Halder, Rashi

[["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","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","1"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","9"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Varbanov, Hristo"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Anderson-Schmidt, Heike"],["dc.contributor.author","Anghelescu, Ion"],["dc.contributor.author","Budde, Monika"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Costa, Joan"],["dc.contributor.author","Medina, Juan"],["dc.contributor.author","Dietrich, Detlef E."],["dc.contributor.author","Figge, Christian"],["dc.contributor.author","Folkerts, Here"],["dc.contributor.author","Gade, Katrin"],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Koller, Manfred"],["dc.contributor.author","Konrad, Carsten"],["dc.contributor.author","Nussbeck, Sara Y."],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Spitzer, Carsten"],["dc.contributor.author","Stierl, Sebastian"],["dc.contributor.author","Stöckel, Judith"],["dc.contributor.author","Thiel, Andreas"],["dc.contributor.author","von Hagen, Martin"],["dc.contributor.author","Zimmermann, Jörg"],["dc.contributor.author","Zitzelsberger, Antje"],["dc.contributor.author","Schulz, Sybille"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Delalle, Ivana"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Dityatev, Alexander"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.date.accessioned","2018-01-09T14:44:03Z"],["dc.date.available","2018-01-09T14:44:03Z"],["dc.date.issued","2017-06-06"],["dc.description.abstract","Schizophrenia is a devastating disease that arises on the background of genetic predisposition and environmental risk factors, such as early life stress (ELS). In this study, we show that ELS-induced schizophrenia-like phenotypes in mice correlate with a widespread increase of histone-deacetylase 1 (Hdac1) expression that is linked to altered DNA methylation. Hdac1 overexpression in neurons of the medial prefrontal cortex, but not in the dorsal or ventral hippocampus, mimics schizophrenia-like phenotypes induced by ELS. Systemic administration of an HDAC inhibitor rescues the detrimental effects of ELS when applied after the manifestation of disease phenotypes. In addition to the hippocampus and prefrontal cortex, mice subjected to ELS exhibit increased Hdac1 expression in blood. Moreover, Hdac1 levels are increased in blood samples from patients with schizophrenia who had encountered ELS, compared with patients without ELS experience. Our data suggest that HDAC1 inhibition should be considered as a therapeutic approach to treat schizophrenia."],["dc.identifier.doi","10.1073/pnas.1613842114"],["dc.identifier.pmid","28533418"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14906"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11605"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1091-6490"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","HDAC1 links early life stress to schizophrenia-like phenotypes"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]