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@INPROCEEDINGS{Zhang:145503,
      author       = {Zhang, L. and Whitworth, A. and Winklhofer, Konstanze F and
                      Schulz, J. B. and Voigt, A.},
      title        = {{PSM}04-06: {M}itochondrial degeneration in {PINK}1
                      loss-of-function isrescued by {TRAP}1},
      journal      = {Journal of neurochemistry},
      volume       = {125},
      number       = {Supplement 1},
      issn         = {0022-3042},
      reportid     = {DZNE-2020-00839},
      pages        = {142-143},
      year         = {2013},
      abstract     = {Mutations in PTEN-induced Kinase 1 (PINK1) cause
                      early-onsetParkinson’s disease (PD). PINK1 is critical to
                      maintain mitochon-drial function and protects cells from
                      oxidative stress by suppressingCytochrome C release and
                      thereby prevents cell death. Alterations inmitochondrial
                      integrity and function is implicated in the etiology ofPD.
                      It is known that application of mitochondrial toxins can
                      causePD. Moreover, not only PINK1-linked but also sporadic
                      PD patientsdisplay impaired function of mitochondrial
                      complex I in post-mortem brains. Recent cell culture
                      analysis implied that the protective effects of PINK1 are
                      dependent on the downstream factorTNF receptor-associated
                      protein 1 (TRAP1). We have recentlyshown that TRAP1
                      mitigates a-Synuclein induced toxicity in fliesand SH-SY5Y
                      cells, highlighting the importance of this protein inPD
                      pathology. So far, no in vivo studies on the interaction of
                      PINK1and TRAP1 have been reported. Here we show that human
                      TRAP1is able to mitigate PINK1 loss-of-function phenotypes
                      in flies,including morphological abnormalities, impaired
                      locomotion,decreased dopamine content and mitochondrial
                      dysfunction. Inaddition, we show that TRAP1 is able to
                      restore mitochondrialintegrity and function found to be
                      impaired in PINK1 silenced SH-SY5Y cells. Thus, our data
                      suggest a functional role of TRAP1 inmaintaining
                      mitochondrial integrity of PINK1 deficient
                      cells.Additionally, we provide evidence for TRAP1’s
                      function withinthe PINK1/Parkin pathway},
      month         = {Apr},
      date          = {2013-04-20},
      organization  = {24th Biennial Meeting of the
                       International Society for
                       Neurochemistry and the American Society
                       for Neurochemistry., Cancun (Mexico),
                       20 Apr 2013 - 24 Apr 2013},
      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)1 / PUB:(DE-HGF)16},
      url          = {https://pub.dzne.de/record/145503},
}