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@ARTICLE{Ku:137434,
      author       = {Kuß, Martin and Adamopoulou, Eleni and Kahle, Philipp J},
      title        = {{I}nterferon-γ induces leucine-rich repeat kinase {LRRK}2
                      via extracellular signal-regulated kinase {ERK}5 in
                      macrophages.},
      journal      = {Journal of neurochemistry},
      volume       = {129},
      number       = {6},
      issn         = {0022-3042},
      address      = {Oxford},
      publisher    = {Wiley-Blackwell},
      reportid     = {DZNE-2020-03756},
      pages        = {980-987},
      year         = {2014},
      abstract     = {The gene encoding leucine-rich repeat kinase 2 (LRRK2)
                      comprises a major risk factor for Parkinson's disease.
                      Recently, it has emerged that LRRK2 plays important roles in
                      the immune system. LRRK2 is induced by interferon-γ
                      (IFN-γ) in monocytes, but the signaling pathway is not
                      known. Here, we show that IFN-γ-mediated induction of LRRK2
                      was suppressed by pharmacological inhibition and RNA
                      interference of the extracellular signal-regulated kinase 5
                      (ERK5). This was confirmed by LRRK2 immunostaining, which
                      also revealed that the morphological responses to IFN-γ
                      were suppressed by ERK5 inhibitor treatment. Both human
                      acute monocytic leukemia THP-1 cells and human peripheral
                      blood monocytes stimulated the ERK5-LRRK2 pathway after
                      differentiation into macrophages. Thus, LRRK2 is induced via
                      a novel, ERK5-dependent IFN-γ signal transduction pathway,
                      pointing to new functions of ERK5 and LRRK2 in human
                      macrophages. Leucine-rich repeat kinase 2 (LRRK2) is a major
                      risk factor for the development of Parkinson's disease (PD).
                      However, the role of LRRK2 in the affected neurons remains
                      enigmatic. Recently, LRRK2 has been reported to be strongly
                      expressed in the immune system. Here, we demonstrate that
                      LRRK2 is induced by Interferon gamma via extracellular
                      signal-regulated kinase 5 (ERK5) in macrophages, thus
                      providing new insights in LRRK2 and ERK5 biology.},
      keywords     = {Protein Serine-Threonine Kinases: biosynthesis / Blotting,
                      Western / Cells, Cultured / Cytokines: metabolism / Enzyme
                      Induction: drug effects / Enzyme Inhibitors: pharmacology /
                      Humans / Immunohistochemistry / Interferon-gamma:
                      antagonists $\&$ inhibitors / Interferon-gamma: pharmacology
                      / Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 /
                      Macrophages: drug effects / Macrophages: enzymology /
                      Mitogen-Activated Protein Kinase 7: antagonists $\&$
                      inhibitors / Mitogen-Activated Protein Kinase 7: physiology
                      / Protein-Serine-Threonine Kinases: biosynthesis / Real-Time
                      Polymerase Chain Reaction / Signal Transduction: drug
                      effects / Cytokines (NLM Chemicals) / Enzyme Inhibitors (NLM
                      Chemicals) / Interferon-gamma (NLM Chemicals) / LRRK2
                      protein, human (NLM Chemicals) / Leucine-Rich Repeat
                      Serine-Threonine Protein Kinase-2 (NLM Chemicals) /
                      Protein-Serine-Threonine Kinases (NLM Chemicals) /
                      Mitogen-Activated Protein Kinase 7 (NLM Chemicals)},
      cin          = {AG N.N. 3 / AG Kahle 2},
      ddc          = {610},
      cid          = {I:(DE-2719)1240015 / I:(DE-2719)1210000-4},
      pnm          = {344 - Clinical and Health Care Research (POF3-344) / 345 -
                      Population Studies and Genetics (POF3-345)},
      pid          = {G:(DE-HGF)POF3-344 / G:(DE-HGF)POF3-345},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:24479685},
      doi          = {10.1111/jnc.12668},
      url          = {https://pub.dzne.de/record/137434},
}