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@ARTICLE{Tedeschi:141516,
      author       = {Tedeschi, Andrea and Dupraz, Sebastian and Curcio, Michele
                      and Laskowski, Claudia J and Schaffran, Barbara and Flynn,
                      Kevin C and Da Silva Santos, Telma and Stern, Sina and
                      Hilton, Brett J and Larson, Molly J E and Gurniak, Christine
                      B and Witke, Walter and Bradke, Frank},
      title        = {{ADF}/{C}ofilin-{M}ediated {A}ctin {T}urnover {P}romotes
                      {A}xon {R}egeneration in the {A}dult {CNS}.},
      journal      = {Neuron},
      volume       = {103},
      number       = {6},
      issn         = {0896-6273},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DZNE-2020-07840},
      pages        = {1073-1085.e6},
      year         = {2019},
      abstract     = {Injured axons fail to regenerate in the adult CNS, which
                      contrasts with their vigorous growth during embryonic
                      development. We explored the potential of re-initiating axon
                      extension after injury by reactivating the molecular
                      mechanisms that drive morphogenetic transformation of
                      neurons during development. Genetic loss- and
                      gain-of-function experiments followed by time-lapse
                      microscopy, in vivo imaging, and whole-mount analysis show
                      that axon regeneration is fueled by elevated actin turnover.
                      Actin depolymerizing factor (ADF)/cofilin controls actin
                      turnover to sustain axon regeneration after spinal cord
                      injury through its actin-severing activity. This pinpoints
                      ADF/cofilin as a key regulator of axon growth competence,
                      irrespective of developmental stage. These findings reveal
                      the central role of actin dynamics regulation in this
                      process and elucidate a core mechanism underlying axon
                      growth after CNS trauma. Thereby, neurons maintain the
                      capacity to stimulate developmental programs during adult
                      life, expanding their potential for plasticity. Thus, actin
                      turnover is a key process for future regenerative
                      interventions.},
      keywords     = {Actins: metabolism / Animals / Axons: metabolism / Axons:
                      pathology / Cofilin 1: genetics / Cofilin 1: metabolism /
                      Cofilin 2: genetics / Cofilin 2: metabolism / Destrin:
                      genetics / Destrin: metabolism / Growth Cones: metabolism /
                      Growth Cones: pathology / Intravital Microscopy / Mice /
                      Microscopy, Confocal / Nerve Regeneration: genetics /
                      Neurons: metabolism / Neurons: pathology / Rats / Spinal
                      Cord Injuries: genetics / Spinal Cord Injuries: metabolism /
                      Spinal Cord Injuries: pathology / Time-Lapse Imaging},
      cin          = {AG Bradke / AG Tavosanis},
      ddc          = {610},
      cid          = {I:(DE-2719)1013002 / I:(DE-2719)1013018},
      pnm          = {341 - Molecular Signaling (POF3-341) / 342 - Disease
                      Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-341 / G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31400829},
      pmc          = {pmc:PMC6763392},
      doi          = {10.1016/j.neuron.2019.07.007},
      url          = {https://pub.dzne.de/record/141516},
}