Quintes, Susanne

[["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.firstpage","1241"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Neural Regeneration Research"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Quintes, Susanne"],["dc.contributor.author","Brinkmann, BastianG"],["dc.date.accessioned","2020-12-10T18:47:43Z"],["dc.date.available","2020-12-10T18:47:43Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.4103/1673-5374.213537"],["dc.identifier.issn","1673-5374"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78863"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Transcriptional inhibition in Schwann cell development and nerve regeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2205"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","FEBS Letters"],["dc.bibliographiccitation.lastpage","2211"],["dc.bibliographiccitation.volume","585"],["dc.contributor.author","Kassmann, Celia M."],["dc.contributor.author","Quintes, Susanne"],["dc.contributor.author","Rietdorf, Jens"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Sereda, Michael Werner"],["dc.contributor.author","Nientiedt, Tobias"],["dc.contributor.author","Saher, Gesine"],["dc.contributor.author","Baes, Myriam"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2022-03-01T11:45:09Z"],["dc.date.available","2022-03-01T11:45:09Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1016/j.febslet.2011.05.032"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103228"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0014-5793"],["dc.title","A role for myelin-associated peroxisomes in maintaining paranodal loops and axonal integrity"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","7632"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","7645"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Fuenfschilling, Ursula"],["dc.contributor.author","Jockusch, Wolf J."],["dc.contributor.author","Sivakumar, Nandhini"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Corthals, Kristina"],["dc.contributor.author","Li, Sai"],["dc.contributor.author","Quintes, Susanne"],["dc.contributor.author","Kim, Younghoon"],["dc.contributor.author","Schaap, Iwan Alexander Taco"],["dc.contributor.author","Rhee, Jeong-Seop"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Saher, Gesine"],["dc.date.accessioned","2018-11-07T09:10:14Z"],["dc.date.available","2018-11-07T09:10:14Z"],["dc.date.issued","2012"],["dc.description.abstract","Cholesterol is an essential membrane component enriched in plasma membranes, growth cones, and synapses. The brain normally synthesizes all cholesterol locally, but the contribution of individual cell types to brain cholesterol metabolism is unknown. To investigate whether cortical projection neurons in vivo essentially require cholesterol biosynthesis and which cell types support neurons, we have conditionally ablated the cholesterol biosynthesis in these neurons in mice either embryonically or postnatally. We found that cortical projection neurons synthesize cholesterol during their entire lifetime. At all stages, they can also benefit from glial support. Adult neurons that lack cholesterol biosynthesis are mainly supported by astrocytes such that their functional integrity is preserved. In contrast, microglial cells support young neurons. However, compensatory efforts of microglia are only transient leading to layer-specific neuronal death and the reduction of cortical projections. Hence, during the phase of maximal membrane growth and maximal cholesterol demand, neuronal cholesterol biosynthesis is indispensable. Analysis of primary neurons revealed that neurons tolerate only slight alteration in the cholesterol content and plasma membrane tension. This quality control allows neurons to differentiate normally and adjusts the extent of neurite outgrowth, the number of functional growth cones and synapses to the available cholesterol. This study highlights both the flexibility and the limits of horizontal cholesterol transfer in vivo and may have implications for the understanding of neurodegenerative diseases."],["dc.identifier.doi","10.1523/JNEUROSCI.1352-11.2012"],["dc.identifier.fs","596609"],["dc.identifier.isi","000304627100022"],["dc.identifier.pmid","22649242"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8454"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26441"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.relation.orgunit","Fakultät für Physik"],["dc.title","Critical Time Window of Neuronal Cholesterol Synthesis during Neurite Outgrowth"],["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.journal","Glia"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Brinkmann, Bastian G."],["dc.contributor.author","Kungl, Theresa"],["dc.contributor.author","Ebert, Matthias"],["dc.contributor.author","Wernick, S."],["dc.contributor.author","Quintes, Susanne"],["dc.contributor.author","Nave, K.-A."],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2018-11-07T10:23:01Z"],["dc.date.available","2018-11-07T10:23:01Z"],["dc.date.issued","2017"],["dc.format.extent","E381"],["dc.identifier.isi","000403071700590"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42381"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley"],["dc.publisher.place","Hoboken"],["dc.relation.conference","13th European Meeting on Glial Cells in Health and Disease"],["dc.relation.eventlocation","Edinburgh, SCOTLAND"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Using mouse models of peripheral neuropathies to study the development of Schmidt-Lanterman incisures"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Brinkmann, Bastian G."],["dc.contributor.author","Quintes, Susanne"],["dc.contributor.author","Ebert, Matthias"],["dc.contributor.author","Keric, Naureen"],["dc.contributor.author","Matz, A."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Nave, K.-A."],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2018-11-07T09:54:17Z"],["dc.date.available","2018-11-07T09:54:17Z"],["dc.date.issued","2015"],["dc.format.extent","E286"],["dc.identifier.isi","000356386700487"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36504"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","12th European Meeting on Glial Cell Function in Health and Disease"],["dc.relation.eventlocation","Bilbao, SPAIN"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","A novel role for Endothelin receptor B signalling in the peripheral nervous system"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","eLife"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Kleinecke, Sandra"],["dc.contributor.author","Richert, Sarah"],["dc.contributor.author","de Hoz, Livia"],["dc.contributor.author","Brügger, Britta"],["dc.contributor.author","Kungl, Theresa"],["dc.contributor.author","Asadollahi, Ebrahim"],["dc.contributor.author","Quintes, Susanne"],["dc.contributor.author","Blanz, Judith"],["dc.contributor.author","McGonigal, Rhona"],["dc.contributor.author","Naseri, Kobra"],["dc.contributor.author","Kassmann, Celia Michèle"],["dc.date.accessioned","2022-03-01T11:44:32Z"],["dc.date.available","2022-03-01T11:44:32Z"],["dc.date.issued","2017"],["dc.description.abstract","Impairment of peripheral nerve function is frequent in neurometabolic diseases, but mechanistically not well understood. Here, we report a novel disease mechanism and the finding that glial lipid metabolism is critical for axon function, independent of myelin itself. Surprisingly, nerves of Schwann cell-specific Pex5 mutant mice were unaltered regarding axon numbers, axonal calibers, and myelin sheath thickness by electron microscopy. In search for a molecular mechanism, we revealed enhanced abundance and internodal expression of axonal membrane proteins normally restricted to juxtaparanodal lipid-rafts. Gangliosides were altered and enriched within an expanded lysosomal compartment of paranodal loops. We revealed the same pathological features in a mouse model of human Adrenomyeloneuropathy, preceding disease-onset by one year. Thus, peroxisomal dysfunction causes secondary failure of local lysosomes, thereby impairing the turnover of gangliosides in myelin. This reveals a new aspect of axon-glia interactions, with Schwann cell lipid metabolism regulating the anchorage of juxtaparanodal Kv1-channels."],["dc.description.abstract","Nerve cells transmit messages along their length in the form of electrical signals. Much like an electrical wire, the nerve fiber or axon is coated by a multiple-layered insulation, called the myelin sheath. However, unlike electrical insulation, the myelin sheath is regularly interrupted to expose short regions of the underlying nerve. These exposed regions and the adjacent regions underneath the myelin contain ion channels that help to propagate electrical signals along the axon. Peroxisomes are compartments in animal cells that process fats. Genetic mutations that prevent peroxisomes from working properly can lead to diseases where the nerves cannot transmit signals correctly. This is thought to be because the nerves lose their myelin sheath, which largely consists of fatty molecules. The nerves outside of the brain and spinal cord are known as peripheral nerves. Kleinecke et al. have now analyzed peripheral nerves from mice that had one of three different genetic mutations, preventing their peroxisomes from working correctly. Even in cases where the mutation severely impaired nerve signaling, the peripheral nerves retained their myelin sheath. The peroxisome mutations did affect a particular type of potassium ion channel and the anchor proteins that hold these channels in place. The role of these potassium ion channels is not fully known, but normally they are only found close to regions of the axon that are not coated by myelin. However, the peroxisome mutations meant that the channels and their protein anchors were now also located along the myelinated segments of the nerve’s axons. This redistribution of the potassium ion channels likely contributes to the peripheral nerves being unable to signal properly. In addition, Kleinecke et al. found that disrupting the peroxisomes also affected another cell compartment, called the lysosome, in the nerve cells that insulate axons with myelin sheaths. Lysosomes help to break down unwanted fat molecules. Mutant mice had more lysosomes than normal, but these lysosomes did not work efficiently. This caused the nerve cells to store more of certain types of molecules, including molecules called glycolipids that stabilize protein anchors, which hold the potassium channels in place. A likely result is that protein anchors that would normally be degraded are not, leading to the potassium channels appearing inappropriately throughout the nerve. Future work is now needed to investigate whether peroxisomal diseases cause similar changes in the brain. The results presented by Kleinecke et al. also suggest that targeting the lysosomes or the potassium channels could present new ways to treat disorders of the peroxisomes."],["dc.description.abstract","Impairment of peripheral nerve function is frequent in neurometabolic diseases, but mechanistically not well understood. Here, we report a novel disease mechanism and the finding that glial lipid metabolism is critical for axon function, independent of myelin itself. Surprisingly, nerves of Schwann cell-specific Pex5 mutant mice were unaltered regarding axon numbers, axonal calibers, and myelin sheath thickness by electron microscopy. In search for a molecular mechanism, we revealed enhanced abundance and internodal expression of axonal membrane proteins normally restricted to juxtaparanodal lipid-rafts. Gangliosides were altered and enriched within an expanded lysosomal compartment of paranodal loops. We revealed the same pathological features in a mouse model of human Adrenomyeloneuropathy, preceding disease-onset by one year. Thus, peroxisomal dysfunction causes secondary failure of local lysosomes, thereby impairing the turnover of gangliosides in myelin. This reveals a new aspect of axon-glia interactions, with Schwann cell lipid metabolism regulating the anchorage of juxtaparanodal Kv1-channels."],["dc.description.abstract","Nerve cells transmit messages along their length in the form of electrical signals. Much like an electrical wire, the nerve fiber or axon is coated by a multiple-layered insulation, called the myelin sheath. However, unlike electrical insulation, the myelin sheath is regularly interrupted to expose short regions of the underlying nerve. These exposed regions and the adjacent regions underneath the myelin contain ion channels that help to propagate electrical signals along the axon. Peroxisomes are compartments in animal cells that process fats. Genetic mutations that prevent peroxisomes from working properly can lead to diseases where the nerves cannot transmit signals correctly. This is thought to be because the nerves lose their myelin sheath, which largely consists of fatty molecules. The nerves outside of the brain and spinal cord are known as peripheral nerves. Kleinecke et al. have now analyzed peripheral nerves from mice that had one of three different genetic mutations, preventing their peroxisomes from working correctly. Even in cases where the mutation severely impaired nerve signaling, the peripheral nerves retained their myelin sheath. The peroxisome mutations did affect a particular type of potassium ion channel and the anchor proteins that hold these channels in place. The role of these potassium ion channels is not fully known, but normally they are only found close to regions of the axon that are not coated by myelin. However, the peroxisome mutations meant that the channels and their protein anchors were now also located along the myelinated segments of the nerve’s axons. This redistribution of the potassium ion channels likely contributes to the peripheral nerves being unable to signal properly. In addition, Kleinecke et al. found that disrupting the peroxisomes also affected another cell compartment, called the lysosome, in the nerve cells that insulate axons with myelin sheaths. Lysosomes help to break down unwanted fat molecules. Mutant mice had more lysosomes than normal, but these lysosomes did not work efficiently. This caused the nerve cells to store more of certain types of molecules, including molecules called glycolipids that stabilize protein anchors, which hold the potassium channels in place. A likely result is that protein anchors that would normally be degraded are not, leading to the potassium channels appearing inappropriately throughout the nerve. Future work is now needed to investigate whether peroxisomal diseases cause similar changes in the brain. The results presented by Kleinecke et al. also suggest that targeting the lysosomes or the potassium channels could present new ways to treat disorders of the peroxisomes."],["dc.identifier.doi","10.7554/eLife.23332"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103046"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","2050-084X"],["dc.title","Peroxisomal dysfunctions cause lysosomal storage and axonal Kv1 channel redistribution in peripheral neuropathy"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1933"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Journal of Neuroscience Research"],["dc.bibliographiccitation.lastpage","1952"],["dc.bibliographiccitation.volume","98"],["dc.contributor.author","Prukop, Thomas"],["dc.contributor.author","Wernick, Stephanie"],["dc.contributor.author","Boussicault, Lydie"],["dc.contributor.author","Ewers, David"],["dc.contributor.author","Jäger, Karoline"],["dc.contributor.author","Adam, Julia"],["dc.contributor.author","Winter, Lorenz"],["dc.contributor.author","Quintes, Susanne"],["dc.contributor.author","Linhoff, Lisa"],["dc.contributor.author","Barrantes‐Freer, Alonso"],["dc.contributor.author","Bartl, Michael"],["dc.contributor.author","Czesnik, Dirk"],["dc.contributor.author","Zschüntzsch, Jana"],["dc.contributor.author","Schmidt, Jens"],["dc.contributor.author","Primas, Gwenaël"],["dc.contributor.author","Laffaire, Julien"],["dc.contributor.author","Rinaudo, Philippe"],["dc.contributor.author","Brureau, Anthony"],["dc.contributor.author","Nabirotchkin, Serguei"],["dc.contributor.author","Schwab, Markus H."],["dc.contributor.author","Nave, Klaus‐Armin"],["dc.contributor.author","Hajj, Rodolphe"],["dc.contributor.author","Cohen, Daniel"],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2021-04-14T08:23:41Z"],["dc.date.available","2021-04-14T08:23:41Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1002/jnr.24679"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81010"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1097-4547"],["dc.relation.issn","0360-4012"],["dc.title","Synergistic PXT3003 therapy uncouples neuromuscular function from dysmyelination in male Charcot–Marie–Tooth disease type 1A (CMT1A) rats"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","202"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Structural Biology"],["dc.bibliographiccitation.lastpage","212"],["dc.bibliographiccitation.volume","173"],["dc.contributor.author","Dučić, Tanja"],["dc.contributor.author","Quintes, Susanne"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Susini, Jean"],["dc.contributor.author","Rak, Margaret"],["dc.contributor.author","Tucoulou, Remi"],["dc.contributor.author","Alevra, Mihai"],["dc.contributor.author","Guttmann, Peter"],["dc.contributor.author","Salditt, Tim"],["dc.date.accessioned","2017-09-07T11:44:21Z"],["dc.date.available","2017-09-07T11:44:21Z"],["dc.date.issued","2011"],["dc.description.abstract","We report elemental mappings on the sub-cellular level of myelinated sciatic neurons isolated from wild type mice, with high spatial resolution. The distribution of P. S. Cl, Na, K, Fe, Mn, Cu was imaged in freeze-dried as well as cryo-preserved specimen, using the recently developed cryogenic sample environment at beamline ID21 at the European Synchrotron Radiation Facility (ESRF). In addition, synchrotron radiation based Fourier transform infrared (FTIR) spectromicroscopy was used as a chemically sensitive imaging method. Finally single fiber diffraction in highly focused hard X-ray beams, and soft X-ray microscopy and tomography in absorption contrast are demonstrated as novel techniques for the study of single nerve fibers. (C) 2010 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.jsb.2010.10.001"],["dc.identifier.gro","3142780"],["dc.identifier.isi","000286846700002"],["dc.identifier.pmid","20950687"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/221"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: DFG Research Center"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1047-8477"],["dc.relation.orgunit","Institut für Röntgenphysik"],["dc.relation.workinggroup","RG Salditt (Structure of Biomolecular Assemblies and X-Ray Physics)"],["dc.subject.gro","x-ray imaging"],["dc.subject.gro","x-ray scattering"],["dc.subject.gro","neuro biophysics"],["dc.title","Structure and composition of myelinated axons: A multimodal synchrotron spectro-microscopy study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6094"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","6104"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Saher, G."],["dc.contributor.author","Quintes, S."],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Wehr, M. C."],["dc.contributor.author","Kramer-Albers, E.-M."],["dc.contributor.author","Brugger, B."],["dc.contributor.author","Nave, K.-A."],["dc.date.accessioned","2021-06-01T10:48:22Z"],["dc.date.available","2021-06-01T10:48:22Z"],["dc.date.issued","2009"],["dc.identifier.doi","10.1523/JNEUROSCI.0686-09.2009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85911"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1529-2401"],["dc.relation.issn","0270-6474"],["dc.title","Cholesterol Regulates the Endoplasmic Reticulum Exit of the Major Membrane Protein P0 Required for Peripheral Myelin Compaction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]