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@ARTICLE{Brady:125959,
      author       = {A. Brady$^*$ and N. Brady$^*$},
      title        = {{M}itophagy programs: mechanisms and physiological
                      implications of mitochondrial targeting by autophagy.},
      journal      = {Cellular and molecular life sciences},
      volume       = {73},
      number       = {4},
      issn         = {1420-9071},
      address      = {Basel},
      publisher    = {Birkhäuser},
      reportid     = {DKFZ-2017-02083},
      pages        = {775 - 795},
      year         = {2016},
      abstract     = {Mitochondria are an essential source of ATP for cellular
                      function, but when damaged, mitochondria generate a plethora
                      of stress signals, which lead to cellular dysfunction and
                      eventually programmed cell death. Thus, a major component of
                      maintaining cellular homeostasis is the recognition and
                      removal of dysfunctional mitochondria through
                      autophagy-mediated degradation, i.e., mitophagy. Mitophagy
                      further constitutes a developmental program, and undergoes a
                      high degree of crosstalk with apoptosis. Reduced
                      mitochondrial quality control is linked to disease
                      pathogenesis, suggesting the importance of process
                      elucidation as a clinical target. Recent work has revealed
                      multiple mitophagy programs that operate independently or
                      undergo crosstalk, and require modulated autophagy receptor
                      activities at outer membranes of mitochondria. Here, we
                      review these mitophagy programs, focusing on pathway
                      mechanisms which recognize and target mitochondria for
                      sequestration by autophagosomes, as well as mechanisms
                      controlling pathway activities. Furthermore, we provide an
                      introduction to the currently available methods for
                      detecting mitophagy.},
      keywords     = {BNIP3 protein, human (NLM Chemicals) / Membrane Proteins
                      (NLM Chemicals) / Microtubule-Associated Proteins (NLM
                      Chemicals) / Proto-Oncogene Proteins (NLM Chemicals) /
                      Ubiquitin (NLM Chemicals) / Ubiquitin-Protein Ligases (NLM
                      Chemicals) / parkin protein (NLM Chemicals)},
      cin          = {B190 / B170},
      ddc          = {570},
      cid          = {I:(DE-He78)B190-20160331 / I:(DE-He78)B170-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26611876},
      pmc          = {pmc:PMC4735260},
      doi          = {10.1007/s00018-015-2087-8},
      url          = {https://inrepo02.dkfz.de/record/125959},
}