Voigt, Aaron

[["dc.bibliographiccitation.firstpage","543"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","American Journal Of Pathology"],["dc.bibliographiccitation.lastpage","552"],["dc.bibliographiccitation.volume","163"],["dc.contributor.author","Grzmil, M."],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Voigt, S."],["dc.contributor.author","Mury, D."],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T10:37:03Z"],["dc.date.available","2018-11-07T10:37:03Z"],["dc.date.issued","2003"],["dc.description.abstract","To analyze differential gene expression of putative prostate tumor markers we compared the expression levels of more than 400 cancer-related genes using the cDNA array technique in a set of capsule-invasive prostate tumor and matched normal prostate tissue. The overexpression. of Bax inhibitor-1 (BI-1) in prostate carcinoma and prostate cancer cell lines was confirmed by using Northern blot and Western blot analyses. Quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) on intact RNAs from 17 paired laser-captured microdissected epithelial tissue samples confirmed up-regulated BI-1 expression in 11 of 17 prostate tumors. In addition, it was demonstrated that BI-1 expression is down-regulated in stromal cells as. compared to matched normal epithelial cells of the prostate. In situ hybridization experiments on prostate sections also revealed that BI-1 expression is mainly restricted to epithelial cells. Furthermore, quantitative RT-PCR on RNAs derived from five benign prostate hyperplasia (BPH) samples showed no significant difference in BI-1 expression as compared to normal epithelial prostate tissue. To determine the function of BI-1 in vitro, human PC-3, LNCaP, and DU-145 prostate carcinoma cells were transfected with small interfering double-strand RNA (siRNA) oligonucleotides against the BI-1 gene leading to a specific down-regulation of BI-1 expression. Furthermore, transfection of PC-3, LNCaP, and DU-145 cells with BI-1 sequence-specific siRNAs caused a significant increase in spontaneous apoptosis in all cell lines. Taken together, our results indicate that the human BI-1 gene contains the potential to serve as a prostate cancer expression marker and as a potential target for developing therapeutic strategies for prostate cancer."],["dc.identifier.doi","10.1016/S0002-9440(10)63682-6"],["dc.identifier.isi","000184366400016"],["dc.identifier.pmid","12875974"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45473"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Investigative Pathology, Inc"],["dc.relation.issn","0002-9440"],["dc.title","Bax inhibitor-1 is overexpressed in prostate cancer and its specific down-regulation by RNA interference leads to cell death in human prostate carcinoma cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1013"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","1023"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Deeg, S."],["dc.contributor.author","Voigt, A."],["dc.contributor.author","Voßfeldt, H."],["dc.contributor.author","Dohm, C. P."],["dc.contributor.author","Karch, A."],["dc.contributor.author","Weishaupt, Jochen"],["dc.contributor.author","Schulz, J. B."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Kermer, P."],["dc.date.accessioned","2017-09-07T11:46:13Z"],["dc.date.available","2017-09-07T11:46:13Z"],["dc.date.issued","2014"],["dc.description.abstract","Spinocerebellar ataxia type 3 (SCA3) is one of at least nine inherited neurodegenerative diseases caused by an expansion of a polyglutamine tract within corresponding disease-specific proteins. In case of SCA3, mutation of Ataxin-3 results in aggregation of misfolded protein, formation of intranuclear as well as cytosolic inclusion bodies and cell death in distinct neuronal populations. Since cyclin-dependent kinase-5 (CDK5) has been shown to exert beneficial effects on aggregate formation and cell death in various polyglutamine diseases, we tested its therapeutic potential for SCA3. Our data show increased caspase-dependent Ataxin-3 cleavage, aggregation, and neurodegeneration in the absence of sufficient CDK5 activity. This disease-propagating effect could be reversed by mutation of the caspase cleavage site in Ataxin-3. Moreover, reduction of CDK5 expression levels by RNAi in vivo enhances SCA3 toxicity as assayed in a Drosophila model for SCA3. In summary, we present CDK5 as a potent neuroprotectant, regulating cleavage and thereby toxicity of Ataxin-3 and other polyglutamine proteins. We propose that increased caspase-dependent cleavage of mutated Ataxin-3, because of missing CDK5 shielding, leads to aggregation and cell death. Moreover, reduction of CDK5 expression levels by RNAi in vivo enhances SCA3 toxicity as assayed in a Drosophila model for SCA3. We think that CDK5 functions as a shield against cleavage-induced toxification and thereby is an interesting target for therapeutic intervention in polyQ disease in general."],["dc.identifier.doi","10.1111/jnc.12684"],["dc.identifier.gro","3142111"],["dc.identifier.isi","000337760500011"],["dc.identifier.pmid","24548080"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/4666"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1471-4159"],["dc.relation.issn","0022-3042"],["dc.title","CDK5 protects from caspase-induced Ataxin-3 cleavage and neurodegeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Butler, Erin K."],["dc.contributor.author","Voigt, Aaron"],["dc.contributor.author","Schulz, Joerg B."],["dc.date.accessioned","2018-11-07T11:25:05Z"],["dc.date.available","2018-11-07T11:25:05Z"],["dc.date.issued","2009"],["dc.format.extent","180"],["dc.identifier.isi","000268550400479"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56553"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.publisher.place","Malden"],["dc.relation.conference","22nd Biennial Meeting of the International-Society-of-Neurochemistry/Asian-Pacific-Society-for-Neuroc hemistry"],["dc.relation.eventlocation","Busan, SOUTH KOREA"],["dc.relation.issn","0022-3042"],["dc.title","ALPHA SYNUCLEIN NEUROTOXICITY MODIFIED BY MITOCHONDRIAL CHAPERONE PROTEIN TRAP1"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","no"],["dc.bibliographiccitation.issue","26"],["dc.bibliographiccitation.journal","ChemInform"],["dc.bibliographiccitation.lastpage","no"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","MURUGAVEL, R."],["dc.contributor.author","VOIGT, A."],["dc.contributor.author","WALAWALKAR, M. G."],["dc.contributor.author","ROESKY, H. W."],["dc.date.accessioned","2021-12-08T12:28:19Z"],["dc.date.available","2021-12-08T12:28:19Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1002/chin.199826357"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/95647"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-476"],["dc.relation.eissn","1522-2667"],["dc.relation.issn","0931-7597"],["dc.rights.uri","http://doi.wiley.com/10.1002/tdm_license_1.1"],["dc.title","ChemInform Abstract: Silanetriols: Preparation and Their Reactions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","225"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","233"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Reich, Arno"],["dc.contributor.author","Spering, Christopher"],["dc.contributor.author","Gertz, Karen"],["dc.contributor.author","Harms, Christoph"],["dc.contributor.author","Gerhardt, Ellen"],["dc.contributor.author","Kronenberg, Golo"],["dc.contributor.author","Nave, Klaus A."],["dc.contributor.author","Schwab, Markus"],["dc.contributor.author","Tauber, Simone C."],["dc.contributor.author","Drinkut, Anja"],["dc.contributor.author","Harms, Kristian"],["dc.contributor.author","Beier, Chrstioph P."],["dc.contributor.author","Voigt, Aaron"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Endres, Matthias"],["dc.contributor.author","Schulz, Joerg B."],["dc.date.accessioned","2018-11-07T09:00:08Z"],["dc.date.available","2018-11-07T09:00:08Z"],["dc.date.issued","2011"],["dc.description.abstract","Death receptor (DR) signaling has a major impact on the outcome of numerous neurological diseases, including ischemic stroke. DRs mediate not only cell death signals, but also proinflammatory responses and cell proliferation. Identification of regulatory proteins that control the switch between apoptotic and alternative DR signaling opens new therapeutic opportunities. Fas apoptotic inhibitory molecule 2 (Faim2) is an evolutionary conserved, neuron-specific inhibitor of Fas/CD95-mediated apoptosis. To investigate its role during development and in disease models, we generated Faim2-deficient mice. The ubiquitous null mutation displayed a viable and fertile phenotype without overt deficiencies. However, lack of Faim2 caused an increase in susceptibility to combined oxygen-glucose deprivation in primary neurons in vitro as well as in caspase-associated cell death, stroke volume, and neurological impairment after cerebral ischemia in vivo. These processes were rescued by lentiviral Faim2 gene transfer. In summary, we provide evidence that Faim2 is a novel neuroprotective molecule in the context of cerebral ischemia."],["dc.identifier.doi","10.1523/JNEUROSCI.2188-10.2011"],["dc.identifier.isi","000285915100026"],["dc.identifier.pmid","21209208"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24077"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.title","Fas/CD95 Regulatory Protein Faim2 Is Neuroprotective after Transient Brain Ischemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1085"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","International Journal of Oncology"],["dc.bibliographiccitation.lastpage","1092"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Grzmil, M."],["dc.contributor.author","Voigt, S."],["dc.contributor.author","Ringert, Rolf-Hermann"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.date.accessioned","2018-11-07T10:49:16Z"],["dc.date.available","2018-11-07T10:49:16Z"],["dc.date.issued","2004"],["dc.description.abstract","Laser microdissection is a valuable tool to prepare pure cell populations from complex tissues for further analyses. Gene expression studies by real-time RT-PCR and cDNA arrays of microdissected tissues are becoming widely used methods. The integrity and quantity of prepared RNA must be proven to ensure reliable results in subsequent applications such as quantitative RT-PCR and cDNA-arrays. In the present study we used RNAlater(TM) protected prostate tissue for laser microdissection of tumor and tumor-free tissues. RNA quality and quantity was assessed using automated capillary gel electrophoresis. By using quantitative real time-RT-PCR before and after mRNA amplification the insulin-like growth factor binding protein-3 (IGFBP-3) gene expression was shown to be down-regulated in three out of five cases and DD3 was up-regulated in cancer tissues in all cases. The up-regulation of DD3 and the down-regulation of IGFBP-3 gene expression in cancer tissue were conserved after RNA amplification. A cDNA microarray also revealed an IGFBP-3 down-regulation in cancer tissue as well as several genes known to be differerentially expressed in prostate cancer. Taken together, we present a novel method for the isolation of intact RNA from laser microdissection-derived prostate cancer tissue useful for downstream applications of real-time RT-PCR and cDNA microarrays."],["dc.identifier.isi","000220779700004"],["dc.identifier.pmid","15067329"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48389"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Professor D A Spandidos"],["dc.relation.issn","1019-6439"],["dc.title","cDNA microarray analysis with amplified RNA after isolation of intact cellular RNA from neoplastic and non-neoplastic prostate tissue separated by laser microdissections"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e12247"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PloS one"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Voigt, Aaron"],["dc.contributor.author","Herholz, David"],["dc.contributor.author","Fiesel, Fabienne C."],["dc.contributor.author","Kaur, Kavita"],["dc.contributor.author","Müller, Daniel"],["dc.contributor.author","Karsten, Peter"],["dc.contributor.author","Weber, Stephanie S."],["dc.contributor.author","Kahle, Philipp J."],["dc.contributor.author","Marquardt, Till"],["dc.contributor.author","Schulz, Jörg"],["dc.date.accessioned","2019-07-09T11:53:07Z"],["dc.date.available","2019-07-09T11:53:07Z"],["dc.date.issued","2010"],["dc.description.abstract","Alteration and/or mutations of the ribonucleoprotein TDP-43 have been firmly linked to human neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). The relative impacts of TDP-43 alteration, mutation, or inherent protein function on neural integrity, however, remain less clear--a situation confounded by conflicting reports based on transient and/or random-insertion transgenic expression. We therefore performed a stringent comparative investigation of impacts of these TDP-43 modifications on neural integrity in vivo. To achieve this, we systematically screened ALS/FTLD-associated and synthetic TDP-43 isoforms via same-site gene insertion and neural expression in Drosophila; followed by transposon-based motor neuron-specific transgenesis in a chick vertebrate system. Using this bi-systemic approach we uncovered a requirement of inherent TDP-43 RNA-binding function--but not ALS/FTLD-linked mutation, mislocalization, or truncation--for TDP-43-mediated neurotoxicity in vivo."],["dc.identifier.doi","10.1371/journal.pone.0012247"],["dc.identifier.fs","573853"],["dc.identifier.pmid","20806063"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6913"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60347"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.subject.ddc","610"],["dc.subject.mesh","Amyotrophic Lateral Sclerosis"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Cell Line"],["dc.subject.mesh","Chickens"],["dc.subject.mesh","DNA-Binding Proteins"],["dc.subject.mesh","Drosophila melanogaster"],["dc.subject.mesh","Frontotemporal Lobar Degeneration"],["dc.subject.mesh","Gene Expression Regulation"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Intracellular Space"],["dc.subject.mesh","Locomotion"],["dc.subject.mesh","Longevity"],["dc.subject.mesh","Male"],["dc.subject.mesh","Motor Neurons"],["dc.subject.mesh","Mutation"],["dc.subject.mesh","Neurons"],["dc.subject.mesh","Organ Specificity"],["dc.subject.mesh","Protein Binding"],["dc.subject.mesh","Protein Transport"],["dc.subject.mesh","RNA"],["dc.title","TDP-43-mediated neuron loss in vivo requires RNA-binding activity."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","UNSP 1437-2096,E;2002,0,08,1362,1364,ftx,en;G15402ST.pdf"],["dc.bibliographiccitation.firstpage","1362"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Synlett"],["dc.bibliographiccitation.lastpage","1364"],["dc.contributor.author","Voigt, T."],["dc.contributor.author","Winsel, H."],["dc.contributor.author","de Meijere, Armin"],["dc.date.accessioned","2018-11-07T10:18:14Z"],["dc.date.available","2018-11-07T10:18:14Z"],["dc.date.issued","2002"],["dc.description.abstract","Aminocyclopropanation of 1-ethenylcycloalkenes 2a-d with N,N-dibenzyl- and N,N-dimethylformamide, respectively, by treatment with cyclohexylmagnesium bromide in the presence of methyltitanium triisopropoxide yielded the exo-(n+3)-N,N-dimethylamino-1-ethenylbicyclo[n.1.0]alkanes 3a-d (58-72%). Compounds 7b-d could be transformed by thermal vinylcyclopropane to cyclopentene rearrangement to the corresponding exo-4-dimethyl-aminobicyclo[n.3.0]alk-1-enes 7b-d (84-90%). Elimination of the dimethylamino group led to the cyclopentadienes 11b-d and 12b-d (72-82%). The 5-dimethylamino-1-ethenylbicyclo[2.1.0]pentane did not undergo the typical vinylcyclopropane rearrangement, but ring-opening at the bridgehead-bridgehead bond to form 1-ethenyl-2-dimethylaminocyclopentene 8."],["dc.identifier.isi","000177216500042"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41397"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0936-5214"],["dc.title","Easy access to (n+3)-dimethylamino-1-ethenylbicyclo[n.1.0]alkanes and their facile conversion to ring-annelated cyclopentadienes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","801"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","807"],["dc.bibliographiccitation.volume","111"],["dc.contributor.author","Sroka, Kamila"],["dc.contributor.author","Voigt, Aaron"],["dc.contributor.author","Deeg, Sebastian"],["dc.contributor.author","Reed, John C."],["dc.contributor.author","Schulz, Jörg B."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Kermer, Pawel"],["dc.date.accessioned","2017-09-07T11:46:46Z"],["dc.date.available","2017-09-07T11:46:46Z"],["dc.date.issued","2009"],["dc.description.abstract","Bcl-2-associated athanogene-1 (BAG1) is a multifunctional protein delivering chaperone-recognized unfolded substrates to the proteasome for degradation. It has been shown to be essential for proper CNS development in vivo, playing a crucial role in neuronal survival and differentiation. With regard to Huntington's disease, a sequestration of BAG1 into inclusion bodies and a neuroprotective effect in double transgenic mice have been reported. Here, we show that BAG1 reduces aggregation and accelerates degradation of mutant huntingtin (htt-mut). Moreover, it reduces nuclear levels of htt-mut. This effect can be overcome by over-expression of seven in absentia homolog 1, an E3 ligase negatively regulated by BAG1 and known to be involved in nuclear import of htt-mut. In vivo, BAG1 proved to be protective in a Drosophila melanogaster Huntington's disease model, preventing photoreceptor cell loss induced by htt-mut. In summary, we present BAG1 as a therapeutic tool modulating key steps in htt toxicity in vitro and ameliorating htt toxicity in vivo."],["dc.identifier.doi","10.1111/j.1471-4159.2009.06363.x"],["dc.identifier.gro","3143030"],["dc.identifier.isi","000270728600016"],["dc.identifier.pmid","19712056"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/499"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: CMPB; High Q foundation; European Commission [MEST-CT-2004-504193]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1471-4159"],["dc.relation.issn","0022-3042"],["dc.title","BAG1 modulates huntingtin toxicity, aggregation, degradation, and subcellular distribution"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1003980"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLoS Genetics"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Ghosh, Aniket"],["dc.contributor.author","Kling, Tina"],["dc.contributor.author","Snaidero, Nicolas"],["dc.contributor.author","Sampaio, Julio L."],["dc.contributor.author","Shevchenko, Andrej"],["dc.contributor.author","Gras, Heribert"],["dc.contributor.author","Geurten, Bart R. H."],["dc.contributor.author","Göpfert, Martin C."],["dc.contributor.author","Schulz, Joerg B."],["dc.contributor.author","Voigt, Aaron"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2018-11-07T09:16:43Z"],["dc.date.available","2018-11-07T09:16:43Z"],["dc.date.issued","2013"],["dc.description.abstract","Glia are of vital importance for all complex nervous system. One of the many functions of glia is to insulate and provide trophic and metabolic support to axons. Here, using glial-specific RNAi knockdown in Drosophila, we silenced 6930 conserved genes in adult flies to identify essential genes and pathways. Among our screening hits, metabolic processes were highly represented, and genes involved in carbohydrate and lipid metabolic pathways appeared to be essential in glia. One critical pathway identified was de novo ceramide synthesis. Glial knockdown of lace, a subunit of the serine palmitoyltransferase associated with hereditary sensory and autonomic neuropathies in humans, resulted in ensheathment defects of peripheral nerves in Drosophila. A genetic dissection study combined with shotgun high-resolution mass spectrometry of lipids showed that levels of ceramide phosphoethanolamine are crucial for axonal ensheathment by glia. A detailed morphological and functional analysis demonstrated that the depletion of ceramide phosphoethanolamine resulted in axonal defasciculation, slowed spike propagation, and failure of wrapping glia to enwrap peripheral axons. Supplementing sphingosine into the diet rescued the neuropathy in flies. Thus, our RNAi study in Drosophila identifies a key role of ceramide phosphoethanolamine in wrapping of axons by glia."],["dc.identifier.doi","10.1371/journal.pgen.1003980"],["dc.identifier.isi","000330533300023"],["dc.identifier.pmid","24348263"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9570"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27999"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1553-7404"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","A Global In Vivo Drosophila RNAi Screen Identifies a Key Role of Ceramide Phosphoethanolamine for Glial Ensheathment of Axons"],["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"]]