Neumann, Heinz

[["dc.bibliographiccitation.journal","FEBS Journal"],["dc.bibliographiccitation.volume","282"],["dc.contributor.author","Hoffmann, C."],["dc.contributor.author","Neumann, H."],["dc.date.accessioned","2018-11-07T09:54:50Z"],["dc.date.available","2018-11-07T09:54:50Z"],["dc.date.issued","2015"],["dc.format.extent","70"],["dc.identifier.isi","000362570601051"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36619"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","40th Congress of the Federation-of-European-Biochemical-Societies (FEBS) The Biochemical Basis of Life"],["dc.relation.eventlocation","Berlin, GERMANY"],["dc.relation.issn","1742-4658"],["dc.relation.issn","1742-464X"],["dc.title","In vivo structural mapping of FACT-histone interactions using genetically encoded crosslinkers"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3495"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","Cell Cycle"],["dc.bibliographiccitation.lastpage","3504"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Shchebet, Andrei"],["dc.contributor.author","Neumann, Heinz"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2018-11-07T08:50:42Z"],["dc.date.available","2018-11-07T08:50:42Z"],["dc.date.issued","2011"],["dc.description.abstract","Many anticancer therapies function largely by inducing DNA double-strand breaks (DSBs) or altering the ability of cancer cells to repair them. Proper and timely DNA repair requires dynamic changes in chromatin assembly and disassembly characterized by histone H3 lysine 56 acetylation (H3K56ac) and phosphorylation of the variant histone H2AX (gamma H2AX). Similarly, histone H2B monoubiquitination (H2Bub1) functions in DNA repair, but its role in controlling dynamic changes in chromatin structure following DSBs and the histone chaperone complexes involved remain unknown. Therefore, we investigated the role of the H2B ubiquitin ligase RNF40 in the DSB response. We show that RNF40 depletion results in sustained H2AX phosphorylation and a decrease in rapid cell cycle checkpoint activation. Furthermore, RNF40 knockdown resulted in decreased H3K56ac and decreased recruitment of the facilitates chromatin transcription (FACT) complex to chromatin following DSB. Knockdown of the FACT component suppressor of Ty homolog-16 (SUPT16H) phenocopied the effects of RNF40 knockdown on both gamma H2AX and H3K56ac following DSB induction. Consistently, both RNF40 and SUPT16H were required for proper DNA end resection and timely DNA repair, suggesting that H2Bub1 and FACT cooperate to increase chromatin dynamics, which facilitates proper checkpoint activation and timely DNA repair. These results provide important mechanistic insights into the tumor suppressor function of H2Bub1 and provide a rational basis for pursuing H2Bub1-based therapies in conjunction with traditional chemo-and radiotherapy."],["dc.identifier.doi","10.4161/cc.10.20.17769"],["dc.identifier.isi","000296570700027"],["dc.identifier.pmid","22031019"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21752"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1538-4101"],["dc.title","The H2B ubiquitin ligase RNF40 cooperates with SUPT16H to induce dynamic changes in chromatin structure during DNA double-strand break repair"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","77"],["dc.bibliographiccitation.issue","6166"],["dc.bibliographiccitation.journal","Science"],["dc.bibliographiccitation.lastpage","80"],["dc.bibliographiccitation.volume","343"],["dc.contributor.author","Wilkins, Bryan J."],["dc.contributor.author","Rall, Nils A."],["dc.contributor.author","Ostwal, Yogesh"],["dc.contributor.author","Kruitwagen, Tom"],["dc.contributor.author","Hiragami-Hamada, Kyoko"],["dc.contributor.author","Winkler, Marco"],["dc.contributor.author","Barral, Yves"],["dc.contributor.author","Fischle, Wolfgang"],["dc.contributor.author","Neumann, Heinz"],["dc.date.accessioned","2018-11-07T09:45:15Z"],["dc.date.available","2018-11-07T09:45:15Z"],["dc.date.issued","2014"],["dc.description.abstract","Metaphase chromosomes are visible hallmarks of mitosis, yet our understanding of their structure and of the forces shaping them is rudimentary. Phosphorylation of histone H3 serine 10 (H3 S10) by Aurora B kinase is a signature event of mitosis, but its function in chromatin condensation is unclear. Using genetically encoded ultraviolet light-inducible cross-linkers, we monitored protein-protein interactions with spatiotemporal resolution in living yeast to identify the molecular details of the pathway downstream of H3 S10 phosphorylation. This modification leads to the recruitment of the histone deacetylase Hst2p that subsequently removes an acetyl group from histone H4 lysine 16, freeing the H4 tail to interact with the surface of neighboring nucleosomes and promoting fiber condensation. This cascade of events provides a condensin-independent driving force of chromatin hypercondensation during mitosis."],["dc.identifier.doi","10.1126/science.1244508"],["dc.identifier.isi","000329162000051"],["dc.identifier.pmid","24385627"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34572"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Advancement Science"],["dc.relation.issn","1095-9203"],["dc.relation.issn","0036-8075"],["dc.title","A Cascade of Histone Modifications Induces Chromatin Condensation in Mitosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2817"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","Journal of Cell Science"],["dc.bibliographiccitation.lastpage","2828"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Desfougeres, Yann"],["dc.contributor.author","Neumann, Heinz"],["dc.contributor.author","Mayer, Andreas"],["dc.date.accessioned","2018-11-07T10:11:33Z"],["dc.date.available","2018-11-07T10:11:33Z"],["dc.date.issued","2016"],["dc.description.abstract","Cells control the size of their compartments relative to cell volume, but there is also size control within each organelle. Yeast vacuoles neither burst nor do they collapse into a ruffled morphology, indicating that the volume of the organellar envelope is adjusted to the amount of content. It is poorly understood how this adjustment is achieved. We show that the accumulating content of yeast vacuoles activates fusion of other vacuoles, thus increasing the volume-to-surface ratio. Synthesis of the dominant compound stored inside vacuoles, polyphosphate, stimulates binding of the chaperone Sec18/NSF to vacuolar SNAREs, which activates them and triggers fusion. SNAREs can only be activated by lumenal, not cytosolic, polyphosphate (polyP). Control of lumenal polyP over SNARE activation in the cytosol requires the cytosolic cyclin-dependent kinase Pho80-Pho85 and the R-SNARE Nyv1. These results suggest that cells can adapt the volume of vacuoles to their content through feedback from the vacuole lumen to the SNAREs on the cytosolic surface of the organelle."],["dc.identifier.doi","10.1242/jcs.184382"],["dc.identifier.isi","000380928600014"],["dc.identifier.pmid","27252384"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40073"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Company Of Biologists Ltd"],["dc.relation.issn","1477-9137"],["dc.relation.issn","0021-9533"],["dc.title","Organelle size control - increasing vacuole content activates SNAREs to augment organelle volume through homotypic fusion"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","73"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","74"],["dc.contributor.author","Liu, Y."],["dc.contributor.author","Heine, H."],["dc.contributor.author","Neumann, H."],["dc.contributor.author","Fassbender, Klaus"],["dc.date.accessioned","2018-11-07T10:36:32Z"],["dc.date.available","2018-11-07T10:36:32Z"],["dc.date.issued","2003"],["dc.identifier.isi","000184938300320"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45349"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.publisher.place","New york"],["dc.relation.conference","6th European Meeting on Glial Cell Function in Health and Disease"],["dc.relation.eventlocation","BERLIN, GERMANY"],["dc.relation.issn","0894-1491"],["dc.title","Cd14-dependent phagocytosis of Alzheimer's amyloid beta-peptide"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","453"],["dc.bibliographiccitation.journal","Metabolic Engineering"],["dc.bibliographiccitation.lastpage","462"],["dc.bibliographiccitation.volume","47"],["dc.contributor.author","Heitmüller, Svenja"],["dc.contributor.author","Neumann-Staubitz, Petra"],["dc.contributor.author","Herrfurth, Cornelia"],["dc.contributor.author","Feussner, Ivo"],["dc.contributor.author","Neumann, Heinz"],["dc.date.accessioned","2020-12-10T15:21:49Z"],["dc.date.available","2020-12-10T15:21:49Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.ymben.2018.04.022"],["dc.identifier.issn","1096-7176"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73173"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Cellular substrate limitations of lysine acetylation turnover by sirtuins investigated with engineered futile cycle enzymes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","267"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Current Opinion in Neurology"],["dc.bibliographiccitation.lastpage","273"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Neumann, H."],["dc.date.accessioned","2018-11-07T10:38:29Z"],["dc.date.available","2018-11-07T10:38:29Z"],["dc.date.issued","2003"],["dc.description.abstract","Purpose of review Axonal dysfunction and damage is an early pathological sign of autoimmune central nervous system disease, viral and bacterial infections, and brain trauma. Axonal injury has attracted considerable interest during the past few years because the degree of axonal damage appears to determine long-term clinical outcome. Recent findings Advanced magnetic resonance spectroscopic imaging techniques have suggested that axonal loss and dysfunction is responsible for the persistent neurological deficits that occur in patients with multiple sclerosis. Histopathological methods have shown that axonal damage is defined primarily by dysfunction of axonal transport, and finally by complete transection and degeneration of axons. Recent studies have demonstrated that the extent of axonal damage in the primary demyelinating lesion of multiple sclerosis patients is associated with the number of activated microglia/macrophages and cytotoxic CD8(+) T lymphocytes. In addition, diffuse axonal dysfunction independent of demyelination develops in normal appearing white matter, possibly due to indirect effects of inflammation. Summary The fact that axonal damage in response to overt inflammatory reactions may occur gradually, leaving a window for therapeutical intervention, has important clinical implications. Determination of the exact molecular mechanism might help in finding new therapies for inflammatory axonal damage."],["dc.identifier.doi","10.1097/01.wco.0000073926.19076.29"],["dc.identifier.isi","000183433800004"],["dc.identifier.pmid","12858061"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45825"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1350-7540"],["dc.title","Molecular mechanisms of axonal damage in inflammatory central nervous system diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","412"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","The FASEB Journal"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Iliev, Asparouh I."],["dc.contributor.author","Stringaris, A. K."],["dc.contributor.author","Nau, R."],["dc.contributor.author","Neumann, H."],["dc.date.accessioned","2018-11-07T10:34:20Z"],["dc.date.available","2018-11-07T10:34:20Z"],["dc.date.issued","2003"],["dc.description.abstract","Innate immune cells express toll-like receptor-9 (TLR9) and respond to unmethylated, CG dinucleotide motif-rich DNA released from bacteria during infection or endogenous cells during autoimmune tissue injury. Oligonucleotides containing CG dinucleotide (CpG-DNA) mimic the effect of unmethylated DNA and stimulate TLR9. CpG-DNA was cytotoxic to neurons in organotypic brain cultures. Neurotoxicity of CpG-DNA was mediated via microglial cells and started primarily from neurites as determined by time-lapse imaging of enhanced green fluorescent protein (EGFP)-transfected neurons. Cultured brain microglial cells expressed TLR9 and responded to CpG-DNA by production of the inflammatory mediators nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha). Blockade of NO synthase and TNF-alpha prevented damage of neurites and neurotoxicity of CpG-DNA. The data suggest that stimulation of microglia via TLR9 and subsequent release of NO and TNF-alpha is a major source of neurotoxicity in bacterial and autoimmune brain tissue injury."],["dc.identifier.doi","10.1096/fj.03-0670fje"],["dc.identifier.isi","000188067500007"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44841"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Federation Amer Soc Exp Biol"],["dc.relation.issn","1530-6860"],["dc.relation.issn","0892-6638"],["dc.title","Neuronal injury mediated via stimulation of microglial toll-like receptor-9 (TLR9)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2057"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","FEBS Letters"],["dc.bibliographiccitation.lastpage","2064"],["dc.bibliographiccitation.volume","586"],["dc.contributor.author","Neumann, Heinz"],["dc.date.accessioned","2018-11-07T09:08:12Z"],["dc.date.available","2018-11-07T09:08:12Z"],["dc.date.issued","2012"],["dc.description.abstract","With few minor variations, the genetic code is universal to all forms of life on our planet. It is difficult to imagine that one day organisms might exist that use an entirely different code to translate the information of their genome. Recent developments in the field of synthetic biology, however, have opened the gate to their creation. The genetic code of several organisms has been expanded by the heterologous expression of evolved aminoacyl-tRNA synthetase/tRNA(CUA) pairs that mediate the incorporation of unnatural amino acids in response to amber codons. These UAAs introduce exciting new features into proteins, such as spectroscopic probes, UV-inducible crosslinkers, and functional groups for bioorthogonal conjugations or posttranslational modifications. Orthogonal ribosomes provide a parallel translational machinery in Escherichia coli that has lost its evolutionary constraints. Evolved variants of these ribosomes translate amber or quadruplet codons with massively enhanced efficiency. Here, I review these recent developments emphasizing their tremendous potential to facilitate biochemical and cell biological studies. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved."],["dc.description.sponsorship","German Research Foundation; University of Gottingen"],["dc.identifier.doi","10.1016/j.febslet.2012.02.002"],["dc.identifier.isi","000306113700006"],["dc.identifier.pmid","22710184"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25974"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0014-5793"],["dc.title","Rewiring translation - Genetic code expansion and its applications"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","792"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","European Journal of Paediatric Neurology"],["dc.bibliographiccitation.lastpage","800"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Storm van's Gravesande, K."],["dc.contributor.author","Calabrese, P."],["dc.contributor.author","Blaschek, A."],["dc.contributor.author","Rostásy, K."],["dc.contributor.author","Huppke, P."],["dc.contributor.author","Rothe, L."],["dc.contributor.author","Mall, V."],["dc.contributor.author","Kessler, J."],["dc.contributor.author","Kalbe, E."],["dc.contributor.author","Kraus, V."],["dc.contributor.author","Dornfeld, E."],["dc.contributor.author","Elpers, C."],["dc.contributor.author","Lohmann, H."],["dc.contributor.author","Weddige, A."],["dc.contributor.author","Hagspiel, S."],["dc.contributor.author","Kirschner, J."],["dc.contributor.author","Brehm, M."],["dc.contributor.author","Blank, C."],["dc.contributor.author","Schubert, J."],["dc.contributor.author","Schimmel, M."],["dc.contributor.author","Pacheè, S."],["dc.contributor.author","Mohrbach, M."],["dc.contributor.author","Karenfort, M."],["dc.contributor.author","Kamp, G."],["dc.contributor.author","Lücke, T."],["dc.contributor.author","Neumann, H."],["dc.contributor.author","Lutz, S."],["dc.contributor.author","Gierse, A."],["dc.contributor.author","Sievers, S."],["dc.contributor.author","Schiffmann, H."],["dc.contributor.author","de Soye, I."],["dc.contributor.author","Trollmann, R."],["dc.contributor.author","Candova, A."],["dc.contributor.author","Rosner, M."],["dc.contributor.author","Neu, A."],["dc.contributor.author","Romer, G."],["dc.contributor.author","Seidel, U."],["dc.contributor.author","John, R."],["dc.contributor.author","Hofmann, C."],["dc.contributor.author","Schulz, A."],["dc.contributor.author","Kinder, S."],["dc.contributor.author","Bertolatus, A."],["dc.contributor.author","Scheidtmann, K."],["dc.contributor.author","Lasogga, R."],["dc.contributor.author","Leiz, S."],["dc.contributor.author","Alber, M."],["dc.contributor.author","Kranz, J."],["dc.contributor.author","Bajer-Kornek, B."],["dc.contributor.author","Seidl, R."],["dc.contributor.author","Novak, A."],["dc.date.accessioned","2020-12-10T14:23:42Z"],["dc.date.available","2020-12-10T14:23:42Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.ejpn.2019.08.006"],["dc.identifier.issn","1090-3798"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72016"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","The Multiple Sclerosis Inventory of Cognition for Adolescents (MUSICADO): A brief screening instrument to assess cognitive dysfunction, fatigue and loss of health-related quality of life in pediatric-onset multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]