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@ARTICLE{Funk:140566,
      author       = {Funk, Natalja and Munz, Marita and Ott, Thomas and
                      Brockmann, Kathrin and Wenninger-Weinzierl, Andrea and
                      Kühn, Ralf and Vogt-Weisenhorn, Daniela and Giesert,
                      Florian and Wurst, Wolfgang and Gasser, Thomas and Biskup,
                      Saskia},
      title        = {{T}he {P}arkinson's disease-linked {L}eucine-rich repeat
                      kinase 2 ({LRRK}2) is required for insulin-stimulated
                      translocation of {GLUT}4.},
      journal      = {Scientific reports},
      volume       = {9},
      number       = {1},
      issn         = {2045-2322},
      address      = {[London]},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {DZNE-2020-06888},
      pages        = {4515},
      year         = {2019},
      abstract     = {Mutations within Leucine-rich repeat kinase 2 (LRRK2) are
                      associated with late-onset Parkinson's disease. The
                      physiological function of LRRK2 and molecular mechanism
                      underlying the pathogenic role of LRRK2 mutations remain
                      uncertain. Here, we investigated the role of LRRK2 in
                      intracellular signal transduction. We find that deficiency
                      of Lrrk2 in rodents affects insulin-dependent translocation
                      of glucose transporter type 4 (GLUT4). This deficit is
                      restored during aging by prolonged insulin-dependent
                      activation of protein kinase B (PKB, Akt) and Akt substrate
                      of 160 kDa (AS160), and is compensated by elevated basal
                      expression of GLUT4 on the cell surface. Furthermore, we
                      find a crucial role of Rab10 phosphorylation by LRRK2 for
                      efficient insulin signal transduction. Translating our
                      findings into human cell lines, we find comparable molecular
                      alterations in fibroblasts from Parkinson's patients with
                      the known pathogenic G2019S LRRK2 mutation. Our results
                      highlight the role of LRRK2 in insulin-dependent signalling
                      with potential therapeutic implications.},
      keywords     = {Animals / Cell Survival: drug effects / Fibroblast Growth
                      Factors: pharmacology / Fibroblasts: cytology / Fibroblasts:
                      metabolism / Glucose Transporter Type 4: metabolism / Humans
                      / Insulin: pharmacology / Leucine-Rich Repeat
                      Serine-Threonine Protein Kinase-2: genetics / Leucine-Rich
                      Repeat Serine-Threonine Protein Kinase-2: metabolism / Mice
                      / Neuronal Outgrowth: drug effects / Parkinson Disease:
                      metabolism / Parkinson Disease: pathology / Phosphorylation
                      / Polymorphism, Single Nucleotide / Proto-Oncogene Proteins
                      c-akt: metabolism / Rats / Signal Transduction: drug effects
                      / rab GTP-Binding Proteins: metabolism},
      cin          = {Tübingen Pre 2020 / Ext UKT / AG Gasser 1 / AG Haass old /
                      AG Wurst},
      ddc          = {600},
      cid          = {I:(DE-2719)6000018 / I:(DE-2719)5000058 /
                      I:(DE-2719)1210000 / I:(DE-2719)1110007 /
                      I:(DE-2719)1140001},
      pnm          = {345 - Population Studies and Genetics (POF3-345) / 342 -
                      Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-345 / G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30872638},
      pmc          = {pmc:PMC6418296},
      doi          = {10.1038/s41598-019-40808-y},
      url          = {https://pub.dzne.de/record/140566},
}