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@ARTICLE{Meka:137919,
      author       = {Meka, Durga Praveen and Müller-Rischart, Anne Kathrin and
                      Nidadavolu, Prakash and Mohammadi, Behnam and Motori, Elisa
                      and Ponna, Srinivas Kumar and Aboutalebi, Helia and Bassal,
                      Mahmoud and Annamneedi, Anil and Finckh, Barbara and
                      Miesbauer, Margit and Rotermund, Natalie and Lohr, Christian
                      and Tatzelt, Jörg and Winklhofer, Konstanze F and Kramer,
                      Edgar R},
      title        = {{P}arkin cooperates with {GDNF}/{RET} signaling to prevent
                      dopaminergic neuron degeneration.},
      journal      = {The journal of clinical investigation},
      volume       = {125},
      number       = {5},
      issn         = {0021-9738},
      address      = {Ann Arbor, Mich.},
      publisher    = {ASCJ},
      reportid     = {DZNE-2020-04241},
      pages        = {1873-1885},
      year         = {2015},
      abstract     = {Parkin and the glial cell line-derived neurotrophic factor
                      (GDNF) receptor RET have both been independently linked to
                      the dopaminergic neuron degeneration that underlies
                      Parkinson's disease (PD). In the present study, we
                      demonstrate that there is genetic crosstalk between parkin
                      and the receptor tyrosine kinase RET in two different mouse
                      models of PD. Mice lacking both parkin and RET exhibited
                      accelerated dopaminergic cell and axonal loss compared with
                      parkin-deficient animals, which showed none, and
                      RET-deficient mice, in which we found moderate degeneration.
                      Transgenic expression of parkin protected the dopaminergic
                      systems of aged RET-deficient mice. Downregulation of either
                      parkin or RET in neuronal cells impaired mitochondrial
                      function and morphology. Parkin expression restored
                      mitochondrial function in GDNF/RET-deficient cells, while
                      GDNF stimulation rescued mitochondrial defects in
                      parkin-deficient cells. In both cases, improved
                      mitochondrial function was the result of activation of the
                      prosurvival NF-κB pathway, which was mediated by RET
                      through the phosphoinositide-3-kinase (PI3K) pathway. Taken
                      together, these observations indicate that parkin and the
                      RET signaling cascade converge to control mitochondrial
                      integrity and thereby properly maintain substantia nigra
                      pars compacta dopaminergic neurons and their innervation in
                      the striatum. The demonstration of crosstalk between parkin
                      and RET highlights the interplay in the protein network that
                      is altered in PD and suggests potential therapeutic targets
                      and strategies to treat PD.},
      keywords     = {Adenosine Triphosphate: biosynthesis / Animals / Anxiety:
                      genetics / Cell Line / Cell Size / Disease Progression /
                      Dopaminergic Neurons: pathology / Exploratory Behavior /
                      Glial Cell Line-Derived Neurotrophic Factor: deficiency /
                      Glial Cell Line-Derived Neurotrophic Factor: genetics /
                      Glial Cell Line-Derived Neurotrophic Factor: physiology /
                      Mice / Mice, Knockout / Mice, Transgenic / Mitochondria:
                      pathology / NF-kappa B: physiology / Nerve Degeneration:
                      pathology / Parkinsonian Disorders: genetics / Parkinsonian
                      Disorders: pathology / Phosphatidylinositol 3-Kinases:
                      physiology / Proto-Oncogene Proteins c-ret: deficiency /
                      Proto-Oncogene Proteins c-ret: genetics / Proto-Oncogene
                      Proteins c-ret: physiology / Recombinant Fusion Proteins:
                      metabolism / Rotarod Performance Test / Signal Transduction
                      / Substantia Nigra: pathology / Ubiquitin-Protein Ligases:
                      deficiency / Ubiquitin-Protein Ligases: genetics /
                      Ubiquitin-Protein Ligases: physiology / Gdnf protein, mouse
                      (NLM Chemicals) / Glial Cell Line-Derived Neurotrophic
                      Factor (NLM Chemicals) / NF-kappa B (NLM Chemicals) /
                      Recombinant Fusion Proteins (NLM Chemicals) / Adenosine
                      Triphosphate (NLM Chemicals) / Ubiquitin-Protein Ligases
                      (NLM Chemicals) / parkin protein (NLM Chemicals) /
                      Phosphatidylinositol 3-Kinases (NLM Chemicals) /
                      Proto-Oncogene Proteins c-ret (NLM Chemicals) / Ret protein,
                      mouse (NLM Chemicals)},
      cin          = {AG Winklhofer},
      ddc          = {610},
      cid          = {I:(DE-2719)5000047},
      pnm          = {341 - Molecular Signaling (POF3-341)},
      pid          = {G:(DE-HGF)POF3-341},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25822020},
      pmc          = {pmc:PMC4611569},
      doi          = {10.1172/JCI79300},
      url          = {https://pub.dzne.de/record/137919},
}