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@ARTICLE{Pilsl:136463,
      author       = {Pilsl, Anna and Winklhofer, Konstanze F},
      title        = {{P}arkin, {PINK}1 and mitochondrial integrity: emerging
                      concepts of mitochondrial dysfunction in {P}arkinson's
                      disease.},
      journal      = {Acta neuropathologica},
      volume       = {123},
      number       = {2},
      issn         = {0001-6322},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DZNE-2020-02785},
      pages        = {173-188},
      year         = {2012},
      abstract     = {Mitochondria are dynamic organelles which are essential for
                      many cellular processes, such as ATP production by oxidative
                      phosphorylation, lipid metabolism, assembly of iron sulfur
                      clusters, regulation of calcium homeostasis, and cell death
                      pathways. The dynamic changes in mitochondrial morphology,
                      connectivity, and subcellular distribution are critically
                      dependent on a highly regulated fusion and fission
                      machinery. Mitochondrial function, dynamics, and quality
                      control are vital for the maintenance of neuronal integrity.
                      Indeed, there is mounting evidence that mitochondrial
                      dysfunction plays a central role in several
                      neurodegenerative diseases. In particular, the
                      identification of genes linked to rare familial variants of
                      Parkinson's disease has fueled research on mitochondrial
                      aspects of the disease etiopathogenesis. Studies on the
                      function of parkin and PINK1, which are associated with
                      autosomal recessive parkinsonism, provided compelling
                      evidence that these proteins can functionally interact to
                      maintain mitochondrial integrity and to promote clearance of
                      damaged and dysfunctional mitochondria. In this review we
                      will summarize current knowledge about the impact of parkin
                      and PINK1 on mitochondria.},
      subtyp        = {Review Article},
      keywords     = {Animals / Humans / Mitochondrial Diseases: genetics /
                      Mitochondrial Diseases: metabolism / Mitochondrial Diseases:
                      physiopathology / Mitochondrial Proteins: genetics /
                      Mitochondrial Proteins: physiology / Parkinson Disease:
                      genetics / Parkinson Disease: metabolism / Parkinson
                      Disease: physiopathology / Parkinsonian Disorders: genetics
                      / Parkinsonian Disorders: metabolism / Parkinsonian
                      Disorders: physiopathology / Protein Kinases: genetics /
                      Protein Kinases: physiology / Ubiquitin-Protein Ligases:
                      genetics / Ubiquitin-Protein Ligases: physiology /
                      Mitochondrial Proteins (NLM Chemicals) / Ubiquitin-Protein
                      Ligases (NLM Chemicals) / parkin protein (NLM Chemicals) /
                      Protein Kinases (NLM Chemicals) / PTEN-induced putative
                      kinase (NLM Chemicals)},
      cin          = {München common / AG Winklhofer},
      ddc          = {610},
      cid          = {I:(DE-2719)6000016 / I:(DE-2719)5000047},
      pnm          = {341 - Molecular Signaling (POF3-341)},
      pid          = {G:(DE-HGF)POF3-341},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:22057787},
      doi          = {10.1007/s00401-011-0902-3},
      url          = {https://pub.dzne.de/record/136463},
}