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@ARTICLE{Aalto:140635,
      author       = {Aalto, Anna L and Mohan, Aravind K and Schwintzer, Lukas
                      and Kupka, Sebastian and Kietz, Christa and Walczak, Henning
                      and Broemer, Meike and Meinander, Annika},
      title        = {{M}1-linked ubiquitination by {LUBEL} is required for
                      inflammatory responses to oral infection in {D}rosophila.},
      journal      = {Cell death and differentiation},
      volume       = {26},
      number       = {5},
      issn         = {1350-9047},
      address      = {London},
      publisher    = {Macmillan},
      reportid     = {DZNE-2020-06957},
      pages        = {860-876},
      year         = {2019},
      abstract     = {Post-translational modifications such as ubiquitination
                      play a key role in regulation of inflammatory nuclear
                      factor-κB (NF-κB) signalling. The Drosophila IκB kinase
                      γ (IKKγ) Kenny is a central regulator of the Drosophila
                      Imd pathway responsible for activation of the NF-κB Relish.
                      We found the Drosophila E3 ligase and HOIL-1L interacting
                      protein (HOIP) orthologue linear ubiquitin E3 ligase (LUBEL)
                      to catalyse formation of M1-linked linear ubiquitin (M1-Ub)
                      chains in flies in a signal-dependent manner upon bacterial
                      infection. Upon activation of the Imd pathway, LUBEL
                      modifies Kenny with M1-Ub chains. Interestingly, the
                      LUBEL-mediated M1-Ub chains seem to be targeted both
                      directly to Kenny and to K63-linked ubiquitin chains
                      conjugated to Kenny by DIAP2. This suggests that DIAP2 and
                      LUBEL work together to promote Kenny-mediated activation of
                      Relish. We found LUBEL-mediated M1-Ub chain formation to be
                      required for flies to survive oral infection with
                      Gram-negative bacteria, for activation of Relish-mediated
                      expression of antimicrobial peptide genes and for pathogen
                      clearance during oral infection. Interestingly, LUBEL is not
                      required for mounting an immune response against systemic
                      infection, as Relish-mediated antimicrobial peptide genes
                      can be expressed in the absence of LUBEL during septic
                      injury. Finally, transgenic induction of LUBEL-mediated
                      M1-Ub drives expression of antimicrobial peptide genes and
                      hyperplasia in the midgut in the absence of infection. This
                      suggests that M1-Ub chains are important for Imd signalling
                      and immune responses in the intestinal epithelia, and that
                      enhanced M1-Ub chain formation is able to drive chronic
                      intestinal inflammation in flies.},
      keywords     = {Animals / Bacterial Infections: genetics / Bacterial
                      Infections: microbiology / Disease Models, Animal /
                      Drosophila: genetics / Drosophila Proteins: genetics /
                      Gram-Negative Bacteria: pathogenicity / Humans / Immunity,
                      Innate: genetics / Inflammation: genetics / Inflammation:
                      microbiology / Inhibitor of Apoptosis Proteins: genetics /
                      Mouth: microbiology / Mouth: pathology / NF-kappa B:
                      genetics / Protein Processing, Post-Translational: genetics
                      / RNA-Binding Proteins: genetics / Signal Transduction:
                      genetics / Transcription Factors: genetics / Ubiquitin:
                      genetics / Ubiquitin-Protein Ligases: genetics /
                      Ubiquitination: genetics},
      cin          = {AG Brömer 1},
      ddc          = {610},
      cid          = {I:(DE-2719)5000021},
      pnm          = {341 - Molecular Signaling (POF3-341)},
      pid          = {G:(DE-HGF)POF3-341},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30026495},
      pmc          = {pmc:PMC6462001},
      doi          = {10.1038/s41418-018-0164-x},
      url          = {https://pub.dzne.de/record/140635},
}