% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Zhu:166690,
      author       = {J.-Y. Zhu and S. B. Hannan$^*$ and N. Dräger$^*$ and N.
                      Vereshchagina and A.-C. Krahl and Y. Fu and C. J. H. Elliott
                      and Z. Han and T. Jahn$^*$ and T. Rasse$^*$},
      title        = {{A}utophagy inhibition rescues structural and functional
                      defects caused by the loss of mitochondrial chaperone
                      {H}sc70-5 in {D}rosophila.},
      journal      = {Autophagy},
      volume       = {17},
      number       = {10},
      issn         = {1554-8635},
      address      = {Abingdon, Oxon},
      publisher    = {Taylor $\&$ Francis},
      reportid     = {DKFZ-2021-00043},
      pages        = {3160-3174},
      year         = {2021},
      note         = {#LA:B180# /2021 Oct;17(10):3160-3174},
      abstract     = {We investigated in larval and adult Drosophila models
                      whether loss of the mitochondrial chaperone Hsc70-5 is
                      sufficient to cause pathological alterations commonly
                      observed in Parkinson disease. At affected larval
                      neuromuscular junctions, no effects on terminal size, bouton
                      size or number, synapse size, or number were observed,
                      suggesting that we studied an early stage of pathogenesis.
                      At this stage, we noted a loss of synaptic vesicle proteins
                      and active zone components, delayed synapse maturation,
                      reduced evoked and spontaneous excitatory junctional
                      potentials, increased synaptic fatigue, and cytoskeleton
                      rearrangements. The adult model displayed ATP depletion,
                      altered body posture, and susceptibility to heat-induced
                      paralysis. Adult phenotypes could be suppressed by knockdown
                      of dj-1β, Lrrk, DCTN2-p50, DCTN1-p150, Atg1, Atg101, Atg5,
                      Atg7, and Atg12. The knockdown of components of the
                      macroautophagy/autophagy machinery or overexpression of
                      human HSPA9 broadly rescued larval and adult phenotypes,
                      while disease-associated HSPA9 variants did not.
                      Overexpression of Pink1 or promotion of autophagy
                      exacerbated defects.},
      keywords     = {Atg1 (Other) / Hsc70-5 (Other) / microtubule (Other) /
                      mitochondria (Other) / mitophagy (Other) / rapamycin (Other)
                      / synapse (Other)},
      cin          = {B180},
      ddc          = {570},
      cid          = {I:(DE-He78)B180-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33404278},
      doi          = {10.1080/15548627.2020.1871211},
      url          = {https://inrepo02.dkfz.de/record/166690},
}