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@INPROCEEDINGS{MllerRischart:145425,
      author       = {Müller-Rischart, Anne Kathrin and Pilsl, Anna and Bouman,
                      Lena and Tatzelt, Jörg and Winklhofer, Konstanze F},
      title        = {{P}arkinson's disease-associated genes and mitochondrial
                      integrity},
      journal      = {Biochimica et biophysica acta / Bioenergetics},
      volume       = {1797},
      issn         = {0005-2728},
      reportid     = {DZNE-2020-00768},
      pages        = {75},
      year         = {2010},
      abstract     = {Parkinson's disease (PD) is the most common movement
                      disorder and the second most common neurodegenerative
                      disease after Alzheimer's disease, affecting an increasing
                      number of patients due to the demographic trend towards an
                      aged population. Oxidative stress, mitochondrial dysfunction
                      and protein aggregation are pathophysiological alterations
                      consistently found in the course of the disease, however,
                      the etiology of sporadic PD still remains enigmatic. Thus,
                      the identification of genes which are reponsible for
                      familial variants was a major breakthrough. Importantly,
                      several PD-linked gene products have a direct or indirect
                      impact on mitochondrial integrity, emphasizing a crucial
                      role of mitochondria in the pathogenesis of PD.
                      Loss-of-function mutations in the E3 ubiquitin ligase parkin
                      or the mitochondrial kinase PINK1 are associated with
                      autosomal recessive parkinsonism. Our previous work revealed
                      that parkin is a stress-responsive protein with a remarkably
                      wide neuroprotective capacity, preventing cell death under
                      various stress conditions. An early consequence of parkin or
                      PINK1 silencing in human cells is a decrease in
                      mitochondrial membrane potential and ATP production and
                      increase in mitochondrial fragmentation. Remarkably, parkin
                      can increase the clearance of dysfunctional mitochondria by
                      mitophagy in a PINK1-dependent manner. We will discuss the
                      underlying mechanisms and present data indicative of a
                      regulatory crosstalk between the autophagic machinery and
                      mitochondrial dynamics.},
      month         = {Jul},
      date          = {2010-07-17},
      organization  = {16th European Bioenergetics
                       Conference, , 17 Jul 2010 - 22 Jul
                       2010},
      cin          = {AG Winklhofer / München Pre 2020 / Ext AG Tatzelt},
      ddc          = {570},
      cid          = {I:(DE-2719)5000047 / I:(DE-2719)6000016 /
                      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/145425},
}