Kerimoglu, Cemil

[["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.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.issue","38"],["dc.bibliographiccitation.journal","Science Advances"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Tonchev, Anton B."],["dc.contributor.author","Sakib, M. Sadman"],["dc.contributor.author","Xie, Yuanbin"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Ulmke, Pauline Antonie"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Abbas, Eman"],["dc.contributor.author","Nguyen, Huong"],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2021-10-01T09:58:33Z"],["dc.date.available","2021-10-01T09:58:33Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1126/sciadv.abc6792"],["dc.identifier.pmid","34524839"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/90085"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/341"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-469"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","2375-2548"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.title","H3 acetylation selectively promotes basal progenitor proliferation and neocortex expansion"],["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","1734"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Stem Cell Reports"],["dc.bibliographiccitation.lastpage","1750"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Nguyen, Huong"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Pirouz, Mehdi"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Kiszka, Kamila A."],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Sakib, M. Sadman"],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Teichmann, Ulrike"],["dc.contributor.author","Seong, Rho H."],["dc.contributor.author","Stoykova, Anastassia"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2020-12-10T15:21:29Z"],["dc.date.available","2020-12-10T15:21:29Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.stemcr.2018.04.014"],["dc.identifier.issn","2213-6711"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73043"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Epigenetic Regulation by BAF Complexes Limits Neural Stem Cell Proliferation by Suppressing Wnt Signaling in Late Embryonic Development"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","546"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.lastpage","554"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Pena-Centeno, Tonatiuh"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Islam, Md Rezaul"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Zhou, Qihui"],["dc.contributor.author","Edbauer, Dieter"],["dc.contributor.author","Dean, Camin"],["dc.contributor.author","Fischer, André"],["dc.date.accessioned","2020-12-10T14:23:00Z"],["dc.date.available","2020-12-10T14:23:00Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.celrep.2018.03.059"],["dc.identifier.issn","2211-1247"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71800"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","RNA-Dependent Intergenerational Inheritance of Enhanced Synaptic Plasticity after Environmental Enrichment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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"]]