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@ARTICLE{Tedeschi:138857,
      author       = {Tedeschi, Andrea and Dupraz, Sebastian and Laskowski,
                      Claudia J and Xue, Jia and Ulas, Thomas and Beyer, Marc and
                      Schultze, Joachim L and Bradke, Frank},
      title        = {{T}he {C}alcium {C}hannel {S}ubunit {A}lpha2delta2
                      {S}uppresses {A}xon {R}egeneration in the {A}dult {CNS}.},
      journal      = {Neuron},
      volume       = {92},
      number       = {2},
      issn         = {0896-6273},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DZNE-2020-05179},
      pages        = {419-434},
      year         = {2016},
      abstract     = {Injuries to the adult CNS often result in permanent
                      disabilities because neurons lose the ability to regenerate
                      their axon during development. Here, whole transcriptome
                      sequencing and bioinformatics analysis followed by gain- and
                      loss-of-function experiments identified Cacna2d2, the gene
                      encoding the Alpha2delta2 subunit of voltage-gated calcium
                      channels (VGCCs), as a developmental switch that limits axon
                      growth and regeneration. Cacna2d2 gene deletion or silencing
                      promoted axon growth in vitro. In vivo, Alpha2delta2
                      pharmacological blockade through Pregabalin (PGB)
                      administration enhanced axon regeneration in adult mice
                      after spinal cord injury (SCI). As PGB is already an
                      established treatment for a wide range of neurological
                      disorders, our findings suggest that targeting Alpha2delta2
                      may be a novel treatment strategy to promote structural
                      plasticity and regeneration following CNS trauma.},
      keywords     = {Animals / Axons: drug effects / Axons: physiology / Calcium
                      Channel Blockers: pharmacology / Calcium Channels: drug
                      effects / Calcium Channels: genetics / Calcium Channels:
                      metabolism / Central Nervous System / Female / Ganglia,
                      Spinal: cytology / Ganglia, Spinal: metabolism / Gene
                      Expression Profiling / Mice / Mice, Inbred C57BL / Mice,
                      Knockout / Neuronal Outgrowth: drug effects / Neuronal
                      Outgrowth: genetics / Neurons: metabolism / Pregabalin:
                      pharmacology / RNA, Messenger: metabolism / Regeneration:
                      drug effects / Regeneration: genetics / Sequence Analysis,
                      RNA / Spinal Cord Injuries: metabolism / Cacna2d2 protein,
                      mouse (NLM Chemicals) / Calcium Channel Blockers (NLM
                      Chemicals) / Calcium Channels (NLM Chemicals) / RNA,
                      Messenger (NLM Chemicals) / Pregabalin (NLM Chemicals)},
      cin          = {AG Bradke / Schultze - PRECISE},
      ddc          = {610},
      cid          = {I:(DE-2719)1013002 / I:(DE-2719)1013031},
      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},
      experiment   = {EXP:(DE-2719)PRECISE-20190321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27720483},
      doi          = {10.1016/j.neuron.2016.09.026},
      url          = {https://pub.dzne.de/record/138857},
}