Lingor, Paul

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Clinical and Translational Medicine"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Caldi Gomes, Lucas"],["dc.contributor.author","Roser, Anna‐Elisa"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Pena Centeno, Tonatiuh"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Schilde, Lukas"],["dc.contributor.author","May, Caroline"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2021-06-01T09:41:18Z"],["dc.date.available","2021-06-01T09:41:18Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1002/ctm2.357"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84876"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","2001-1326"],["dc.relation.issn","2001-1326"],["dc.title","MicroRNAs from extracellular vesicles as a signature for Parkinson's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","89"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Virology"],["dc.bibliographiccitation.lastpage","95"],["dc.bibliographiccitation.volume","311"],["dc.contributor.author","Kügler, S"],["dc.contributor.author","Schöll, U"],["dc.contributor.author","Zolotukhin, S"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2021-06-01T10:50:07Z"],["dc.date.available","2021-06-01T10:50:07Z"],["dc.date.issued","2003"],["dc.description.abstract","Adeno-associated- (AAV) based vectors are promising tools for gene therapy applications in several organs, including the brain, but are limited by their small genome size. Two short promoters, the human synapsin 1 gene promoter (hSYN) and the murine cytomegalovirus immediate early promoter (mCMV), were evaluated in bicistronic AAV-2 vectors for their expression profiles in cultured primary brain cells and in the rat brain. Whereas transgene expression from the hSYN promoter was exclusively neuronal, the murine CMV promoter targeted expression mainly to astrocytes in vitro and showed weak transgene expression in vivo in retinal and cortical neurons, but strong expression in thalamic neurons. We propose that neuron specific transgene expression in combination with enhanced transgene capacity will further substantially improve AAV based vector technology. (C) 2003 Elsevier Science (USA). All rights reserved."],["dc.identifier.doi","10.1016/S0042-6822(03)00162-4"],["dc.identifier.gro","3144097"],["dc.identifier.isi","000184042900010"],["dc.identifier.pmid","12832206"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86537"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0042-6822"],["dc.title","Differential transgene expression in brain cells in vivo and in vitro from AAV-2 vectors with small transcriptional control units"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","148"],["dc.bibliographiccitation.lastpage","163"],["dc.bibliographiccitation.seriesnr","557"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.editor","Bähr, Mathias"],["dc.date.accessioned","2018-04-23T11:48:10Z"],["dc.date.available","2018-04-23T11:48:10Z"],["dc.date.issued","2006"],["dc.identifier.doi","10.1007/0-387-30128-3_9"],["dc.identifier.gro","3142089"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13466"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.publisher","Eurekah.com and Springer Science+Business Media, 2006"],["dc.publisher.place","Boston, MA"],["dc.relation.crisseries","Advances in Experimental Medicine and Biology"],["dc.relation.isbn","978-0-387-30128-0"],["dc.relation.ispartof","Brain Repair"],["dc.relation.ispartofseries","Advances in Experimental Medicine and Biology; 557"],["dc.title","Brain Repair: Experimental Treatment Strategies, Neuroprotective and Repair Strategies in the Lesioned Adult CNS"],["dc.type","book_chapter"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","72"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","86"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Ribas, Vinicius Toledo"],["dc.contributor.author","Koch, Jan C."],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2018-01-09T11:14:21Z"],["dc.date.available","2018-01-09T11:14:21Z"],["dc.date.issued","2017"],["dc.description.abstract","Axonal degeneration is one of the initial steps in many traumatic and neurodegenerative central nervous system (CNS) disorders and thus a promising therapeutic target. A focal axonal lesion is followed by acute axonal degeneration (AAD) of both adjacent axon parts, before proximal and distal parts follow different degenerative fates at later time points. Blocking calcium influx by calcium channel inhibitors was previously shown to attenuate AAD after optic nerve crush (ONC). However, it remains unclear whether the attenuation of AAD also promotes consecutive axonal regeneration. Here, we used a rat ONC model to study the effects of calcium channel inhibitors on axonal degeneration, retinal ganglion cell (RGC) survival, and axonal regeneration, as well as the molecular mechanisms involved. Application of calcium channel inhibitors attenuated AAD after ONC and preserved axonal integrity as visualized by live imaging of optic nerve axons. Consecutively, this resulted in improved survival of RGCs and improved axonal regeneration at 28 days after ONC. We show further that calcium channel inhibition attenuated lesion-induced calpain activation in the proximity of the crush and inhibited the activation of the c-Jun N-terminal kinase pathway. Pro-survival signaling via Akt in the retina was also increased. Our data thus show that attenuation of AAD improves consecutive neuronal survival and axonal regeneration and that calcium channel inhibitors could be valuable tools for therapeutic interventions in traumatic and degenerative CNS disorders."],["dc.identifier.doi","10.1007/s12035-015-9676-2"],["dc.identifier.pmid","26732591"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11580"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1559-1182"],["dc.title","Attenuation of Axonal Degeneration by Calcium Channel Inhibitors Improves Retinal Ganglion Cell Survival and Regeneration After Optic Nerve Crush"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","651"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cell Death and Differentiation"],["dc.bibliographiccitation.lastpage","661"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Meuer, K."],["dc.contributor.author","Suppanz, I. E."],["dc.contributor.author","Lingor, P."],["dc.contributor.author","Planchamp, V."],["dc.contributor.author","Göricke, B."],["dc.contributor.author","Fichtner, L."],["dc.contributor.author","Braus, G. H."],["dc.contributor.author","Dietz, G. P. H."],["dc.contributor.author","Jakobs, S."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Weishaupt, J. H."],["dc.date.accessioned","2017-09-07T11:49:50Z"],["dc.date.available","2017-09-07T11:49:50Z"],["dc.date.issued","2007"],["dc.description.abstract","Under physiological conditions, mitochondrial morphology dynamically shifts between a punctuate appearance and tubular networks. However, little is known about upstream signal transduction pathways that regulate mitochondrial morphology. We show that mitochondrial fission is a very early and kinetically invariant event during neuronal cell death, which causally contributes to cytochrome c release and neuronal apoptosis. Using a small molecule CDK5 inhibitor, as well as a dominant-negative CDK5 mutant and RNAi knockdown experiments, we identified CDK5 as an upstream signalling kinase that regulates mitochondrial fission during apoptosis of neurons. Vice versa, our study shows that mitochondrial fission is a modulator contributing to CDK5-mediated neurotoxicity. Thereby, we provide a link that allows integration of CDK5 into established neuronal apoptosis pathways."],["dc.identifier.doi","10.1038/sj.cdd.4402087"],["dc.identifier.gro","3143515"],["dc.identifier.isi","000245102900002"],["dc.identifier.pmid","17218957"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1038"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1350-9047"],["dc.title","Cyclin-dependent kinase 5 is an upstream regulator of mitochondrial fission during neuronal apoptosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1355"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Alzheimer's Disease"],["dc.bibliographiccitation.lastpage","1361"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Gmitterova, Karin"],["dc.contributor.author","Varges, Daniela"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Zafar, Saima"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2020-12-10T18:44:13Z"],["dc.date.available","2020-12-10T18:44:13Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3233/JAD-191153"],["dc.identifier.eissn","1875-8908"],["dc.identifier.issn","1387-2877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78369"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Chromogranin A Analysis in the Differential Diagnosis Across Lewy Body Disorders"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3472"],["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","FEBS Journal"],["dc.bibliographiccitation.lastpage","3483"],["dc.bibliographiccitation.volume","278"],["dc.contributor.author","Koch, J. C."],["dc.contributor.author","Barski, E."],["dc.contributor.author","Lingor, P."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Michel, U."],["dc.date.accessioned","2017-09-07T11:43:25Z"],["dc.date.available","2017-09-07T11:43:25Z"],["dc.date.issued","2011"],["dc.description.abstract","Repressor element-1 silencing transcription factor (REST) is a transcriptional repressor of neuron-specific genes that binds to a conserved DNA element, the neuron restrictive silencer element (NRSE/RE1). Interestingly, increased REST activity is found in several neurological diseases like Huntington's disease and cerebral ischemia. Recently, it was shown that NRSE dsRNA, a double-stranded non-coding RNA can bind to REST during a defined period of neuronal differentiation, and thereby changes REST from a transcriptional repressor to an activator of neuron-specific genes. Here, we analyzed the effects of NRSE dsRNA expression in primary retinal ganglion cells. We found that NRSE dsRNA expression vectors significantly enhance neurite outgrowth even when axonal degeneration is induced by neurotrophin deprivation. Transfection of HEK cells with NRSE dsRNA-expressing vectors altered their morphology leading to the formation of thin processes and induced the expression of neurofilament-68. Surprisingly, control vectors containing REST-binding sites, but not expressing NRSE dsRNA, resulted in the same effects, also in the retinal ganglion cell model. Reporter assays and retention of REST in the cytoplasm with a labeled NRSE/RE1-containing plasmid incapable of entering the nucleus suggest that sequestration of REST in the cytoplasm is the reason for the observed effects. No evidence for a biological function of NRSE dsRNA could be found in these models. We conclude that sequestration of REST leads to enhanced neurite outgrowth in retinal ganglion cells and that an increased activity of REST, as it is found in several neurodegenerative diseases, can be effectively modulated by sequestration of REST with plasmids containing NRSE/RE1 sites."],["dc.identifier.doi","10.1111/j.1742-4658.2011.08269.x"],["dc.identifier.gro","3142674"],["dc.identifier.isi","000294810600024"],["dc.identifier.pmid","21790997"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/104"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1742-464X"],["dc.title","Plasmids containing NRSE/RE1 sites enhance neurite outgrowth of retinal ganglion cells via sequestration of REST independent of NRSE dsRNA expression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","685"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","697"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Balke, Dirk"],["dc.contributor.author","Tatenhorst, Lars"],["dc.contributor.author","Dambeck, Vivian"],["dc.contributor.author","Ribas, Vinicius Toledo"],["dc.contributor.author","Vahsen, Björn F."],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2020-12-10T14:14:28Z"],["dc.date.available","2020-12-10T14:14:28Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s12035-019-01744-0"],["dc.identifier.eissn","1559-1182"],["dc.identifier.issn","0893-7648"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71353"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","AAV-Mediated Expression of Dominant-Negative ULK1 Increases Neuronal Survival and Enhances Motor Performance in the MPTP Mouse Model of Parkinson’s Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","335"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Experimental Brain Research"],["dc.bibliographiccitation.lastpage","342"],["dc.bibliographiccitation.volume","161"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Scholl, U."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Kugler, S."],["dc.date.accessioned","2017-09-07T11:54:31Z"],["dc.date.available","2017-09-07T11:54:31Z"],["dc.date.issued","2005"],["dc.description.abstract","The Semliki Forest virus (SFV) system has been shown to be highly efficient in transduction of cell lines and primary cells. We employed a novel \"noncytotoxic\" SFV(PD) vector for transduction of primary ventral midbrain floor cultures in vitro and rat substantia nigra in vivo. Rapid protein expression was noted with preferential transduction of neuronal cells including the dopaminergic subpopulation. To examine the suitability of the SFV vector system for functional gene expression, SFV(PD) vectors encoding for antiapoptotic proteins Bcl-X-L and XIAP were designed. Despite effective transgene expression, SFV(PD) vectors were unable to rescue dopaminergic neurons from MPP+-induced apoptosis. In vivo, virus injection into substantia nigra resulted in fast onset of transgene expression, but elicited an activation of microglia and an inflammation response. We conclude that the use of novel SFV(PD) vectors is currently limited by persistent neurotoxicity of the vector system. Although SFV(PD) vectors may be useful for protein localization studies in dopaminergic neurons, functional applications will require the development of even less cytopathic vector systems."],["dc.identifier.doi","10.1007/s00221-004-2077-9"],["dc.identifier.gro","3143883"],["dc.identifier.isi","000227236900009"],["dc.identifier.pmid","15502982"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1446"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0014-4819"],["dc.title","Functional applications of novel Semliki Forest virus vectors are limited by vector toxicity in cultures of primary neurons in vitro and in the substantia nigra in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","152"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of the Neurological Sciences"],["dc.bibliographiccitation.lastpage","154"],["dc.bibliographiccitation.volume","331"],["dc.contributor.author","Schmidt, Holger"],["dc.contributor.author","Kretzschmar, Benedikt"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Pauli, Silke"],["dc.contributor.author","Schramm, Peter"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Brockmann, Knut"],["dc.date.accessioned","2018-11-07T09:21:15Z"],["dc.date.available","2018-11-07T09:21:15Z"],["dc.date.issued","2013"],["dc.description.abstract","Adult-onset Alexander disease (AOAD) is a rare leukoencephalopathy affecting predominantly the brainstem and cervical cord with insidious onset of clinical features. Acute onset is very rare and has yet been described only twice, to our knowledge. We report a 32-year-old hitherto healthy male who, after excessive consumption of alcohol, presented with stroke-like onset of symptoms including rigidospasticity, loss of consciousness, and bulbar dysfunction. MRI features comprised bilateral T2-hyperintensities of frontal white matter and basal ganglia as well as atrophy of medulla oblongata with a peculiar \"tadpole\" appearance, a pattern characteristic of AOAD. Mutation analysis of the GFAP gene revealed a heterozygous de novo 9-bp microduplication in exon 1. Adult Alexander disease may present with stroke-like features. MRI patterns of chronic neurodegenerative conditions may be recognizable even in acute neurological emergencies. (C) 2013 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jns.2013.05.006"],["dc.identifier.isi","000322415000030"],["dc.identifier.pmid","23706596"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29072"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0022-510X"],["dc.title","Acute onset of adult Alexander disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]