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@ARTICLE{Bruch:137639,
      author       = {Bruch, Julius and Xu, Hong and De Andrade, Anderson and
                      Höglinger, Günter},
      title        = {{M}itochondrial complex 1 inhibition increases 4-repeat
                      isoform tau by {SRSF}2 upregulation.},
      journal      = {PLOS ONE},
      volume       = {9},
      number       = {11},
      issn         = {1932-6203},
      address      = {San Francisco, California, US},
      publisher    = {PLOS},
      reportid     = {DZNE-2020-03961},
      pages        = {e113070},
      year         = {2014},
      abstract     = {Progressive Supranuclear Palsy (PSP) is a neurodegenerative
                      disorder characterised by intracellular aggregation of the
                      microtubule-associated protein tau. The tau protein exists
                      in 6 predominant isoforms. Depending on alternative splicing
                      of exon 10, three of these isoforms have four
                      microtubule-binding repeat domains (4R), whilst the others
                      only have three (3R). In PSP there is an excess of the 4R
                      tau isoforms, which are thought to contribute significantly
                      to the pathological process. The cause of this 4R increase
                      is so far unknown. Several lines of evidence link
                      mitochondrial complex I inhibition to the pathogenesis of
                      PSP. We demonstrate here for the first time that annonacin
                      and MPP(+), two prototypical mitochondrial complex I
                      inhibitors, increase the 4R isoforms of tau in human
                      neurons. We show that the splicing factor SRSF2 is necessary
                      to increase 4R tau with complex I inhibition. We also found
                      SRSF2, as well as another tau splicing factor, TRA2B, to be
                      increased in brains of PSP patients. Thereby, we provide new
                      evidence that mitochondrial complex I inhibition may
                      contribute as an upstream event to the pathogenesis of PSP
                      and suggest that splicing factors may represent an
                      attractive therapeutic target to intervene in the disease
                      process.},
      keywords     = {Alternative Splicing / Electron Transport Complex I:
                      antagonists $\&$ inhibitors / Electron Transport Complex I:
                      metabolism / Female / Furans: pharmacology / Gene Expression
                      Regulation: drug effects / Humans / Lactones: pharmacology /
                      Nuclear Proteins: metabolism / Oxidative Stress / Protein
                      Interaction Domains and Motifs / RNA Isoforms /
                      Ribonucleoproteins: metabolism / Serine-Arginine Splicing
                      Factors / Supranuclear Palsy, Progressive: genetics /
                      Supranuclear Palsy, Progressive: metabolism / Up-Regulation
                      / tau Proteins: chemistry / tau Proteins: genetics / tau
                      Proteins: metabolism / Furans (NLM Chemicals) / Lactones
                      (NLM Chemicals) / Nuclear Proteins (NLM Chemicals) / RNA
                      Isoforms (NLM Chemicals) / Ribonucleoproteins (NLM
                      Chemicals) / tau Proteins (NLM Chemicals) / SRSF2 protein,
                      human (NLM Chemicals) / Serine-Arginine Splicing Factors
                      (NLM Chemicals) / annonacin (NLM Chemicals) / Electron
                      Transport Complex I (NLM Chemicals)},
      cin          = {AG Höglinger 1},
      ddc          = {610},
      cid          = {I:(DE-2719)1110002},
      pnm          = {344 - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25402454},
      pmc          = {pmc:PMC4234644},
      doi          = {10.1371/journal.pone.0113070},
      url          = {https://pub.dzne.de/record/137639},
}