Shomroni, Orr

[["dc.bibliographiccitation.artnumber","160090"],["dc.bibliographiccitation.journal","Scientific Data"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Centeno, Tonatiuh Pena"],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Hennion, Magali"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Vidal, Ramon"],["dc.contributor.author","Rahman, Raza-Ur"],["dc.contributor.author","Bonn, Stefan"],["dc.date.accessioned","2017-09-07T11:52:23Z"],["dc.date.available","2017-09-07T11:52:23Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1038/sdata.2016.90"],["dc.identifier.gro","3144912"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14127"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2588"],["dc.notes.intern","Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","public"],["dc.relation.issn","2052-4463"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Genome-wide chromatin and gene expression profiling during memory formation and maintenance in adult mice"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","647"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","661"],["dc.bibliographiccitation.volume","154"],["dc.contributor.author","Ripamonti, Silvia"],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Rhee, Jeong Seop"],["dc.contributor.author","Chowdhury, Kamal"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Hellmann, Klaus Peter"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Tirard, Marilyn"],["dc.date.accessioned","2021-04-14T08:26:35Z"],["dc.date.available","2021-04-14T08:26:35Z"],["dc.date.issued","2020"],["dc.description.abstract","SUMOylation is a dynamic post-translational protein modification that primarily takes place in cell nuclei, where it plays a key role in multiple DNA-related processes. In neurons, the SUMOylation-dependent control of a subset of neuronal transcription factors is known to regulate various aspects of nerve cell differentiation, development, and function. In an unbiased screen for endogenous SUMOylation targets in the developing mouse brain, based on a His6-HA-SUMO1 knock-in mouse line, we previously identified the transcription factor Zinc finger and BTB domain-containing 20 (Zbtb20) as a new SUMO1-conjugate. We show here that the three key SUMO paralogues SUMO1, SUMO2, and SUMO3 can all be conjugated to Zbtb20 in vitro in HEK293FT cells, and we confirm the SUMOylation of Zbtb20 in vivo in mouse brain. Using primary hippocampal neurons from wild-type and Zbtb20 knock-out (KO) mice as a model system, we then demonstrate that the expression of Zbtb20 is required for proper nerve cell development and neurite growth and branching. Furthermore, we show that the SUMOylation of Zbtb20 is essential for its function in this context, and provide evidence indicating that SUMOylation affects the Zbtb20-dependent transcriptional profile of neurons. Our data highlight the role of SUMOylation in the regulation of neuronal transcription factors that determine nerve cell development, and they demonstrate that key functions of the transcription factor Zbtb20 in neuronal development and neurite growth are under obligatory SUMOylation control."],["dc.identifier.doi","10.1111/jnc.15008"],["dc.identifier.pmid","32233089"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82001"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/73"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | A09: SUMOylation und Neddylation in Synapsen"],["dc.relation","SFB 1286 | Z02: Integrative Datenanalyse und -interpretation. Generierung einer synaptisch-integrativen Datenstrategie (SynIDs)"],["dc.relation.eissn","1471-4159"],["dc.relation.issn","0022-3042"],["dc.relation.workinggroup","RG Bonn"],["dc.relation.workinggroup","RG Brose"],["dc.rights","CC BY 4.0"],["dc.title","SUMOylation controls the neurodevelopmental function of the transcription factor Zbtb20"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1006802"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PLOS Pathogens"],["dc.bibliographiccitation.lastpage","33"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Thüne, Katrin"],["dc.contributor.author","Martí, Eulàlia"],["dc.contributor.author","Kanata, Eirini"],["dc.contributor.author","Dafou, Dimitra"],["dc.contributor.author","Díaz-Lucena, Daniela"],["dc.contributor.author","Vivancos, Ana"],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Zafar, Saima"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Fernández-Borges, Natalia"],["dc.contributor.author","Andréoletti, Olivier"],["dc.contributor.author","del Río, José Antonio"],["dc.contributor.author","Díez, Juana"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Sklaviadis, Theodoros"],["dc.contributor.author","Torres, Juan Maria"],["dc.contributor.author","Ferrer, Isidre"],["dc.contributor.author","Zerr, Inga"],["dc.creator.editor","Bartz, Jason C."],["dc.date.accessioned","2018-04-23T11:47:15Z"],["dc.date.available","2018-04-23T11:47:15Z"],["dc.date.issued","2018"],["dc.description.abstract","Increasing evidence indicates that microRNAs (miRNAs) are contributing factors to neurodegeneration. Alterations in miRNA signatures have been reported in several neurodegenerative dementias, but data in prion diseases are restricted to ex vivo and animal models. The present study identified significant miRNA expression pattern alterations in the frontal cortex and cerebellum of sporadic Creutzfeldt-Jakob disease (sCJD) patients. These changes display a highly regional and disease subtype-dependent regulation that correlates with brain pathology. We demonstrate that selected miRNAs are enriched in sCJD isolated Argonaute(Ago)-binding complexes in disease, indicating their incorporation into RNA-induced silencing complexes, and further suggesting their contribution to disease-associated gene expression changes. Alterations in the miRNA-mRNA regulatory machinery and perturbed levels of miRNA biogenesis key components in sCJD brain samples reported here further implicate miRNAs in sCJD gene expression (de)regulation. We also show that a subset of sCJD-altered miRNAs are commonly changed in Alzheimer’s disease, dementia with Lewy bodies and fatal familial insomnia, suggesting potential common mechanisms underlying these neurodegenerative processes. Additionally, we report no correlation between brain and cerebrospinal fluid (CSF) miRNA-profiles in sCJD, indicating that CSF-miRNA profiles do not faithfully mirror miRNA alterations detected in brain tissue of human prion diseases. Finally, utilizing a sCJD MM1 mouse model, we analyzed the miRNA deregulation patterns observed in sCJD in a temporal manner. While fourteen sCJD-related miRNAs were validated at clinical stages, only two of those were changed at early symptomatic phase, suggesting that the miRNAs altered in sCJD may contribute to later pathogenic processes. Altogether, the present work identifies alterations in the miRNA network, biogenesis and miRNA-mRNA silencing machinery in sCJD, whereby contributions to disease mechanisms deserve further investigation."],["dc.identifier.doi","10.1371/journal.ppat.1006802"],["dc.identifier.gro","3142194"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15708"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13314"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","1553-7374"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Regional and subtype-dependent miRNA signatures in sporadic Creutzfeldt-Jakob disease are accompanied by alterations in miRNA silencing machinery and biogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1300"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Genes & Development"],["dc.bibliographiccitation.lastpage","1312"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Nemajerova, Alice"],["dc.contributor.author","Kramer, Daniela"],["dc.contributor.author","Siller, Saul S."],["dc.contributor.author","Herr, Christian"],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Pena, Tonatiuh"],["dc.contributor.author","Suazo, Cristina Gallinas"],["dc.contributor.author","Glaser, Katharina"],["dc.contributor.author","Wildung, Merit"],["dc.contributor.author","Steffen, Henrik"],["dc.contributor.author","Sriraman, Anusha"],["dc.contributor.author","Oberle, Fabian"],["dc.contributor.author","Wienken, Magdalena"],["dc.contributor.author","Hennion, Magali"],["dc.contributor.author","Vidal, Ramon"],["dc.contributor.author","Royen, Bettina"],["dc.contributor.author","Alevra, Mihai"],["dc.contributor.author","Schild, Detlev"],["dc.contributor.author","Bals, Robert"],["dc.contributor.author","Doenitz, Juergen"],["dc.contributor.author","Riedel, Dietmar"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Takemaru, Ken-Ichi"],["dc.contributor.author","Moll, Ute M."],["dc.contributor.author","Lize, Muriel"],["dc.date.accessioned","2018-11-07T10:13:24Z"],["dc.date.available","2018-11-07T10:13:24Z"],["dc.date.issued","2016"],["dc.description.abstract","Motile multiciliated cells (MCCs) have critical roles in respiratory health and disease and are essential for cleaning inhaled pollutants and pathogens from airways. Despite their significance for human disease, the transcriptional control that governs multiciliogenesis remains poorly understood. Here we identify TP73, a p53 homolog, as governing the program for airway multiciliogenesis. Mice with TP73 deficiency suffer from chronic respiratory tract infections due to profound defects in ciliogenesis and complete loss of mucociliary clearance. Organotypic airway cultures pinpoint TAp73 as necessary and sufficient for basal body docking, axonemal extension, and motility during the differentiation of MCC progenitors. Mechanistically, cross-species genomic analyses and complete ciliary rescue of knockout MCCs identify TAp73 as the conserved central transcriptional integrator of multiciliogenesis. TAp73 directly activates the key regulators FoxJ1, Rfx2, Rfx3, and miR34bc plus nearly 50 structural and functional ciliary genes, some of which are associated with human ciliopathies. Our results position TAp73 as a novel central regulator of MCC differentiation."],["dc.identifier.doi","10.1101/gad.279836.116"],["dc.identifier.isi","000378084000006"],["dc.identifier.pmid","27257214"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40428"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cold Spring Harbor Lab Press, Publications Dept"],["dc.relation.issn","1549-5477"],["dc.relation.issn","0890-9369"],["dc.title","TAp73 is a central transcriptional regulator of airway multiciliogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2205"],["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","Bioinformatics"],["dc.bibliographiccitation.lastpage","2207"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Vizcaino, Julio C. Garcia"],["dc.contributor.author","Vidal, Ramon"],["dc.contributor.author","Rahman, Raza-Ur"],["dc.contributor.author","Centeno, Tonatiuh Pena"],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Suberviola, Irantzu"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Bonn, Stefan"],["dc.date.accessioned","2017-09-07T11:43:44Z"],["dc.date.available","2017-09-07T11:43:44Z"],["dc.date.issued","2015"],["dc.description.abstract","Oasis is a web application that allows for the fast and flexible online analysis of small-RNA-seq (sRNA-seq) data. It was designed for the end user in the lab, providing an easy-to-use web frontend including video tutorials, demo data and best practice step-by-step guidelines on how to analyze sRNA-seq data. Oasis' exclusive selling points are a differential expression module that allows for the multivariate analysis of samples, a classification module for robust biomarker detection and an advanced programming interface that supports the batch submission of jobs. Both modules include the analysis of novel miRNAs, miRNA targets and functional analyses including GO and pathway enrichment. Oasis generates downloadable interactive web reports for easy visualization, exploration and analysis of data on a local system. Finally, Oasis' modular workflow enables for the rapid (re-) analysis of data."],["dc.identifier.doi","10.1093/bioinformatics/btv113"],["dc.identifier.gro","3141872"],["dc.identifier.isi","000357425800020"],["dc.identifier.pmid","25701573"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2012"],["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","1460-2059"],["dc.relation.issn","1367-4803"],["dc.title","Oasis: online analysis of small RNA deep sequencing data"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["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"]]