Kerimoglu, Cemil

[["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","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"]]

[["dc.bibliographiccitation.firstpage","538"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.lastpage","548"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Sakib, M Sadman"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Urbanke, Hendrik"],["dc.contributor.author","Kranz, Andrea"],["dc.contributor.author","Stewart, Adrian Francis"],["dc.date.accessioned","2018-01-09T14:45:29Z"],["dc.date.available","2018-01-09T14:45:29Z"],["dc.date.issued","2017-07-18"],["dc.description.abstract","Kmt2a and Kmt2b are H3K4 methyltransferases of the Set1/Trithorax class. We have recently shown the importance of Kmt2b for learning and memory. Here, we report that Kmt2a is also important in memory formation. We compare the decrease in H3K4 methylation and de-regulation of gene expression in hippocampal neurons of mice with knockdown of either Kmt2a or Kmt2b. Kmt2a and Kmt2b control largely distinct genomic regions and different molecular pathways linked to neuronal plasticity. Finally, we show that the decrease in H3K4 methylation resulting from Kmt2a knockdown partially recapitulates the pattern previously reported in CK-p25 mice, a model for neurodegeneration and memory impairment. Our findings point to the distinct functions of even closely related histone-modifying enzymes and provide essential insight for the development of more efficient and specific epigenetic therapies against brain diseases."],["dc.identifier.doi","10.1016/j.celrep.2017.06.072"],["dc.identifier.pmid","28723559"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11606"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","2211-1247"],["dc.title","KMT2A and KMT2B Mediate Memory Function by Affecting Distinct Genomic Regions"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["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.artnumber","514"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Translational Psychiatry"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Goldberg, Maria"],["dc.contributor.author","Islam, Md Rezaul"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Lancelin, Camille"],["dc.contributor.author","Gisa, Verena"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Krüger, Dennis M."],["dc.contributor.author","Marquardt, Till"],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Fischer, André"],["dc.date.accessioned","2021-12-01T09:23:16Z"],["dc.date.available","2021-12-01T09:23:16Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract MicroRNAs have been linked to synaptic plasticity and memory function and are emerging as potential biomarkers and therapeutic targets for cognitive diseases. Most of these data stem from the analysis of model systems or postmortem tissue from patients which mainly represents an advanced stage of pathology. Due to the in-accessibility of human brain tissue upon experimental manipulation, it is still challenging to identify microRNAs relevant to human cognition, which is however a key step for future translational studies. Here, we employ exercise as an experimental model for memory enhancement in healthy humans with the aim to identify microRNAs linked to memory function. By analyzing the circulating smallRNAome we find a cluster of 18 microRNAs that are highly correlated to cognition. MicroRNA-409-5p and microRNA-501-3p were the most significantly regulated candidates. Functional analysis revealed that the two microRNAs are important for neuronal integrity, synaptic plasticity, and morphology. In conclusion, we provide a novel approach to identify microRNAs linked to human memory function."],["dc.identifier.doi","10.1038/s41398-021-01627-w"],["dc.identifier.pii","1627"],["dc.identifier.pmid","34625536"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94605"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/350"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/137"],["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","2158-3188"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.rights","CC BY 4.0"],["dc.title","Exercise as a model to identify microRNAs linked to human cognition: a role for microRNA-409 and microRNA-501"],["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","121"],["dc.bibliographiccitation.journal","Neurobiology of Disease"],["dc.bibliographiccitation.lastpage","135"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Paiva, Isabel"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Lázaro, Diana F."],["dc.contributor.author","Jerčić, Kristina Gotovac"],["dc.contributor.author","Hentrich, Thomas"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Pinho, Raquel"],["dc.contributor.author","Szegő, Èva M."],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Islam, Rezaul"],["dc.contributor.author","Xylaki, Mary"],["dc.contributor.author","Caldi Gomes, Lucas A."],["dc.contributor.author","Roser, Anna-Elisa"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Schulze-Hentrich, Julia M."],["dc.contributor.author","Borovečki, Fran"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Outeiro, Tiago F."],["dc.date.accessioned","2020-12-10T15:20:24Z"],["dc.date.available","2020-12-10T15:20:24Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.nbd.2018.08.001"],["dc.identifier.pmid","30092270"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72660"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/35"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B06: Die Rolle von RNA in Synapsenphysiologie und Neurodegeneration"],["dc.relation.workinggroup","RG Outeiro (Experimental Neurodegeneration)"],["dc.title","Alpha-synuclein deregulates the expression of COL4A2 and impairs ER-Golgi function"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]