Sereda, Michael Werner

[["dc.bibliographiccitation.firstpage","1050"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","1059"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Quintes, Susanne"],["dc.contributor.author","Brinkmann, Bastian G"],["dc.contributor.author","Ebert, Madlen"],["dc.contributor.author","Fröb, Franziska"],["dc.contributor.author","Kungl, Theresa"],["dc.contributor.author","Arlt, Friederike A"],["dc.contributor.author","Tarabykin, Victor"],["dc.contributor.author","Huylebroeck, Danny"],["dc.contributor.author","Meijer, Dies"],["dc.contributor.author","Suter, Ueli"],["dc.contributor.author","Wegner, Michael"],["dc.contributor.author","Sereda, Michael W"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2020-12-10T18:09:31Z"],["dc.date.available","2020-12-10T18:09:31Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1038/nn.4321"],["dc.identifier.eissn","1546-1726"],["dc.identifier.issn","1097-6256"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73679"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Zeb2 is essential for Schwann cell differentiation, myelination and nerve repair"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Annals of Clinical and Translational Neurology"],["dc.contributor.author","Epplen, Dirk B."],["dc.contributor.author","Prukop, Thomas"],["dc.contributor.author","Nientiedt, Tobias"],["dc.contributor.author","Albrecht, Philipp"],["dc.contributor.author","Arlt, Friederike A."],["dc.contributor.author","Stassart, Ruth M."],["dc.contributor.author","Kassmann, Celia M."],["dc.contributor.author","Methner, Axel"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2019-07-09T11:41:24Z"],["dc.date.available","2019-07-09T11:41:24Z"],["dc.date.issued","2015"],["dc.description.abstract","Objective: Pelizaeus–Merzbacher disease (PMD) is a progressive and lethal leukodystrophy caused by mutations affecting the proteolipid protein (PLP1) gene. The most common cause of PMD is a duplication of PLP1 and at present there is no curative therapy available. Methods: By using transgenic mice carrying additional copies of Plp1, we investigated whether curcumin diet ameliorates PMD symptoms. The diet of Plp1 transgenic mice was supplemented with curcumin for 10 consecutive weeks followed by phenotypical, histological and immunohistochemical analyses of the central nervous system. Plp1 transgenic and wild-type mice fed with normal chow served as controls. Results: Curcumin improved the motor phenotype performance of Plp1 transgenic mice by 50% toward wild-type level and preserved myelinated axons by 35% when compared to Plp1 transgenic controls. Furthermore, curcumin reduced astrocytosis, microgliosis and lymphocyte infiltration in Plp1 transgenic mice. Curcumin diet did not affect the pathologically increased Plp1 mRNA abundance. However, high glutathione levels indicating an oxidative misbalance in the white matter of Plp1 transgenic mice were restored by curcumin treatment. Interpretation: Curcumin may potentially serve as an antioxidant therapy of PMD caused by PLP1 gene duplication. ª"],["dc.identifier.doi","10.1002/acn3.219"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12013"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58419"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/201535/EU//NGIDD"],["dc.relation.euproject","Ngidd"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Curcumin therapy in a Plp1 transgenic mouse model of Pelizaeus-Merzbacher disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","201"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Orphanet journal of rare diseases"],["dc.bibliographiccitation.lastpage","16"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Chumakov, Ilya"],["dc.contributor.author","Milet, Aude"],["dc.contributor.author","Cholet, Nathalie"],["dc.contributor.author","Primas, Gwenaël"],["dc.contributor.author","Boucard, Aurélie"],["dc.contributor.author","Pereira, Yannick"],["dc.contributor.author","Graudens, Esther"],["dc.contributor.author","Mandel, Jonas"],["dc.contributor.author","Laffaire, Julien"],["dc.contributor.author","Foucquier, Julie"],["dc.contributor.author","Glibert, Fabrice"],["dc.contributor.author","Bertrand, Viviane"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Vial, Emmanuel"],["dc.contributor.author","Guedj, Mickaël"],["dc.contributor.author","Hajj, Rodolphe"],["dc.contributor.author","Nabirotchkin, Serguei"],["dc.contributor.author","Cohen, Daniel"],["dc.date.accessioned","2019-07-09T11:41:08Z"],["dc.date.available","2019-07-09T11:41:08Z"],["dc.date.issued","2014"],["dc.description.abstract","Charcot-Marie-Tooth disease type 1A (CMT1A) is the most common inherited sensory and motor peripheral neuropathy. It is caused by PMP22 overexpression which leads to defects of peripheral myelination, loss of long axons, and progressive impairment then disability. There is no treatment available despite observations that monotherapeutic interventions slow progression in rodent models. We thus hypothesized that a polytherapeutic approach using several drugs, previously approved for other diseases, could be beneficial by simultaneously targeting PMP22 and pathways important for myelination and axonal integrity. A combination of drugs for CMT1A polytherapy was chosen from a group of authorised drugs for unrelated diseases using a systems biology approach, followed by pharmacological safety considerations. Testing and proof of synergism of these drugs were performed in a co-culture model of DRG neurons and Schwann cells derived from a Pmp22 transgenic rat model of CMT1A. Their ability to lower Pmp22 mRNA in Schwann cells relative to house-keeping genes or to a second myelin transcript (Mpz) was assessed in a clonal cell line expressing these genes. Finally in vivo efficacy of the combination was tested in two models: CMT1A transgenic rats, and mice that recover from a nerve crush injury, a model to assess neuroprotection and regeneration. Combination of (RS)-baclofen, naltrexone hydrochloride and D-sorbitol, termed PXT3003, improved myelination in the Pmp22 transgenic co-culture cellular model, and moderately down-regulated Pmp22 mRNA expression in Schwannoma cells. In both in vitro systems, the combination of drugs was revealed to possess synergistic effects, which provided the rationale for in vivo clinical testing of rodent models. In Pmp22 transgenic CMT1A rats, PXT3003 down-regulated the Pmp22 to Mpz mRNA ratio, improved myelination of small fibres, increased nerve conduction and ameliorated the clinical phenotype. PXT3003 also improved axonal regeneration and remyelination in the murine nerve crush model. Based on these observations in preclinical models, a clinical trial of PTX3003 in CMT1A, a neglected orphan disease, is warranted. If the efficacy of PTX3003 is confirmed, rational polytherapy based on novel combinations of existing non-toxic drugs with pleiotropic effects may represent a promising approach for rapid drug development."],["dc.identifier.doi","10.1186/s13023-014-0201-x"],["dc.identifier.fs","606978"],["dc.identifier.pmid","25491744"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11689"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58355"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1750-1172"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Polytherapy with a combination of three repurposed drugs (PXT3003) down-regulates Pmp22 over-expression and improves myelination, axonal and functional parameters in models of CMT1A neuropathy."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["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","72"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","87"],["dc.bibliographiccitation.volume","135"],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Schlotter-Weigel, Beate"],["dc.contributor.author","Schnizer, Tuuli J."],["dc.contributor.author","Wichert, Sven P."],["dc.contributor.author","Stassart, Ruth Martha"],["dc.contributor.author","Hoerste, Gerd Meyer Zu"],["dc.contributor.author","Klink, Axel"],["dc.contributor.author","Weiss, Bernhard G."],["dc.contributor.author","Haag, Uwe"],["dc.contributor.author","Walter, Maggie C."],["dc.contributor.author","Rautenstrauss, Bernd"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Rossner, Moritz J."],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2018-11-07T09:15:45Z"],["dc.date.available","2018-11-07T09:15:45Z"],["dc.date.issued","2012"],["dc.description.abstract","Charcot-Marie-Tooth disease is the most common inherited neuropathy and a duplication of the peripheral myelin protein 22 gene causes the most frequent subform Charcot-Marie-Tooth 1A. Patients develop a slowly progressive dysmyelinating and demyelinating peripheral neuropathy and distally pronounced muscle atrophy. The amount of axonal loss determines disease severity. Although patients share an identical monogenetic defect, the disease progression is strikingly variable and the impending disease course can not be predicted in individual patients. Despite promising experimental data, recent therapy trials have failed. Established clinical outcome measures are thought to be too insensitive to detect amelioration within trials. Surrogate biomarkers of disease severity in Charcot-Marie-Tooth 1A are thus urgently needed. Peripheral myelin protein 22 transgenic rats harbouring additional copies of the peripheral myelin protein 22 gene ('Charcot-Marie-Tooth rats'), which were kept on an outbred background mimic disease hallmarks and phenocopy the variable disease severity of patients with Charcot-Marie-Tooth 1A. Hence, we used the Charcot-Marie-Tooth rat to dissect prospective and surrogate markers of disease severity derived from sciatic nerve and skin tissue messenger RNA extracts. Gene set enrichment analysis of sciatic nerve transcriptomes revealed that dysregulation of lipid metabolism associated genes such as peroxisome proliferator-activated receptor gamma constitutes a modifier of present and future disease severity. Importantly, we directly validated disease severity markers from the Charcot-Marie-Tooth rats in 46 patients with Charcot-Marie-Tooth 1A. Our data suggest that the combination of age and cutaneous messenger RNA levels of glutathione S-transferase theta 2 and cathepsin A composes a strong indicator of disease severity in patients with Charcot-Marie-Tooth 1A, as quantified by the Charcot-Marie-Tooth Neuropathy Score. This translational approach, utilizing a transgenic animal model, demonstrates that transcriptional analysis of skin biopsy is suitable to identify biomarkers of Charcot-Marie-Tooth 1A."],["dc.identifier.doi","10.1093/brain/awr322"],["dc.identifier.isi","000300044400016"],["dc.identifier.pmid","22189569"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13524"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27771"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A rat model of Charcot-Marie-Tooth disease 1A recapitulates disease variability and supplies biomarkers of axonal loss in patients"],["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.issue","2"],["dc.bibliographiccitation.journal","Journal of the Peripheral Nervous System"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Prukop, Thomas"],["dc.contributor.author","Milet, A."],["dc.contributor.author","Stenzel, J."],["dc.contributor.author","Cholet, N."],["dc.contributor.author","Nabirotchkin, S."],["dc.contributor.author","Hajj, R."],["dc.contributor.author","Nave, K-A"],["dc.contributor.author","Chumakov, I."],["dc.contributor.author","Cohen, Doron"],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2018-11-07T09:56:13Z"],["dc.date.available","2018-11-07T09:56:13Z"],["dc.date.issued","2015"],["dc.format.extent","213"],["dc.identifier.isi","000360214600327"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36911"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","Biennial Meeting of the Peripheral-Nerve-Society"],["dc.relation.eventlocation","Quebec, CANADA"],["dc.relation.issn","1529-8027"],["dc.relation.issn","1085-9489"],["dc.title","AN EXPERIMENTAL TRIAL OF AN EARLY ONSET TREATMENT WITH A COMBINATIONAL DRUG (PXT3003) CONSISTING OF BACLOFEN, NALTREXONE AND SORBITOL IN THE CMT1A RAT MODEL"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3465"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Journal of Neuroscience Research"],["dc.bibliographiccitation.lastpage","3479"],["dc.bibliographiccitation.volume","87"],["dc.contributor.author","Schardt, Anke"],["dc.contributor.author","Brinkmann, Bastian G."],["dc.contributor.author","Mitkovski, Miso"],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2018-11-07T11:22:05Z"],["dc.date.available","2018-11-07T11:22:05Z"],["dc.date.issued","2009"],["dc.description.abstract","During myelin formation, vast amounts of specialized membrane proteins and lipids are trafficked toward the growing sheath in cell surface-directed transport vesicles. Soluble N-ethylmaleimide-sensitive factor (NSF) attachment proteins (SNAPs) are important components of molecular complexes required for membrane fusion. We have analyzed the expression profile and molecular interactions of SNAP-29 in the nervous system. In addition to its known enrichment in neuronal synapses, SNAP-29 is abundant in oligodendrocytes during myelination and in noncompact myelin of the peripheral nervous system. By yeast two-hybrid screen and coimmunoprecipitation, we found that the GTPases Rab3A, Rab24, and septin 4 bind to the N-terminal domain of SNAP-29. The interaction with Rab24 or septin 4 was GTP independent. In contrast, interaction between SNAP-29 and Rab3A was GTP dependent, and colocalization was extensive both in synapses and in myelinating glia. In HEK293 cells, cytoplasmic SNAP-29 pools were redistributed upon coexpression with Rab3A, and surface-directed trafficking of myelin proteolipid protein was enhanced by overexpression of SNAP-29 and Rab3A. Interestingly, the abundance of SNAP-29 in sciatic nerves was increased during remyelination and in a rat model of Charcot-Marie-Tooth disease, two pathological situations with increased myelin membrane biogenesis. We suggest that Rab3A may regulate SNAP-29-mediated membrane fusion during myelination. (C) 2009 Wiley-Liss, Inc."],["dc.description.sponsorship","DFG [SFB 523]; BMBF (Leukonet)"],["dc.identifier.doi","10.1002/jnr.22005"],["dc.identifier.isi","000270843400023"],["dc.identifier.pmid","19170188"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55921"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0360-4012"],["dc.title","The SNARE Protein SNAP-29 Interacts With the GTPase Rab3A: Implications for Membrane Trafficking in Myelinating Glia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Juergens, T."],["dc.contributor.author","Glaser, Raoul"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Brinkmann, Bastian G."],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T11:25:14Z"],["dc.date.available","2018-11-07T11:25:14Z"],["dc.date.issued","2009"],["dc.format.extent","S180"],["dc.identifier.isi","000269652500538"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56580"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","25th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis"],["dc.relation.eventlocation","Dusseldorf, GERMANY"],["dc.relation.issn","1352-4585"],["dc.title","Propagation of cortical spreading depression inversely correlates with cortical myelin content"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3973"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA"],["dc.bibliographiccitation.lastpage","3978"],["dc.bibliographiccitation.volume","109"],["dc.contributor.author","Makoukji, Joelle"],["dc.contributor.author","Belle, Martin"],["dc.contributor.author","Meffre, Delphine"],["dc.contributor.author","Stassart, Ruth"],["dc.contributor.author","Grenier, Julien"],["dc.contributor.author","Shackleford, Ghjuvan'Ghjacumu"],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Fonte, Cosima"],["dc.contributor.author","Branchu, Julien"],["dc.contributor.author","Goulard, Marie"],["dc.contributor.author","de Waele, Catherine"],["dc.contributor.author","Charbonnier, Frederic"],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Baulieu, Etienne-Emile"],["dc.contributor.author","Schumacher, Michael"],["dc.contributor.author","Bernard, Sophie"],["dc.contributor.author","Massaad, Charbel"],["dc.date.accessioned","2018-11-07T09:12:24Z"],["dc.date.available","2018-11-07T09:12:24Z"],["dc.date.issued","2012"],["dc.description.abstract","Glycogen synthase kinase 3 beta (GSK3 beta) inhibitors, especially the mood stabilizer lithium chloride, are also used as neuroprotective or anti-inflammatory agents. We studied the influence of LiCl on the remyelination of peripheral nerves. We showed that the treatment of adult mice with LiCl after facial nerve crush injury stimulated the expression of myelin genes, restored the myelin structure, and accelerated the recovery of whisker movements. LiCl treatment also promoted remyelination of the sciatic nerve after crush. We also demonstrated that peripheral myelin gene MPZ and PMP22 promoter activities, transcripts, and protein levels are stimulated by GSK3 beta inhibitors (LiCl and SB216763) in Schwann cells as well as in sciatic and facial nerves. LiCl exerts its action in Schwann cells by increasing the amount of beta-catenin and provoking its nuclear localization. We showed by ChIP experiments that LiCl treatment drives beta-catenin to bind to T-cell factor/lymphoid-enhancer factor response elements identified in myelin genes. Taken together, our findings open perspectives in the treatment of nerve demyelination by administering GSK3 beta inhibitors such as lithium."],["dc.identifier.doi","10.1073/pnas.1121367109"],["dc.identifier.isi","000301117700073"],["dc.identifier.pmid","22355115"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26939"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Lithium enhances remyelination of peripheral nerves"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1840"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Akkermann, Dagmar"],["dc.contributor.author","Schütza, Vlad"],["dc.contributor.author","Abdelaal, Tamer A."],["dc.contributor.author","Hermes, Doris"],["dc.contributor.author","Schäffner, Erik"],["dc.contributor.author","Soto-Bernardini, M. Clara"],["dc.contributor.author","Götze, Tilmann"],["dc.contributor.author","Klink, Axel"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Krueger, Martin"],["dc.contributor.author","Kungl, Theresa"],["dc.contributor.author","Frydrychowicz, Clara"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Mueller, Wolf C."],["dc.contributor.author","Bechmann, Ingo"],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Schwab, Markus H."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Stassart, Ruth M."],["dc.date.accessioned","2019-07-09T11:51:38Z"],["dc.date.available","2019-07-09T11:51:38Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1038/s41467-019-09886-4"],["dc.identifier.pmid","30992451"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16160"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59979"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Publisher Correction: NRG1 type I dependent autoparacrine stimulation of Schwann cells in onion bulbs of peripheral neuropathies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]