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@INPROCEEDINGS{MllerRischart:145610,
      author       = {Müller-Rischart, Anne Kathrin and Tatzelt, Jörg and
                      Winklhofer, Konstanze F},
      title        = {{P}arkin: {A} stress-protective {E}3 ubiquitin ligase
                      maintaining mitochondrial integrity},
      journal      = {Biochimica et biophysica acta / Bioenergetics},
      volume       = {1817},
      number       = {Sup},
      issn         = {0005-2728},
      reportid     = {DZNE-2020-00940},
      pages        = {S77 - S78},
      year         = {2012},
      abstract     = {Mitochondrial dysfunction has long been implicated in the
                      etiopathogenesis of Parkinson's disease (PD), based on the
                      observation that mitochondrial toxins can cause parkinsonism
                      in humans and animal models. Research into the function and
                      dysfunction of PD-associated genes revealed that at least
                      some of these genes interface with pathways regulating
                      various aspects of mitochondrial biology. Mutations in the
                      parkin gene, encoding an E3 ubiquitin ligase, are
                      responsible for the majority of autosomal recessive
                      parkinsonism. Our previous work revealed that parkin is a
                      stress-inducible protein with a wide neuroprotective
                      capacity, preventing cell death under various stress
                      conditions. We now present evidence that the acute
                      stress-protective activity of parkin and its capacity to
                      induce mitophagy are mediated by two separate and
                      independent pathways. While a functional autophagic
                      machinery and expression of the mitochondrial kinase PINK1
                      is required for parkin-induced mitophagy, these components
                      are dispensable for the anti-apoptotic activity of parkin.
                      We identified a signaling pathway that is essential for the
                      anti-apoptotic activity of parkin but not for induction of
                      mitophagy. In support of this concept, parkin seems to exert
                      adaptive effects on mitochondria depending on the severity
                      of mitochondrial damage. Parkin prevents stress-induced cell
                      death under moderate stress conditions with only minor
                      mitochondrial defects. However, when mitochondria are
                      irreversibly damaged in response to severe stress, parkin
                      can promote their elimination via mitophagy.},
      month         = {Sep},
      date          = {2012-09-15},
      organization  = {17th European Bioenergetics Conference
                       (EBEC), Freiburg (Germany), 15 Sep 2012
                       - 20 Sep 2012},
      cin          = {AG Winklhofer / Ext AG Tatzelt},
      ddc          = {570},
      cid          = {I:(DE-2719)5000047 / I:(DE-2719)5000053},
      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)1 / PUB:(DE-HGF)16},
      url          = {https://pub.dzne.de/record/145610},
}