Winkler, Anne

[["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"]]

[["dc.bibliographiccitation.artnumber","6530"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Kettwig, Matthias"],["dc.contributor.author","Ternka, Katharina"],["dc.contributor.author","Wendland, Kristin"],["dc.contributor.author","Krüger, Dennis Manfred"],["dc.contributor.author","Zampar, Silvia"],["dc.contributor.author","Schob, Charlotte"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Aich, Abhishek"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Sakib, M. Sadman"],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2021-12-01T09:23:01Z"],["dc.date.available","2021-12-01T09:23:01Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Infantile-onset RNaseT2 deficient leukoencephalopathy is characterised by cystic brain lesions, multifocal white matter alterations, cerebral atrophy, and severe psychomotor impairment. The phenotype is similar to congenital cytomegalovirus brain infection and overlaps with type I interferonopathies, suggesting a role for innate immunity in its pathophysiology. To date, pathophysiological studies have been hindered by the lack of mouse models recapitulating the neuroinflammatory encephalopathy found in patients. In this study, we generated Rnaset2 −/− mice using CRISPR/Cas9-mediated genome editing. Rnaset2 −/− mice demonstrate upregulation of interferon-stimulated genes and concurrent IFNAR1-dependent neuroinflammation, with infiltration of CD8 + effector memory T cells and inflammatory monocytes into the grey and white matter. Single nuclei RNA sequencing reveals homeostatic dysfunctions in glial cells and neurons and provide important insights into the mechanisms of hippocampal-accentuated brain atrophy and cognitive impairment. The Rnaset2 −/− mice may allow the study of CNS damage associated with RNaseT2 deficiency and may be used for the investigation of potential therapies."],["dc.identifier.doi","10.1038/s41467-021-26880-x"],["dc.identifier.pii","26880"],["dc.identifier.pmid","34764281"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94539"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/361"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/48"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/141"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B06: Die Rolle von RNA in Synapsenphysiologie und Neurodegeneration"],["dc.relation.eissn","2041-1723"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.relation.workinggroup","RG Gärtner"],["dc.relation.workinggroup","RG Rehling (Mitochondrial Protein Biogenesis)"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.rights","CC BY 4.0"],["dc.title","Interferon-driven brain phenotype in a mouse model of RNaseT2 deficient leukoencephalopathy"],["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","6382"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.lastpage","6395"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Li, Huaibiao"],["dc.contributor.author","Frappart, Lucien"],["dc.contributor.author","Moll, Jürgen"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Kroll, Torsten"],["dc.contributor.author","Hamann, Jana"],["dc.contributor.author","Kufferath, Iris"],["dc.contributor.author","Groth, Marco"],["dc.contributor.author","Taudien, Stefan"],["dc.contributor.author","Schütte, Moritz"],["dc.contributor.author","Yaspo, Marie-Laure"],["dc.contributor.author","Heuer, Heike"],["dc.contributor.author","Lange, Bodo M.H."],["dc.contributor.author","Platzer, Matthias"],["dc.contributor.author","Zatloukal, Kurt"],["dc.contributor.author","Herrlich, Peter"],["dc.contributor.author","Ploubidou, Aspasia"],["dc.date.accessioned","2020-12-10T18:37:43Z"],["dc.date.available","2020-12-10T18:37:43Z"],["dc.date.issued","2016"],["dc.description.abstract","Hypofertility is a risk factor for the development of testicular germ cell tumors (TGCT), but the initiating event linking these pathologies is unknown. We hypothesized that excessive planar division of undifferentiated germ cells promotes their self-renewal and TGCT development. However, our results obtained from mouse models and seminoma patients demonstrated the opposite. Defective planar divisions of undifferentiated germ cells caused their premature exit from the seminiferous tubule niche, resulting in germ cell depletion, hypofertility, intratubular germ cell neoplasias, and seminoma development. Oriented divisions of germ cells, which determine their fate, were regulated by spindle-associated RHAMM-a function we found to be abolished in 96% of human seminomas. Mechanistically, RHAMM expression is regulated by the testis-specific polyadenylation protein CFIm25, which is downregulated in the human seminomas. These results suggested that spindle misorientation is oncogenic, not by promoting selfrenewing germ cell divisions within the niche, but by prematurely displacing proliferating cells from their normal epithelial milieu. Furthermore, they suggested RHAMM loss-of-function and spindle misorientation as an initiating event underlying both hypofertility and TGCT initiation. These findings identify spindle-associated RHAMM as an intrinsic regulator of male germ cell fate and as a gatekeeper preventing initiation of TGCTs."],["dc.identifier.doi","10.1158/0008-5472.CAN-16-0179"],["dc.identifier.eissn","1538-7445"],["dc.identifier.isi","000387446700026"],["dc.identifier.issn","0008-5472"],["dc.identifier.pmid","27543603"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77075"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","1538-7445"],["dc.relation.issn","0008-5472"],["dc.title","Impaired Planar Germ Cell Division in the Testis, Caused by Dissociation of RHAMM from the Spindle, Results in Hypofertility and Seminoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","43"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","58"],["dc.bibliographiccitation.volume","132"],["dc.contributor.author","Kinzel, Silke"],["dc.contributor.author","Lehmann-Horn, Klaus"],["dc.contributor.author","Torke, Sebastian"],["dc.contributor.author","Haeusler, Darius"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Payne, Natalie L."],["dc.contributor.author","Feldmann, Linda"],["dc.contributor.author","Saiz, Albert"],["dc.contributor.author","Reindl, Markus"],["dc.contributor.author","Lalive, Patrice H."],["dc.contributor.author","Bernard, Claude C."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2018-11-07T10:12:20Z"],["dc.date.available","2018-11-07T10:12:20Z"],["dc.date.issued","2016"],["dc.description.abstract","In the pathogenesis of central nervous system (CNS) demyelinating disorders, antigen-specific B cells are implicated to act as potent antigen-presenting cells (APC), eliciting waves of inflammatory CNS infiltration. Here, we provide the first evidence that CNS-reactive antibodies (Ab) are similarly capable of initiating an encephalitogenic immune response by targeting endogenous CNS antigen to otherwise inert myeloid APC. In a transgenic mouse model, constitutive production of Ab against myelin oligodendrocyte glycoprotein (MOG) was sufficient to promote spontaneous experimental autoimmune encephalomyelitis (EAE) in the absence of B cells, when mice endogenously contained MOG-recognizing T cells. Adoptive transfer studies corroborated that anti-MOG Ab triggered activation and expansion of peripheral MOG-specific T cells in an Fc-dependent manner, subsequently causing EAE. To evaluate the underlying mechanism, anti-MOG Ab were added to a co-culture of myeloid APC and MOG-specific T cells. At otherwise undetected concentrations, anti-MOG Ab enabled Fc-mediated APC recognition of intact MOG; internalized, processed and presented MOG activated na < ve T cells to differentiate in an encephalitogenic manner. In a series of translational experiments, anti-MOG Ab from two patients with an acute flare of CNS inflammation likewise facilitated detection of human MOG. Jointly, these observations highlight Ab-mediated opsonization of endogenous CNS auto-antigen as a novel disease- and/or relapse-triggering mechanism in CNS demyelinating disorders."],["dc.identifier.doi","10.1007/s00401-016-1559-8"],["dc.identifier.isi","000378811600003"],["dc.identifier.pmid","27022743"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14069"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40217"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Myelin-reactive antibodies initiate T cell-mediated CNS autoimmune disease by opsonization of endogenous antigen"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","523"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","538"],["dc.bibliographiccitation.volume","127"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Kayser, Dieter M."],["dc.contributor.author","Thal, Dietmar Rudolf"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T09:42:12Z"],["dc.date.available","2018-11-07T09:42:12Z"],["dc.date.issued","2014"],["dc.description.abstract","Neuromyelitis optica (NMO) is a chronic, mostly relapsing inflammatory demyelinating disease of the CNS characterized by serum anti-aquaporin 4 (AQP4) antibodies in the majority of patients. Anti-AQP4 antibodies derived from NMO patients target and deplete astrocytes in experimental models when co-injected with complement. However, the time course and mechanisms of oligodendrocyte loss and demyelination and the fate of oligodendrocyte precursor cells (OPC) have not been examined in detail. Also, no studies regarding astrocyte repopulation of experimental NMO lesions have been reported. We utilized two rat models using either systemic transfer or focal intracerebral injection of recombinant human anti-AQP4 antibodies to generate NMO-like lesions. Time-course experiments were performed to examine oligodendroglial and astroglial damage and repair. In addition, oligodendrocyte pathology was studied in early human NMO lesions. Apart from early complement-mediated astrocyte destruction, we observed a prominent, very early loss of oligodendrocytes and oligodendrocyte precursor cells (OPCs) as well as a delayed loss of myelin. Astrocyte repopulation of focal NMO lesions was already substantial after 1 week. Olig2-positive OPCs reappeared before NogoA-positive, mature oligodendrocytes. Thus, using two experimental models that closely mimic the human disease, our study demonstrates that oligodendrocyte and OPC loss is an extremely early feature in the formation of human and experimental NMO lesions and leads to subsequent, delayed demyelination, highlighting an important difference in the pathogenesis of MS and NMO."],["dc.identifier.doi","10.1007/s00401-013-1220-8"],["dc.identifier.isi","000332957400005"],["dc.identifier.pmid","24292009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33902"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","Early loss of oligodendrocytes in human and experimental neuromyelitis optica lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1196"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1209"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Bergner, Caroline G."],["dc.contributor.author","Meer, Franziska"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Türkmen, Mevlude"],["dc.contributor.author","Valizada, Emil"],["dc.contributor.author","Fitzner, Dirk"],["dc.contributor.author","Hametner, Simon"],["dc.contributor.author","Hartmann, Christian"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2022-03-01T11:45:41Z"],["dc.date.available","2022-03-01T11:45:41Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/glia.23598"],["dc.identifier.eissn","1098-1136"],["dc.identifier.issn","0894-1491"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103412"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.rights.uri","http://creativecommons.org/licenses/by-nc-nd/4.0/"],["dc.title","Microglia damage precedes major myelin breakdown in X‐linked adrenoleukodystrophy and metachromatic leukodystrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Experimental Medicine"],["dc.bibliographiccitation.volume","217"],["dc.contributor.author","Cunha, Maria Inês"],["dc.contributor.author","Su, Minhui"],["dc.contributor.author","Cantuti-Castelvetri, Ludovico"],["dc.contributor.author","Müller, Stephan A."],["dc.contributor.author","Schifferer, Martina"],["dc.contributor.author","Djannatian, Minou"],["dc.contributor.author","Alexopoulos, Ioannis"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","van Ham, Tjakko J."],["dc.contributor.author","Schmid, Bettina"],["dc.contributor.author","Lichtenthaler, Stefan F."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2020-12-10T18:15:37Z"],["dc.date.available","2020-12-10T18:15:37Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1084/jem.20191390"],["dc.identifier.pmid","32078678"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/74902"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/24"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["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 Cantuti"],["dc.relation.workinggroup","RG Simons (The Biology of Glia in Development and Disease)"],["dc.relation.workinggroup","RG Schifferer"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.title","Pro-inflammatory activation following demyelination is required for myelin clearance and oligodendrogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","57"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Singh, Shailender"],["dc.contributor.author","Dallenga, Tobias"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Roemer, Shanu"],["dc.contributor.author","Maruschak, Brigitte"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T10:26:08Z"],["dc.date.available","2018-11-07T10:26:08Z"],["dc.date.issued","2017"],["dc.description.abstract","Background: Axonal damage and loss substantially contribute to the incremental accumulation of clinical disability in progressive multiple sclerosis. Here, we assessed the amount of Wallerian degeneration in brain tissue of multiple sclerosis patients in relation to demyelinating lesion activity and asked whether a transient blockade of Wallerian degeneration decreases axonal loss and clinical disability in a mouse model of inflammatory demyelination. Methods: Wallerian degeneration and acute axonal damage were determined immunohistochemically in the periplaque white matter of multiple sclerosis patients with early actively demyelinating lesions, chronic active lesions, and inactive lesions. Furthermore, we studied the effects of Wallerian degeneration blockage on clinical severity, inflammatory pathology, acute axonal damage, and long-term axonal loss in experimental autoimmune encephalomyelitis using Wallerian degeneration slow (WldS) mutant mice. Results: The highest numbers of axons undergoing Wallerian degeneration were found in the perilesional white matter of multiple sclerosis patients early in the disease course and with actively demyelinating lesions. Furthermore, Wallerian degeneration was more abundant in patients harboring chronic active as compared to chronic inactive lesions. No co-localization of neuropeptide Y-Y1 receptor, a bona fide immunohistochemical marker of Wallerian degeneration, with amyloid precursor protein, frequently used as an indicator of acute axonal transport disturbance, was observed in human and mouse tissue, indicating distinct axon-degenerative processes. Experimentally, a delay of Wallerian degeneration, as observed in WldS mice, did not result in a reduction of clinical disability or acute axonal damage in experimental autoimmune encephalomyelitis, further supporting that acute axonal damage as reflected by axonal transport disturbances does not share common molecular mechanisms with Wallerian degeneration. Furthermore, delaying Wallerian degeneration did not result in a net rescue of axons in late lesion stages of experimental autoimmune encephalomyelitis. Conclusions: Our data indicate that in multiple sclerosis, ongoing demyelination in focal lesions is associated with axonal degeneration in the perilesional white matter, supporting a role for focal pathology in diffuse white matter damage. Also, our results suggest that interfering with Wallerian degeneration in inflammatory demyelination does not suffice to prevent acute axonal damage and finally axonal loss."],["dc.identifier.doi","10.1186/s12974-017-0831-8"],["dc.identifier.isi","000397153100002"],["dc.identifier.pmid","28302146"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14381"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42975"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1742-2094"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Relationship of acute axonal damage, Wallerian degeneration, and clinical disability in multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","7"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","8"],["dc.bibliographiccitation.volume","275"],["dc.contributor.author","Kinzel, Silke"],["dc.contributor.author","Lehmann-Horn, Klaus"],["dc.contributor.author","Zamvil, Scott S."],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Bernard, Claude C."],["dc.contributor.author","Stadelmann-Nessler, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2018-11-07T09:33:33Z"],["dc.date.available","2018-11-07T09:33:33Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1016/j.jneuroim.2014.08.026"],["dc.identifier.isi","000345192100019"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31990"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.eventlocation","Mainz, GERMANY"],["dc.relation.issn","1872-8421"],["dc.relation.issn","0165-5728"],["dc.title","Myelin-specific antibodies trigger spontaneous CNS autoimmune disease in the absence of myelin-specific B cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","314"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.lastpage","322"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Weil, Marie-Theres"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Romanelli, Elisa"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Enz, Lukas"],["dc.contributor.author","Goebels, Norbert"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Kerschensteiner, Martin"],["dc.contributor.author","Schaeren-Wiemers, Nicole"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2018-11-07T10:11:38Z"],["dc.date.available","2018-11-07T10:11:38Z"],["dc.date.issued","2016"],["dc.description.abstract","Breakdown of myelin sheaths is a pathological hallmark of several autoimmune diseases of the nervous system. We employed autoantibody-mediated animal models of demyelinating diseases, including a rat model of neuromyelitis optica (NMO), to target myelin and found that myelin lamellae are broken down into vesicular structures at the innermost region of the myelin sheath. We demonstrated that myelin basic proteins (MBP), which form a polymer in between the myelin membrane layers, are targeted in these models. Elevation of intracellular Ca2+ levels resulted in MBP network disassembly and myelin vesiculation. We propose that the aberrant phase transition of MBP molecules from their cohesive to soluble and non-adhesive state is a mechanism triggering myelin breakdown in NMO and possibly in other demyelinating diseases."],["dc.identifier.doi","10.1016/j.celrep.2016.06.008"],["dc.identifier.isi","000380262300005"],["dc.identifier.pmid","27346352"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13675"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40088"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","2211-1247"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Loss of Myelin Basic Protein Function Triggers Myelin Breakdown in Models of Demyelinating Diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]