Kaurani, Lalit

[["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","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.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.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"]]