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@ARTICLE{Aalto:163763,
      author       = {Aalto, Anna and Martínez-Chacón, Gabriela and Kietz,
                      Christa and Tsyganova, Nadezhda and Kreutzer, Joose and
                      Kallio, Pasi and Broemer, Meike and Meinander, Annika},
      title        = {{M}1-linked ubiquitination facilitates {NF}-κ{B}
                      activation and survival during sterile inflammation.},
      journal      = {The FEBS journal},
      volume       = {289},
      number       = {17},
      issn         = {0014-2956},
      address      = {Oxford [u.a.]},
      publisher    = {Wiley-Blackwell},
      reportid     = {DZNE-2022-00502},
      pages        = {5180-5197},
      year         = {2022},
      note         = {CC BY-NC-ND:
                      https://creativecommons.org/licenses/by-nc-nd/4.0/},
      abstract     = {Methionine 1 (M1)-linked ubiquitination plays a key role in
                      the regulation of inflammatory nuclear factor-κB (NF-κB)
                      signalling and is important for clearance of pathogen
                      infection in Drosophila melanogaster. M1-linked ubiquitin
                      (M1-Ub) chains are assembled by the linear ubiquitin E3
                      ligase (LUBEL) in flies. Here, we have studied the role of
                      LUBEL in sterile inflammation induced by different types of
                      cellular stresses. We have found that the LUBEL catalyses
                      formation of M1-Ub chains in response to hypoxic, oxidative
                      and mechanical stress conditions. LUBEL is shown to be
                      important for flies to survive low oxygen conditions and
                      paraquat-induced oxidative stress. This protective action
                      seems to be driven by stress-induced activation of the
                      NF-κB transcription factor Relish via the immune deficiency
                      (Imd) pathway. In addition to LUBEL, the intracellular
                      mediators of Relish activation, including the transforming
                      growth factor activating kinase 1 (Tak1), Drosophila
                      inhibitor of apoptosis (IAP) Diap2, the IκB kinase γ
                      (IKKγ) Kenny and the initiator caspase Death-related
                      ced-3/Nedd2-like protein (Dredd), but not the membrane
                      receptor peptidoglycan recognition protein (PGRP)-LC, are
                      shown to be required for sterile inflammatory response and
                      survival. Finally, we showed that the stress-induced
                      upregulation of M1-Ub chains in response to hypoxia,
                      oxidative and mechanical stress is also induced in mammalian
                      cells and protects from stress-induced cell death. Taken
                      together, our results suggest that M1-Ub chains are
                      important for NF-κB signalling in inflammation induced by
                      stress conditions often observed in chronic inflammatory
                      diseases and cancer.},
      keywords     = {Animals / Drosophila: metabolism / Drosophila Proteins:
                      genetics / Drosophila Proteins: metabolism / Drosophila
                      melanogaster: metabolism / Inflammation: genetics / MAP
                      Kinase Kinase Kinases: metabolism / Mammals: metabolism /
                      Methionine: metabolism / NF-kappa B: genetics / NF-kappa B:
                      metabolism / Ubiquitin: metabolism / Ubiquitination / NF-κB
                      (Other) / cell stress (Other) / hypoxia (Other) / linear
                      ubiquitin chain (Other) / sterile inflammation (Other)},
      cin          = {AG Brömer 2},
      ddc          = {610},
      cid          = {I:(DE-2719)1013021},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC9543601},
      pubmed       = {pmid:35263507},
      doi          = {10.1111/febs.16425},
      url          = {https://pub.dzne.de/record/163763},
}