Möbius, Wiebke

[["dc.bibliographiccitation.artnumber","e1006290"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","PLoS genetics"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Hu, Bo"],["dc.contributor.author","Arpag, Sezgi"],["dc.contributor.author","Zhang, Xuebao"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Werner, Hauke"],["dc.contributor.author","Sosinsky, Gina"],["dc.contributor.author","Ellisman, Mark"],["dc.contributor.author","Zhang, Yang"],["dc.contributor.author","Hamilton, Audra"],["dc.contributor.author","Chernoff, Jonathan"],["dc.contributor.author","Li, Jun"],["dc.date.accessioned","2019-07-09T11:42:46Z"],["dc.date.available","2019-07-09T11:42:46Z"],["dc.date.issued","2016-09-01"],["dc.description.abstract","Schwann cells in the peripheral nervous systems extend their membranes to wrap axons concentrically and form the insulating sheath, called myelin. The spaces between layers of myelin are sealed by myelin junctions. This tight insulation enables rapid conduction of electric impulses (action potentials) through axons. Demyelination (stripping off the insulating sheath) has been widely regarded as one of the most important mechanisms altering the action potential propagation in many neurological diseases. However, the effective nerve conduction is also thought to require a proper myelin seal through myelin junctions such as tight junctions and adherens junctions. In the present study, we have demonstrated the disruption of myelin junctions in a mouse model (Pmp22+/-) of hereditary neuropathy with liability to pressure palsies (HNPP) with heterozygous deletion of Pmp22 gene. We observed a robust increase of F-actin in Pmp22+/- nerve regions where myelin junctions were disrupted, leading to increased myelin permeability. These abnormalities were present long before segmental demyelination at the late phase of Pmp22+/- mice. Moreover, the increase of F-actin levels correlated with an enhanced activity of p21-activated kinase (PAK1), a molecule known to regulate actin polymerization. Pharmacological inhibition of PAK normalized levels of F-actin, and completely prevented the progression of the myelin junction disruption and nerve conduction failure in Pmp22+/- mice. Our findings explain how abnormal myelin permeability is caused in HNPP, leading to impaired action potential propagation in the absence of demyelination. We call it \"functional demyelination\", a novel mechanism upstream to the actual stripping of myelin that is relevant to many demyelinating diseases. This observation also provides a potential therapeutic approach for HNPP."],["dc.identifier.doi","10.1371/journal.pgen.1006290"],["dc.identifier.pmid","27583434"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13698"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58738"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1553-7404"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Tuning PAK Activity to Rescue Abnormal Myelin Permeability in HNPP."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","277"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Cell"],["dc.bibliographiccitation.lastpage","290"],["dc.bibliographiccitation.volume","156"],["dc.contributor.author","Snaidero, Nicolas"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Czopka, Tim"],["dc.contributor.author","Hekking, Liesbeth H. P."],["dc.contributor.author","Mathisen, Cliff"],["dc.contributor.author","Verkleij, Dick"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Edgar, Julia M."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Lyons, David A."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2018-11-07T09:45:05Z"],["dc.date.available","2018-11-07T09:45:05Z"],["dc.date.issued","2014"],["dc.description.abstract","Central nervous system myelin is a multilayered membrane sheath generated by oligodendrocytes for rapid impulse propagation. However, the underlying mechanisms of myelin wrapping have remained unclear. Using an integrative approach of live imaging, electron microscopy, and genetics, we show that new myelin membranes are incorporated adjacent to the axon at the innermost tongue. Simultaneously, newly formed layers extend laterally, ultimately leading to the formation of a set of closely apposed paranodal loops. An elaborated system of cytoplasmic channels within the growing myelin sheath enables membrane trafficking to the leading edge. Most of these channels close with ongoing development but can be reopened in adults by experimentally raising phosphatidylinositol-(3,4,5)-triphosphate levels, which reinitiates myelin growth. Our model can explain assembly of myelin as a multilayered structure, abnormal myelin outfoldings in neurological disease, and plasticity of myelin biogenesis observed in adult life."],["dc.identifier.doi","10.1016/j.cell.2013.11.044"],["dc.identifier.isi","000329912200027"],["dc.identifier.pmid","24439382"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34540"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","1097-4172"],["dc.relation.issn","0092-8674"],["dc.title","Myelin Membrane Wrapping of CNS Axons by PI(3,4,5) P3-Dependent Polarized Growth at the Inner Tongue"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.contributor.author","Brás, Inês Caldeira"],["dc.contributor.author","Khani, Mohammad Hossein"],["dc.contributor.author","Vasili, Eftychia"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Riedel, Dietmar"],["dc.contributor.author","Parfentev, Iwan"],["dc.contributor.author","Gerhardt, Ellen"],["dc.contributor.author","Fahlbusch, Christiane"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Zweckstetter, Markus"],["dc.contributor.author","Gollisch, Tim"],["dc.contributor.author","Outeiro, Tiago Fleming"],["dc.date.accessioned","2022-02-23T16:36:34Z"],["dc.date.available","2022-02-23T16:36:34Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1101/2021.07.18.452825"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/100391"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/327"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/128"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B08: Definition von Kaskaden molekularer Veränderungen bei Synucleinopathien während der Neurodegeneration"],["dc.relation.workinggroup","RG Gollisch (Sensory Processing in the Retina)"],["dc.relation.workinggroup","RG Möbius"],["dc.relation.workinggroup","RG Outeiro (Experimental Neurodegeneration)"],["dc.relation.workinggroup","RG Urlaub (Bioanalytische Massenspektrometrie)"],["dc.title","Common molecular mechanisms underlie the transfer of alpha-synuclein, Tau and huntingtin and modulate spontaneous activity in neuronal cells"],["dc.type","preprint"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Moore, Sharlen"],["dc.contributor.author","Meschkat, Martin"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Trevisiol, Andrea"],["dc.contributor.author","Tzvetanova, Iva D."],["dc.contributor.author","Battefeld, Arne"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Kole, Maarten H. P."],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","de Hoz, Livia"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2021-04-14T08:31:48Z"],["dc.date.available","2021-04-14T08:31:48Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1038/s41467-020-19152-7"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83719"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2041-1723"],["dc.title","A role of oligodendrocytes in information processing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","167"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","168"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Syed, Yasir A."],["dc.contributor.author","Zhao, Chao"],["dc.contributor.author","Mahad, Don"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Altmann, Friedrich"],["dc.contributor.author","Foss, Franziska"],["dc.contributor.author","Gonzalez, G. A."],["dc.contributor.author","Sentuerk, Aycan"],["dc.contributor.author","Acker-Palmer, Amparo"],["dc.contributor.author","Lubec, Gert"],["dc.contributor.author","Lilley, Kathryn"],["dc.contributor.author","Franklin, Robin J. M."],["dc.contributor.author","Nave, Klaus-A."],["dc.contributor.author","Kotter, Mark R. N."],["dc.date.accessioned","2018-11-07T10:22:08Z"],["dc.date.available","2018-11-07T10:22:08Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1007/s00401-017-1712-z"],["dc.identifier.isi","000403235900014"],["dc.identifier.pmid","28484846"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42220"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","Antibody-mediated neutralization of myelin-associated EphrinB3 accelerates CNS remyelination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1042"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Cell"],["dc.bibliographiccitation.lastpage","1054"],["dc.bibliographiccitation.volume","150"],["dc.contributor.author","Senthilan, Pingkalai R."],["dc.contributor.author","Piepenbrock, David"],["dc.contributor.author","Ovezmyradov, Guvanch"],["dc.contributor.author","Nadrowski, Bjoern"],["dc.contributor.author","Bechstedt, Susanne"],["dc.contributor.author","Pauls, Stephanie"],["dc.contributor.author","Winkler, Margret"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Howard, Jonathon"],["dc.contributor.author","Göpfert, Martin C."],["dc.date.accessioned","2018-11-07T09:07:03Z"],["dc.date.available","2018-11-07T09:07:03Z"],["dc.date.issued","2012"],["dc.description.abstract","The Drosophila auditory organ shares equivalent transduction mechanisms with vertebrate hair cells, and both are specified by atonal family genes. Using a whole-organ knockout strategy based on atonal, we have identified 274 Drosophila auditory organ genes. Only four of these genes had previously been associated with fly hearing, yet one in five of the genes that we identified has a human cognate that is implicated in hearing disorders. Mutant analysis of 42 genes shows that more than half of them contribute to auditory organ function, with phenotypes including hearing loss, auditory hypersusceptibility, and ringing ears. We not only discover ion channels and motors important for hearing, but also show that auditory stimulus processing involves chemoreceptor proteins as well as phototransducer components. Our findings demonstrate mechanosensory roles for ionotropic receptors and visual rhodopsins and indicate that different sensory modalities utilize common signaling cascades."],["dc.identifier.doi","10.1016/j.cell.2012.06.043"],["dc.identifier.isi","000308500200017"],["dc.identifier.pmid","22939627"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25700"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","0092-8674"],["dc.title","Drosophila Auditory Organ Genes and Genetic Hearing Defects"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","282"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","282"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Meyer zu Horste, Gerd"],["dc.contributor.author","Prukop, Thomas"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2022-03-01T11:44:49Z"],["dc.date.available","2022-03-01T11:44:49Z"],["dc.date.issued","2007"],["dc.identifier.doi","10.1002/ana.21134"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103128"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1531-8249"],["dc.relation.iserratumof","/handle/2/52190"],["dc.relation.issn","0364-5134"],["dc.title","Correction"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","erratum_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e3000943"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","PLoS Biology"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Trevisiol, Andrea"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Steyer, Anna M."],["dc.contributor.author","Gregor, Ingo"],["dc.contributor.author","Nardis, Christos"],["dc.contributor.author","Winkler, Ulrike"],["dc.contributor.author","Köhler, Susanne"],["dc.contributor.author","Restrepo, Alejandro"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.date.accessioned","2021-04-14T08:31:16Z"],["dc.date.available","2021-04-14T08:31:16Z"],["dc.date.issued","2020"],["dc.description.abstract","In several neurodegenerative disorders, axonal pathology may originate from impaired oligodendrocyte-to-axon support of energy substrates. We previously established transgenic mice that allow measuring axonal ATP levels in electrically active optic nerves. Here, we utilize this technique to explore axonal ATP dynamics in the Plpnull/y mouse model of spastic paraplegia. Optic nerves from Plpnull/y mice exhibited lower and more variable basal axonal ATP levels and reduced compound action potential (CAP) amplitudes, providing a missing link between axonal pathology and a role of oligodendrocytes in brain energy metabolism. Surprisingly, when Plpnull/y optic nerves are challenged with transient glucose deprivation, both ATP levels and CAP decline slower, but recover faster upon reperfusion of glucose. Structurally, myelin sheaths display an increased frequency of cytosolic channels comprising glucose and monocarboxylate transporters, possibly facilitating accessibility of energy substrates to the axon. These data imply that complex metabolic alterations of the axon–myelin unit contribute to the phenotype of Plpnull/y mice."],["dc.identifier.doi","10.1371/journal.pbio.3000943"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83539"],["dc.identifier.url","https://for2848.gwdguser.de/literature/publications/20"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","FOR 2848: Architektur und Heterogenität der inneren mitochondrialen Membran auf der Nanoskala"],["dc.relation","FOR 2848 | P08: Strukturelle und funktionale Veränderungen der inneren mitochondrialen Membran axonaler Mitochondrien in vivo in einem dymyelinisierenden Mausmodell"],["dc.relation.eissn","1545-7885"],["dc.relation.workinggroup","RG Möbius"],["dc.rights","CC BY 4.0"],["dc.title","Structural myelin defects are associated with low axonal ATP levels but rapid recovery from energy deprivation in a mouse model of spastic paraplegia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.contributor.author","Djannatian, Minou"],["dc.contributor.author","Weikert, Ulrich"],["dc.contributor.author","Safaiyan, Shima"],["dc.contributor.author","Wrede, Christoph"],["dc.contributor.author","Deichsel, Cassandra"],["dc.contributor.author","Kislinger, Georg"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Campbell, Douglas S."],["dc.contributor.author","van Ham, Tjakko"],["dc.contributor.author","Schmid, Bettina"],["dc.contributor.author","Hegermann, Jan"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Schifferer, Martina"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2022-08-19T08:17:44Z"],["dc.date.available","2022-08-19T08:17:44Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1101/2021.02.02.429485"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113031"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/14"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | B01: The role of inflammatory cytokine signaling for efficient remyelination in multiple sclerosis"],["dc.relation.workinggroup","RG Schifferer"],["dc.relation.workinggroup","RG Simons (The Biology of Glia in Development and Disease)"],["dc.title","Myelin biogenesis is associated with pathological ultrastructure that is resolved by microglia during development"],["dc.type","preprint"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.volume","131"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Weil, Marie-Theres"],["dc.contributor.author","Gao, Ming"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Thal, Dietmar R."],["dc.contributor.author","Chang, Mayland"],["dc.contributor.author","Opdenakker, Ghislain"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2021-04-14T08:28:11Z"],["dc.date.available","2021-04-14T08:28:11Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1172/JCI141694"],["dc.identifier.pmid","33645550"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82526"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/22"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | B02: Inflammatory neurodegeneration and repair mechanisms in childhood onset autoimmune and neurometabolic demyelinating CNS disease"],["dc.relation.eissn","1558-8238"],["dc.relation.issn","0021-9738"],["dc.relation.workinggroup","RG Odoardi (Echtzeitdarstellung neuroimmunologischer Prozesse)"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.title","Blood-brain barrier resealing in neuromyelitis optica occurs independently of astrocyte regeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]