDAC inhibitors was shown to be neuroprotective and to initiate neuroregenerative processes. However, little is known about the role of individual HDAC proteins during the pathogenesis of brain diseases. HDAC1 was found to be upregulated in patients suffering from neuropsychiatric diseases. Here, we show that virus-mediated overexpression of neuronal HDAC1 in the adult mouse hippocampus specifically affects the extinction of contextual fear memories, while other cognitive abilities were unaffected. In subsequent experiments we show that under physiological conditions, hippocampal HDAC1 is required for extinction learning via a mechanism that involves H3K9 deacetylation and subsequent trimethylation of target genes. In conclusion, our data show that hippocampal HDAC1 has a specific role in memory function."],["dc.identifier.doi","10.1523/JNEUROSCI.0079-12.2012"],["dc.identifier.gro","3142550"],["dc.identifier.isi","000302793500005"],["dc.identifier.pmid","22496552"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8456"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8913"],["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.issn","0270-6474"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","HDAC1 Regulates Fear Extinction in Mice"],["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.issue","11"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Islam, Md Rezaul; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Kaurani, Lalit; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Berulava, Tea; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Heilbronner, Urs; 3Institute of Psychiatric Phenomics and Genomics (IPPG), University Hospital Ludwig‐Maximilians‐University Munich Munich Germany"],["dc.contributor.affiliation","Budde, Monika; 3Institute of Psychiatric Phenomics and Genomics (IPPG), University Hospital Ludwig‐Maximilians‐University Munich Munich Germany"],["dc.contributor.affiliation","Centeno, Tonatiuh Pena; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Elerdashvili, Vakthang; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Zafieriou, Maria‐Patapia; 4Institute of Pharmacology and Toxicology University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Benito, Eva; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Sertel, Sinem M; 5Department of Neuro‐ and Sensory Physiology University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Goldberg, Maria; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Senner, Fanny; 3Institute of Psychiatric Phenomics and Genomics (IPPG), University Hospital Ludwig‐Maximilians‐University Munich Munich Germany"],["dc.contributor.affiliation","Kalman, Janos L; 3Institute of Psychiatric Phenomics and Genomics (IPPG), University Hospital Ludwig‐Maximilians‐University Munich Munich Germany"],["dc.contributor.affiliation","Burkhardt, Susanne; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Oepen, Anne Sophie; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Sakib, Mohammad Sadman; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Kerimoglu, Cemil; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Wirths, Oliver; 2Department for Psychiatry and Psychotherapy University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Bickeböller, Heike; 7Department of Genetic Epidemiology University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Bartels, Claudia; 2Department for Psychiatry and Psychotherapy University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Brosseron, Frederic; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Buerger, Katharina; 10German Center for Neurodegenerative Diseases (DZNE, Munich) Munich Germany"],["dc.contributor.affiliation","Cosma, Nicoleta‐Carmen; 12Department of Psychiatry and Psychotherapy Charité – Universitätsmedizin Berlin Berlin Germany"],["dc.contributor.affiliation","Fliessbach, Klaus; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Heneka, Michael T.; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Janowitz, Daniel; 11Institute for Stroke and Dementia Research (ISD) University Hospital LMU Munich Munich Germany"],["dc.contributor.affiliation","Kilimann, Ingo; 13German Center for Neurodegenerative Diseases (DZNE) Rostock Germany"],["dc.contributor.affiliation","Kleinedam, Luca; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Laske, Christoph; 14Department of Psychosomatic Medicine Rostock University Medical Center Rostock Germany"],["dc.contributor.affiliation","Metzger, Coraline D; 16German Center for Neurodegenerative Diseases (DZNE) Magdeburg Germany"],["dc.contributor.affiliation","Munk, Matthias H; 15Section for Dementia Research Hertie Institute for Clinical Brain Research and Department of Psychiatry and Psychotherapy University of Tübingen Tübingen Germany"],["dc.contributor.affiliation","Perneczky, Robert; 6Department of Psychiatry and Psychotherapy Ludwig‐Maximilians‐University Munich München Germany"],["dc.contributor.affiliation","Peters, Oliver; 12Department of Psychiatry and Psychotherapy Charité – Universitätsmedizin Berlin Berlin Germany"],["dc.contributor.affiliation","Priller, Josef; 22German Center for Neurodegenerative Diseases (DZNE) Berlin Germany"],["dc.contributor.affiliation","Rauchmann, Boris S.; 6Department of Psychiatry and Psychotherapy Ludwig‐Maximilians‐University Munich München Germany"],["dc.contributor.affiliation","Roy, Nina; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Schneider, Anja; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Spottke, Annika; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Spruth, Eike J; 22German Center for Neurodegenerative Diseases (DZNE) Berlin Germany"],["dc.contributor.affiliation","Teipel, Stefan; 13German Center for Neurodegenerative Diseases (DZNE) Rostock Germany"],["dc.contributor.affiliation","Tscheuschler, Maike; 25Department of Psychiatry Medical Faculty University of Cologne Cologne Germany"],["dc.contributor.affiliation","Wagner, Michael; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Wiltfang, Jens; 2Department for Psychiatry and Psychotherapy University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Düzel, Emrah; 16German Center for Neurodegenerative Diseases (DZNE) Magdeburg Germany"],["dc.contributor.affiliation","Jessen, Frank; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Rizzoli, Silvio O; 5Department of Neuro‐ and Sensory Physiology University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Zimmermann, Wolfram‐Hubertus; 4Institute of Pharmacology and Toxicology University Medical Center Göttingen Göttingen Germany"],["dc.contributor.author","Islam, Md Rezaul"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Berulava, Tea"],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Budde, Monika"],["dc.contributor.author","Centeno, Tonatiuh Pena"],["dc.contributor.author","Elerdashvili, Vakthang"],["dc.contributor.author","Zafieriou, Maria‐Patapia"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Sertel, Sinem M."],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Rizzoli, Silvio O."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.authorgroup","Delcode Study Group"],["dc.date.accessioned","2021-12-01T09:24:01Z"],["dc.date.available","2021-12-01T09:24:01Z"],["dc.date.issued","2021"],["dc.date.updated","2022-03-21T13:34:49Z"],["dc.description.abstract","Abstract While some individuals age without pathological memory impairments, others develop age‐associated cognitive diseases. Since changes in cognitive function develop slowly over time in these patients, they are often diagnosed at an advanced stage of molecular pathology, a time point when causative treatments fail. Thus, there is great need for the identification of inexpensive and minimal invasive approaches that could be used for screening with the aim to identify individuals at risk for cognitive decline that can then undergo further diagnostics and eventually stratified therapies. In this study, we use an integrative approach combining the analysis of human data and mechanistic studies in model systems to identify a circulating 3‐microRNA signature that reflects key processes linked to neural homeostasis and inform about cognitive status. We furthermore provide evidence that expression changes in this signature represent multiple mechanisms deregulated in the aging and diseased brain and are a suitable target for RNA therapeutics."],["dc.description.abstract","SYNOPSIS image Alzheimer\\’s disease (AD) is usually diagnosed at an advanced stage of molecular pathology, a time point when causative treatments fail. This study aimed to identify a minimally invasive biomarker that can help to identify individuals at risk for cognitive decline before clinical manifestation. Circulating microRNAs are linked to cognitive function in young and healthy humans. A circulating 3‐microRNA signature is identified using a longitudinal mouse model of age‐associated memory decline. The expression of the 3‐microRNA signature is increased in patients with mild cognitive impairment (MCI) and is associated with future conversion from MCI to AD. Targeting all 3‐ microRNAs using anti‐miRs ameliorates cognitive decline in AD mice."],["dc.description.abstract","Alzheimer\\’s disease (AD) is usually diagnosed at an advanced stage of molecular pathology, a time point when causative treatments fail. This study aimed to identify a minimally invasive biomarker that can help to identify individuals at risk for cognitive decline before clinical manifestation. image"],["dc.description.sponsorship","EC|H2020|H2020 Priority Excellent Science|H2020 European Research Council (ERC) http://dx.doi.org/10.13039/100010663"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG) http://dx.doi.org/10.13039/501100001659"],["dc.description.sponsorship","Bundesministerium für Bildung und Forschung (BMBF) http://dx.doi.org/10.13039/501100002347"],["dc.description.sponsorship","HHS|NIH|OSC|Common Fund (NIH Common Fund) http://dx.doi.org/10.13039/100015326"],["dc.identifier.doi","10.15252/emmm.202013659"],["dc.identifier.pmid","34633146"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94824"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/411"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/150"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B06: Die Rolle von RNA in Synapsenphysiologie und Neurodegeneration"],["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 Zafeiriou (3D Electrically Excitable Cell Networks – Brain and Heart)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited."],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","A microRNA signature that correlates with cognition and is a target against cognitive decline"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]