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@ARTICLE{Voigt:136092,
      author       = {Voigt, Aaron and Herholz, David and Fiesel, Fabienne C and
                      Kaur, Kavita and Müller, Daniel and Karsten, Peter and
                      Weber, Stephanie S and Kahle, Phillip and Marquardt, Till
                      and Schulz, Jörg B},
      title        = {{TDP}-43-mediated neuron loss in vivo requires
                      {RNA}-binding activity.},
      journal      = {PLOS ONE},
      volume       = {5},
      number       = {8},
      issn         = {1932-6203},
      address      = {San Francisco, California, US},
      publisher    = {PLOS},
      reportid     = {DZNE-2020-02414},
      pages        = {e12247},
      year         = {2010},
      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.},
      keywords     = {Amyotrophic Lateral Sclerosis: genetics / Animals / Cell
                      Line / Chickens: genetics / Chickens: metabolism / Chickens:
                      physiology / DNA-Binding Proteins: genetics / DNA-Binding
                      Proteins: metabolism / Drosophila melanogaster: cytology /
                      Drosophila melanogaster: genetics / Drosophila melanogaster:
                      metabolism / Drosophila melanogaster: physiology /
                      Frontotemporal Lobar Degeneration: genetics / Gene
                      Expression Regulation / Humans / Intracellular Space:
                      metabolism / Locomotion / Longevity / Male / Motor Neurons:
                      metabolism / Mutation / Neurons: cytology / Neurons:
                      metabolism / Organ Specificity / Protein Binding / Protein
                      Transport / RNA: metabolism / DNA-Binding Proteins (NLM
                      Chemicals) / RNA (NLM Chemicals)},
      cin          = {AG Krauß / AG Kahle 2 / Tübingen Pre 2020},
      ddc          = {610},
      cid          = {I:(DE-2719)1011006 / I:(DE-2719)1210000-4 /
                      I:(DE-2719)6000018},
      pnm          = {345 - Population Studies and Genetics (POF3-345) / 342 -
                      Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-345 / G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:20806063},
      pmc          = {pmc:PMC2923622},
      doi          = {10.1371/journal.pone.0012247},
      url          = {https://pub.dzne.de/record/136092},
}