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@ARTICLE{LechadoTerradas:266473,
      author       = {Lechado-Terradas, Anna and Schepers, Sandra and Zittlau,
                      Katharina I. and Sharma, Karan and Ok, Orkun and Fitzgerald,
                      Julia C. and Geimer, Stefan and Westermann, Benedikt and
                      Macek, Boris and Kahle, Philipp},
      title        = {{P}arkin-dependent mitophagy occurs via
                      proteasome-dependent steps sequentially targeting separate
                      mitochondrial sub-compartments for autophagy},
      journal      = {Autophagy reports},
      volume       = {1},
      number       = {1},
      issn         = {2769-4127},
      address      = {London},
      publisher    = {Taylor $\&$ Francis Group},
      reportid     = {DZNE-2023-01158},
      pages        = {576 - 602},
      year         = {2022},
      abstract     = {PINK1/parkin-dependent mitophagy initially involves
                      (phospho)ubiquitin-directed proteasome-dependent degradation
                      of certain outer mitochondrial membrane (OMM) proteins (e.g.
                      mitofusins) and the recruitment of autophagy adaptors to a
                      group of ubiquitinated OMM proteins, eventually leading to
                      autophagic removal of damaged mitochondria in stressed
                      cells. Here we provide evidence that mitochondrial
                      degradation occurs via stepwise delivery of separate
                      mitochondrial sub-compartments for autophagic degradation.
                      OMM and inner mitochondrial material appears to become
                      separately isolated for autophagolysosomal degradation, not
                      only in parkin-overexpressing HeLa cells but also in cells
                      that express endogenous parkin (human embryonic kidney cells
                      and neural progenitor cells) with slower mitophagy kinetics.
                      The remaining inner mitochondrial material becomes degraded
                      only after much prolonged membrane depolarization,
                      potentially involving another proteasome-sensitive step. The
                      present combined microscopy and proteomics analyses support
                      the idea that cell stress-induced parkin-dependent mitophagy
                      is a complex multi-step process with distinct mitochondrial
                      sub-compartments being separately targeted for autophagic
                      degradation.},
      cin          = {AG Kahle},
      ddc          = {610},
      cid          = {I:(DE-2719)1210000-4},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.1080/27694127.2022.2143214},
      url          = {https://pub.dzne.de/record/266473},
}