Fichtner, Lars

[["dc.bibliographiccitation.firstpage","2978"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.lastpage","2984"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Meyer, G. P."],["dc.contributor.author","Wollert, K. C."],["dc.contributor.author","Lotz, J."],["dc.contributor.author","Pirr, J."],["dc.contributor.author","Rager, U."],["dc.contributor.author","Lippolt, P."],["dc.contributor.author","Hahn, A."],["dc.contributor.author","Fichtner, S."],["dc.contributor.author","Schaefer, A."],["dc.contributor.author","Arseniev, L."],["dc.contributor.author","Drexler, H."],["dc.date.accessioned","2022-06-08T07:59:08Z"],["dc.date.available","2022-06-08T07:59:08Z"],["dc.date.issued","2009"],["dc.identifier.doi","10.1093/eurheartj/ehp374"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/110643"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-575"],["dc.relation.eissn","1522-9645"],["dc.relation.issn","0195-668X"],["dc.title","Intracoronary bone marrow cell transfer after myocardial infarction: 5-year follow-up from the randomized-controlled BOOST trial"],["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","3256"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","EMBO Journal"],["dc.bibliographiccitation.lastpage","3268"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Karpinar, Damla Pinar"],["dc.contributor.author","Balija, Madhu Babu Gajula"],["dc.contributor.author","Kügler, Sebastian"],["dc.contributor.author","Opazo, Felipe"],["dc.contributor.author","Rezaei-Ghaleh, Nasrollah"],["dc.contributor.author","Wender, Nora"],["dc.contributor.author","Kim, Hai-Young"],["dc.contributor.author","Taschenberger, Grit"],["dc.contributor.author","Falkenburger, Bjoern H."],["dc.contributor.author","Heise, Henrike"],["dc.contributor.author","Kumar, Ashutosh"],["dc.contributor.author","Riedel, Dietmar"],["dc.contributor.author","Fichtner, Lars"],["dc.contributor.author","Voigt, Aaron"],["dc.contributor.author","Braus, Gerhard H."],["dc.contributor.author","Giller, Karin"],["dc.contributor.author","Becker, Stefan"],["dc.contributor.author","Herzig, Alf"],["dc.contributor.author","Baldus, Marc"],["dc.contributor.author","Jaeckle, Herbert"],["dc.contributor.author","Eimer, Stefan"],["dc.contributor.author","Schulz, Joerg B."],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Zweckstetter, Markus"],["dc.date.accessioned","2017-09-07T11:46:48Z"],["dc.date.available","2017-09-07T11:46:48Z"],["dc.date.issued","2009"],["dc.description.abstract","The relation of alpha-synuclein (alpha S) aggregation to Parkinson's disease (PD) has long been recognized, but the mechanism of toxicity, the pathogenic species and its molecular properties are yet to be identified. To obtain insight into the function different aggregated alpha S species have in neurotoxicity in vivo, we generated alpha S variants by a structure-based rational design. Biophysical analysis revealed that the alpha S mutants have a reduced fibrillization propensity, but form increased amounts of soluble oligomers. To assess their biological response in vivo, we studied the effects of the biophysically defined pre-fibrillar alpha S mutants after expression in tissue culture cells, in mammalian neurons and in PD model organisms, such as Caenorhabditis elegans and Drosophila melanogaster. The results show a striking correlation between alpha S aggregates with impaired beta-structure, neuronal toxicity and behavioural defects, and they establish a tight link between the biophysical properties of multimeric aS species and their in vivo function. The EMBO Journal (2009) 28, 3256-3268. doi:10.1038/emboj.2009.257; Published online 10 September 2009"],["dc.identifier.doi","10.1038/emboj.2009.257"],["dc.identifier.gro","3143038"],["dc.identifier.isi","000271008200017"],["dc.identifier.pmid","19745811"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/508"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0261-4189"],["dc.title","Pre‐fibrillar α‐synuclein variants with impaired β‐structure increase neurotoxicity in Parkinson's disease models"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","68"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Biology of the Cell"],["dc.bibliographiccitation.lastpage","77"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Padmanabhan, Nirmala"],["dc.contributor.author","Fichtner, Lars"],["dc.contributor.author","Dickmanns, Achim"],["dc.contributor.author","Ficner, Ralf"],["dc.contributor.author","Schulz, Joerg B."],["dc.contributor.author","Braus, Gerhard H."],["dc.date.accessioned","2017-09-07T11:47:35Z"],["dc.date.available","2017-09-07T11:47:35Z"],["dc.date.issued","2009"],["dc.description.abstract","Ynm3 is the only budding yeast protein possessing a combination of serine protease and postsynaptic density 95/disclarge/zona occludens domains, a defining feature of the high temperature requirement A (HtrA) protein family. The bacterial HtrA/DegP is involved in protective stress response to aid survival at higher temperatures. The role of mammalian mitochondrial HtrA2/Omi in protein quality control is unclear, although loss of its protease activity results in susceptibility toward Parkinson's disease, in which mitochondrial dysfunction and impairment of protein folding and degradation are key pathogenetic features. We studied the role of the budding yeast HtrA, Ynm3, with respect to unfolding stresses. Similar to Escherichia coli DegP, we find that Ynm3 is a dual chaperone-protease. Its proteolytic activity is crucial for cell survival at higher temperature. Ynm3 also exhibits strong general chaperone activity, a novel finding for a eukaryotic HtrA member. We propose that the chaperone activity of Ynm3 may be important to improve the efficiency of proteolysis of aberrant proteins by averting the formation of nonproductive toxic aggregates and presenting them in a soluble state to its protease domain. Suppression studies with Delta ynm3 led to the discovery of chaperone activity in a nucleolar peptidyl-prolyl cis-trans isomerase, Fpr3, which could partly relieve the heat sensitivity of Delta ynm3."],["dc.identifier.doi","10.1091/mbc.E08-02-0178"],["dc.identifier.gro","3143174"],["dc.identifier.isi","000262134800007"],["dc.identifier.pmid","18946088"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5930"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/659"],["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.publisher","Amer Soc Cell Biology"],["dc.relation.issn","1059-1524"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","The Yeast HtrA Orthologue Ynm3 Is a Protease with Chaperone Activity that Aids Survival Under Heat Stress"],["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","1276"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Molecular Microbiology"],["dc.bibliographiccitation.lastpage","1289"],["dc.bibliographiccitation.volume","66"],["dc.contributor.author","Fichtner, Lars"],["dc.contributor.author","Schulze, Florian"],["dc.contributor.author","Braus, Gerhard H."],["dc.date.accessioned","2018-11-07T10:49:39Z"],["dc.date.available","2018-11-07T10:49:39Z"],["dc.date.issued","2007"],["dc.description.abstract","Cell-cell and cell-surface adherence represents initial steps in forming multicellular aggregates or in establishing cell-surface interactions. The commonly used Saccharomyces cerevisiae laboratory strain S288c carries a flo8 mutation, and is only able to express the flocculin-encoding genes FLO1 and FLO11, when FLO8 is restored. We show here that the two flocculin genes exhibit differences in regulation to execute distinct functions under various environmental conditions. In contrast to the laboratory strain Sigma 1278b, haploids of the S288c genetic background require FLO1 for cell-cell and cell-substrate adhesion, whereas FLO11 is required for pseudohyphae formation of diploids. In contrast to FLO11, FLO1 repression requires the Sin4p mediator tail component, but is independent of the repressor Sfl1p. FLO1 regulation also differs from FLO11, because it requires neither the KSS1 MAP kinase cascade nor the pathways which lead to the transcription factors Gcn4p or Msn1p. The protein kinase A pathway and the transcription factors Flo8p and Mss11p are the major regulators for FLO1 expression. Therefore, S. cerevisiae is prepared to simultaneously express two genes of its otherwise silenced FLO reservoir resulting in an appropriate cellular surface for different environments."],["dc.identifier.doi","10.1111/j.1365-2958.2007.06014.x"],["dc.identifier.isi","000250917200018"],["dc.identifier.pmid","18001350"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48479"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1365-2958"],["dc.relation.issn","0950-382X"],["dc.title","Differential Flo8p-dependent regulation of FLO1 and FLO11 for cell-cell and cell-substrate adherence of S-cerevisiae S288c"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]