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","289"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cell and Tissue Research"],["dc.bibliographiccitation.lastpage","311"],["dc.bibliographiccitation.volume","349"],["dc.contributor.author","Lingor, P."],["dc.contributor.author","Koch, J. C."],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Bähr, M."],["dc.date.accessioned","2017-09-07T11:48:50Z"],["dc.date.available","2017-09-07T11:48:50Z"],["dc.date.issued","2012"],["dc.description.abstract","Degeneration of the axon is an important step in the pathomechanism of traumatic, inflammatory and degenerative neurological diseases. Increasing evidence suggests that axonal degeneration occurs early in the course of these diseases and therefore represents a promising target for future therapeutic strategies. We review the evidence for axonal destruction from pathological findings and animal models with particular emphasis on neurodegenerative and neurotraumatic disorders. We discuss the basic morphological and temporal modalities of axonal degeneration (acute, chronic and focal axonal degeneration and Wallerian degeneration). Based on the mechanistic concepts, we then delineate in detail the major molecular mechanisms that underlie the degenerative cascade, such as calcium influx, axonal transport, protein aggregation and autophagy. We finally concentrate on putative therapeutic targets based on the mechanistic prerequisites."],["dc.identifier.doi","10.1007/s00441-012-1362-3"],["dc.identifier.gro","3142506"],["dc.identifier.isi","000305405800023"],["dc.identifier.pmid","22392734"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8101"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8865"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0302-766X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject","Neurodegeneration; Neurotrauma; Wallerian degeneration; Calcium Autophagy"],["dc.title","Axonal degeneration as a therapeutic target in the CNS"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["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.artnumber","e1811"],["dc.bibliographiccitation.journal","Cell Death and Disease"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Koch, J. C."],["dc.contributor.author","Bitow, F."],["dc.contributor.author","Haack, J."],["dc.contributor.author","D'Hedouville, Z."],["dc.contributor.author","Zhang, J-N"],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Michel, U."],["dc.contributor.author","Oliveira, L. M. A."],["dc.contributor.author","Jovin, T. M."],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Tatenhorst, L."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Lingor, P."],["dc.date.accessioned","2017-09-07T11:43:42Z"],["dc.date.available","2017-09-07T11:43:42Z"],["dc.date.issued","2015"],["dc.description.abstract","Many neuropathological and experimental studies suggest that the degeneration of dopaminergic terminals and axons precedes the demise of dopaminergic neurons in the substantia nigra, which finally results in the clinical symptoms of Parkinson disease (PD). The mechanisms underlying this early axonal degeneration are, however, still poorly understood. Here, we examined the effects of overexpression of human wildtype alpha-synuclein (alpha Syn-WT), a protein associated with PD, and its mutant variants alpha Syn-A30P and -A53T on neurite morphology and functional parameters in rat primary midbrain neurons (PMN). Moreover, axonal degeneration after overexpression of alpha Syn-WT and -A30P was analyzed by live imaging in the rat optic nerve in vivo. We found that overexpression of alpha Syn-WT and of its mutants A30P and A53T impaired neurite outgrowth of PMN and affected neurite branching assessed by Sholl analysis in a variant-dependent manner. Surprisingly, the number of primary neurites per neuron was increased in neurons transfected with alpha Syn. Axonal vesicle transport was examined by live imaging of PMN co-transfected with EGFP-labeled synaptophysin. Overexpression of all alpha Syn variants significantly decreased the number of motile vesicles and decelerated vesicle transport compared with control. Macroautophagic flux in PMN was enhanced by alpha Syn-WT and -A53T but not by alpha Syn-A30P. Correspondingly, colocalization of alpha Syn and the autophagy marker LC3 was reduced for alpha Syn-A30P compared with the other alpha Syn variants. The number of mitochondria colocalizing with LC3 as a marker for mitophagy did not differ among the groups. In the rat optic nerve, both alpha Syn-WT and -A30P accelerated kinetics of acute axonal degeneration following crush lesion as analyzed by in vivo live imaging. We conclude that alpha Syn overexpression impairs neurite outgrowth and augments axonal degeneration, whereas axonal vesicle transport and autophagy are severely altered."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.1038/cddis.2015.169"],["dc.identifier.gro","3141868"],["dc.identifier.isi","000358788800011"],["dc.identifier.pmid","26158517"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12015"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1967"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","2041-4889"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject","Central nervous system; Molecular neuroscience; Parkinson's disease"],["dc.title","Alpha-Synuclein affects neurite morphology, autophagy, vesicle transport and axonal degeneration in CNS neurons"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["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"]]