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@ARTICLE{Stern:162729,
      author       = {Stern, Sina and Hilton, Brett Jason and Burnside, Emily and
                      Dupraz, Sebastian and Handley, Emily and Gonyer, Jessica and
                      Brakebusch, Cord and Bradke, Frank},
      title        = {{R}ho{A} drives actin compaction to restrict axon
                      regeneration and astrocyte reactivity after {CNS} injury.},
      journal      = {Neuron},
      volume       = {109},
      number       = {21},
      issn         = {0896-6273},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DZNE-2021-01386},
      pages        = {3436 - 3455.e9},
      year         = {2021},
      abstract     = {An inhibitory extracellular milieu and neuron-intrinsic
                      processes prevent axons from regenerating in the adult
                      central nervous system (CNS). Here we show how the two
                      aspects are interwoven. Genetic loss-of-function experiments
                      determine that the small GTPase RhoA relays extracellular
                      inhibitory signals to the cytoskeleton by adapting
                      mechanisms set in place during neuronal polarization. In
                      response to extracellular inhibitors, neuronal RhoA
                      restricts axon regeneration by activating myosin II to
                      compact actin and, thereby, restrain microtubule protrusion.
                      However, astrocytic RhoA restricts injury-induced
                      astrogliosis through myosin II independent of microtubules
                      by activating Yes-activated protein (YAP) signaling.
                      Cell-type-specific deletion in spinal-cord-injured mice
                      shows that neuronal RhoA activation prevents axon
                      regeneration, whereas astrocytic RhoA is beneficial for
                      regenerating axons. These data demonstrate how extracellular
                      inhibitors regulate axon regeneration, shed light on the
                      capacity of reactive astrocytes to be growth inhibitory
                      after CNS injury, and reveal cell-specific RhoA targeting as
                      a promising therapeutic avenue.},
      keywords     = {Actins: metabolism / Animals / Astrocytes: metabolism /
                      Axons: metabolism / Central Nervous System: metabolism /
                      Central Nervous System: pathology / Central Nervous System
                      Diseases: metabolism / Central Nervous System Diseases:
                      pathology / Mice / Nerve Regeneration: physiology / rhoA
                      GTP-Binding Protein: metabolism / F-actin density (Other) /
                      RhoA (Other) / YAP signaling (Other) / astrocyte reactivity
                      (Other) / axon regeneration (Other) / microtubule protrusion
                      (Other) / myosin II (Other)},
      cin          = {AG Bradke},
      ddc          = {610},
      cid          = {I:(DE-2719)1013002},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34508667},
      doi          = {10.1016/j.neuron.2021.08.014},
      url          = {https://pub.dzne.de/record/162729},
}