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@ARTICLE{Klein:137272,
      author       = {Klein, Pontus and Müller-Rischart, Anne Kathrin and
                      Motori, Elisa and Schönbauer, Cornelia and Schnorrer, Frank
                      and Winklhofer, Konstanze F and Klein, Rüdiger},
      title        = {{R}et rescues mitochondrial morphology and muscle
                      degeneration of {D}rosophila {P}ink1 mutants.},
      journal      = {The EMBO journal},
      volume       = {33},
      number       = {4},
      issn         = {0261-4189},
      address      = {Hoboken, NJ [u.a.]},
      publisher    = {Wiley},
      reportid     = {DZNE-2020-03594},
      pages        = {341-355},
      year         = {2014},
      abstract     = {Parkinson's disease (PD)-associated Pink1 and Parkin
                      proteins are believed to function in a common pathway
                      controlling mitochondrial clearance and trafficking. Glial
                      cell line-derived neurotrophic factor (GDNF) and its
                      signaling receptor Ret are neuroprotective in toxin-based
                      animal models of PD. However, the mechanism by which
                      GDNF/Ret protects cells from degenerating remains unclear.
                      We investigated whether the Drosophila homolog of Ret can
                      rescue Pink1 and park mutant phenotypes. We report that a
                      signaling active version of Ret (Ret(MEN₂B) rescues muscle
                      degeneration, disintegration of mitochondria and ATP content
                      of Pink1 mutants. Interestingly, corresponding phenotypes of
                      park mutants were not rescued, suggesting that the
                      phenotypes of Pink1 and park mutants have partially
                      different origins. In human neuroblastoma cells, GDNF
                      treatment rescues morphological defects of PINK1 knockdown,
                      without inducing mitophagy or Parkin recruitment. GDNF also
                      rescues bioenergetic deficits of PINK knockdown cells.
                      Furthermore, overexpression of Ret(MEN₂B) significantly
                      improves electron transport chain complex I function in
                      Pink1 mutant Drosophila. These results provide a novel
                      mechanism underlying Ret-mediated cell protection in a
                      situation relevant for human PD.},
      keywords     = {Adenosine Triphosphate: metabolism / Animals / Apoptosis /
                      Autophagy / Cell Line, Tumor / Disease Models, Animal /
                      Dopamine: metabolism / Drosophila Proteins: deficiency /
                      Drosophila Proteins: genetics / Drosophila Proteins:
                      physiology / Drosophila melanogaster: genetics / Drosophila
                      melanogaster: growth $\&$ development / Electron Transport
                      Complex I: physiology / Genes, Lethal / Glial Cell
                      Line-Derived Neurotrophic Factor: pharmacology / Humans /
                      Mitochondria, Muscle: ultrastructure / Muscular Atrophy:
                      prevention $\&$ control / Neuroblastoma: pathology /
                      Neurons: ultrastructure / Oxygen Consumption / Parkinson
                      Disease / Phenotype / Protein Kinases: deficiency / Protein
                      Kinases: genetics / Protein-Serine-Threonine Kinases:
                      deficiency / Protein-Serine-Threonine Kinases: genetics /
                      Protein-Serine-Threonine Kinases: physiology /
                      Proto-Oncogene Proteins c-ret: genetics / Proto-Oncogene
                      Proteins c-ret: physiology / Pupa / Signal Transduction:
                      physiology / Ubiquitin-Protein Ligases: deficiency /
                      Ubiquitin-Protein Ligases: genetics / Drosophila Proteins
                      (NLM Chemicals) / Glial Cell Line-Derived Neurotrophic
                      Factor (NLM Chemicals) / Adenosine Triphosphate (NLM
                      Chemicals) / Ubiquitin-Protein Ligases (NLM Chemicals) /
                      Protein Kinases (NLM Chemicals) / Proto-Oncogene Proteins
                      c-ret (NLM Chemicals) / Ret protein, Drosophila (NLM
                      Chemicals) / PINK1 protein, Drosophila (NLM Chemicals) /
                      PTEN-induced putative kinase (NLM Chemicals) /
                      Protein-Serine-Threonine Kinases (NLM Chemicals) / park
                      protein, Drosophila (NLM Chemicals) / Electron Transport
                      Complex I (NLM Chemicals) / Dopamine (NLM Chemicals)},
      cin          = {AG Winklhofer},
      ddc          = {570},
      cid          = {I:(DE-2719)5000047},
      pnm          = {341 - Molecular Signaling (POF3-341)},
      pid          = {G:(DE-HGF)POF3-341},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:24473149},
      pmc          = {pmc:PMC3983680},
      doi          = {10.1002/embj.201284290},
      url          = {https://pub.dzne.de/record/137272},
}