Marquardt, Till

[["dc.bibliographiccitation.firstpage","974"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Current opinion in neurobiology"],["dc.bibliographiccitation.lastpage","982"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Wang, Liang"],["dc.contributor.author","Marquardt, Till"],["dc.date.accessioned","2019-07-09T11:40:47Z"],["dc.date.available","2019-07-09T11:40:47Z"],["dc.date.issued","2013-12-01"],["dc.description.abstract","A remarkable feature of nervous system development is the ability of axons emerging from newly formed neurons to traverse, by cellular scale, colossal distances to appropriate targets. The earliest axons achieve this in an essentially axon-free environment, but the vast majority of axons eventually grow along a scaffold of nerve tracts created by earlier extending axons. Signal exchange between sequentially or simultaneously extending axons may well represent the predominant mode of axonal navigation, but proportionally few efforts have so far been directed at deciphering the underlying mechanisms. This review intends to provide a conceptual update on the cellular and molecular principles driving axon-axon interactions, with emphasis on those contributing to the fidelity of axonal navigation, sorting and connectivity during nerve and circuit assembly."],["dc.identifier.doi","10.1016/j.conb.2013.08.004"],["dc.identifier.pmid","23973157"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11325"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58250"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1873-6882"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Axons"],["dc.subject.mesh","Cell Communication"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Neurogenesis"],["dc.subject.mesh","Signal Transduction"],["dc.title","What axons tell each other: axon-axon signaling in nerve and circuit assembly."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["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"]]