Halder, Rashi

[["dc.bibliographiccitation.artnumber","82"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","ISME Communications"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","De Saedeleer, Bianca"],["dc.contributor.author","Malabirade, Antoine"],["dc.contributor.author","Ramiro-Garcia, Javier"],["dc.contributor.author","Habier, Janine"],["dc.contributor.author","Trezzi, Jean-Pierre"],["dc.contributor.author","Peters, Samantha L."],["dc.contributor.author","Daujeumont, Annegrät"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Jäger, Christian"],["dc.contributor.author","Busi, Susheel Bhanu"],["dc.contributor.author","Wilmes, Paul"],["dc.contributor.author","Mollenhauer, Brit"],["dc.date.accessioned","2022-04-01T10:02:41Z"],["dc.date.available","2022-04-01T10:02:41Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract The human gut microbiome produces a complex mixture of biomolecules that interact with human physiology and play essential roles in health and disease. Crosstalk between micro-organisms and host cells is enabled by different direct contacts, but also by the export of molecules through secretion systems and extracellular vesicles. The resulting molecular network, comprised of various biomolecular moieties, has so far eluded systematic study. Here we present a methodological framework, optimized for the extraction of the microbiome-derived, extracellular biomolecular complement, including nucleic acids, (poly)peptides, and metabolites, from flash-frozen stool samples of healthy human individuals. Our method allows simultaneous isolation of individual biomolecular fractions from the same original stool sample, followed by specialized omic analyses. The resulting multi-omics data enable coherent data integration for the systematic characterization of this molecular complex. Our results demonstrate the distinctiveness of the different extracellular biomolecular fractions, both in terms of their taxonomic and functional composition. This highlights the challenge of inferring the extracellular biomolecular complement of the gut microbiome based on single-omic data. The developed methodological framework provides the foundation for systematically investigating mechanistic links between microbiome-secreted molecules, including those that are typically vesicle-associated, and their impact on host physiology in health and disease."],["dc.identifier.doi","10.1038/s43705-021-00078-0"],["dc.identifier.pii","78"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105980"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2730-6151"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Systematic characterization of human gut microbiome-secreted molecules by integrated multi-omics"],["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","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.journal","Der Internist"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Lbik, D."],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Mohamed, Belal A."],["dc.contributor.author","Halder, R."],["dc.contributor.author","Fischer, A."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Toischer, Karl"],["dc.date.accessioned","2018-11-07T10:15:52Z"],["dc.date.available","2018-11-07T10:15:52Z"],["dc.date.issued","2016"],["dc.format.extent","S51"],["dc.identifier.isi","000375417500098"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40906"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","1432-1289"],["dc.relation.issn","0020-9554"],["dc.title","Maximal resolution of the heart transcriptome with cell type specific profiling"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","2136"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","2146"],["dc.bibliographiccitation.volume","124"],["dc.contributor.author","Bang, Claudia"],["dc.contributor.author","Batkai, Sandor"],["dc.contributor.author","Dangwal, Seema"],["dc.contributor.author","Gupta, Shashi Kumar"],["dc.contributor.author","Foinquinos, Ariana"],["dc.contributor.author","Holzmann, Angelika"],["dc.contributor.author","Just, Annette"],["dc.contributor.author","Remke, Janet"],["dc.contributor.author","Zimmer, Karina"],["dc.contributor.author","Zeug, Andre"],["dc.contributor.author","Ponimaskin, Evgeni"],["dc.contributor.author","Schmiedl, Andreas"],["dc.contributor.author","Yin, Xiaoke"],["dc.contributor.author","Mayr, Manuel"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Engelhardt, Stefan"],["dc.contributor.author","Wei, Yuanyuan"],["dc.contributor.author","Schober, Andreas"],["dc.contributor.author","Fiedler, Jan"],["dc.contributor.author","Thum, Thomas"],["dc.date.accessioned","2017-09-07T11:46:17Z"],["dc.date.available","2017-09-07T11:46:17Z"],["dc.date.issued","2014"],["dc.description.abstract","In response to stress, the heart undergoes extensive cardiac remodeling that results in cardiac fibrosis and pathological growth of cardiomyocytes (hypertrophy), which contribute to heart failure. Alterations in microRNA (miRNA) levels are associated with dysfunctional gene expression profiles associated with many cardiovascular disease conditions; however, miRNAs have emerged recently as paracrine signaling mediators. Thus, we investigated a potential paracrine miRNA crosstalk between cardiac fibroblasts and cardiomyocytes and found that cardiac fibroblasts secrete miRNA-enriched exosomes. Surprisingly, evaluation of the miRNA content of cardiac fibroblast-derived exosomes revealed a relatively high abundance of many miRNA passenger strands (\"star\" miRNAs), which normally undergo intracellular degradation. Using confocal imaging and coculture assays, we identified fibroblast exosomal-derived miR-21_3p (miR-21 ) as a potent paracrineacting RNA molecule that induces cardiomyocyte hypertrophy. Proteome profiling identified sorbin and SH3 domain-containing protein 2 (SORBS2) and PDZ and LIM domain 5 (PDLIM5) as miR-21 targets, and silencing SORBS2 or PDLIM5 in cardiomyocytes induced hypertrophy. Pharmacological inhibition of miR-21 in a mouse model of Ang II-induced cardiac hypertrophy attenuated pathology. These findings demonstrate that cardiac fibroblasts secrete star miRNA-enriched exosomes and identify fibroblast-derived miR-21 as a paracrine signaling mediator of cardiomyocyte hypertrophy that has potential as a therapeutic target."],["dc.identifier.doi","10.1172/JCI70577"],["dc.identifier.gro","3142136"],["dc.identifier.isi","000335424500028"],["dc.identifier.pmid","24743145"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/4944"],["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","1558-8238"],["dc.relation.issn","0021-9738"],["dc.title","Cardiac fibroblast-derived microRNA passenger strand-enriched exosomes mediate cardiomyocyte hypertrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","9"],["dc.bibliographiccitation.journal","Molecular Therapy - Nucleic Acids"],["dc.bibliographiccitation.lastpage","22"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Roser, Anna-Elisa"],["dc.contributor.author","Caldi Gomes, Lucas"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Tönges, Lars"],["dc.contributor.author","Tatenhorst, Lars"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2020-12-10T15:20:36Z"],["dc.date.available","2020-12-10T15:20:36Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.omtn.2018.01.005"],["dc.identifier.issn","2162-2531"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72737"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","miR-182-5p and miR-183-5p Act as GDNF Mimics in Dopaminergic Midbrain Neurons"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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"]]

[["dc.bibliographiccitation.firstpage","102"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","110"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Hennion, Magali"],["dc.contributor.author","Vidal, Ramon O."],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Rahman, Raza-Ur"],["dc.contributor.author","Rajput, Ashish"],["dc.contributor.author","Centeno, Tonatiuh Pena"],["dc.contributor.author","van Bebber, Frauke"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Garcia Vizcaino, Julio C."],["dc.contributor.author","Schuetz, Anna-Lena"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Navarro Sala, Magdalena"],["dc.contributor.author","Bahari Javan, Sanaz"],["dc.contributor.author","Haass, Christian"],["dc.contributor.author","Schmid, Bettina"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Bonn, Stefan"],["dc.date.accessioned","2018-05-30T15:01:05Z"],["dc.date.available","2018-05-30T15:01:05Z"],["dc.date.issued","2016"],["dc.description.abstract","The ability to form memories is a prerequisite for an organism's behavioral adaptation to environmental changes. At the molecular level, the acquisition and maintenance of memory requires changes in chromatin modifications. In an effort to unravel the epigenetic network underlying both short- and long-term memory, we examined chromatin modification changes in two distinct mouse brain regions, two cell types and three time points before and after contextual learning. We found that histone modifications predominantly changed during memory acquisition and correlated surprisingly little with changes in gene expression. Although long-lasting changes were almost exclusive to neurons, learning-related histone modification and DNA methylation changes also occurred in non-neuronal cell types, suggesting a functional role for non-neuronal cells in epigenetic learning. Finally, our data provide evidence for a molecular framework of memory acquisition and maintenance, wherein DNA methylation could alter the expression and splicing of genes involved in functional plasticity and synaptic wiring."],["dc.identifier.doi","10.1038/nn.4194"],["dc.identifier.pmid","26656643"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/14808"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1546-1726"],["dc.title","DNA methylation changes in plasticity genes accompany the formation and maintenance of memory"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]