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@ARTICLE{MllerRischart:136839,
      author       = {Müller-Rischart, A. Kathrin and Pilsl, Anna and Beaudette,
                      Patrick and Patra, Maria and Hadian, Kamyar and Funke, Maria
                      and Peis, Regina and Deinlein, Alexandra and Schweimer,
                      Carolin and Kuhn, Peer-Hendrik and Lichtenthaler, Stefan F
                      and Motori, Elisa and Hrelia, Silvana and Wurst, Wolfgang
                      and Trümbach, Dietrich and Langer, Thomas and Krappmann,
                      Daniel and Dittmar, Gunnar and Tatzelt, Jörg and
                      Winklhofer, Konstanze F},
      title        = {{T}he {E}3 ligase parkin maintains mitochondrial integrity
                      by increasing linear ubiquitination of {NEMO}.},
      journal      = {Molecular cell},
      volume       = {49},
      number       = {5},
      issn         = {1097-2765},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DZNE-2020-03161},
      pages        = {908-921},
      year         = {2013},
      abstract     = {Parkin, a RING-between-RING-type E3 ubiquitin ligase
                      associated with Parkinson's disease, has a wide
                      neuroprotective activity, preventing cell death in various
                      stress paradigms. We identified a stress-protective pathway
                      regulated by parkin that links NF-κB signaling and
                      mitochondrial integrity via linear ubiquitination. Under
                      cellular stress, parkin is recruited to the linear ubiquitin
                      assembly complex and increases linear ubiquitination of
                      NF-κB essential modulator (NEMO), which is essential for
                      canonical NF-κB signaling. As a result, the mitochondrial
                      guanosine triphosphatase OPA1 is transcriptionally
                      upregulated via NF-κB-responsive promoter elements for
                      maintenance of mitochondrial integrity and protection from
                      stress-induced cell death. Parkin-induced stress protection
                      is lost in the absence of either NEMO or OPA1, but not in
                      cells defective for the mitophagy pathway. Notably, in
                      parkin-deficient cells linear ubiquitination of NEMO,
                      activation of NF-κB, and upregulation of OPA1 are
                      significantly reduced in response to TNF-α stimulation,
                      supporting the physiological relevance of parkin in
                      regulating this antiapoptotic pathway.},
      keywords     = {Animals / Apoptosis / Fibroblasts: metabolism / HEK293
                      Cells / Humans / Intracellular Signaling Peptides and
                      Proteins: genetics / Intracellular Signaling Peptides and
                      Proteins: metabolism / Mice / Mice, Knockout / Mitochondria:
                      metabolism / NF-kappa B: genetics / NF-kappa B: metabolism /
                      Neurons: metabolism / Parkinson Disease: genetics /
                      Parkinson Disease: metabolism / Signal Transduction /
                      Transfection / Ubiquitin-Protein Ligases: genetics /
                      Ubiquitin-Protein Ligases: metabolism / Ubiquitination:
                      genetics / Intracellular Signaling Peptides and Proteins
                      (NLM Chemicals) / NEMO protein, mouse (NLM Chemicals) /
                      NF-kappa B (NLM Chemicals) / Ubiquitin-Protein Ligases (NLM
                      Chemicals) / parkin protein (NLM Chemicals)},
      cin          = {AG Lichtenthaler / AG Wurst},
      ddc          = {610},
      cid          = {I:(DE-2719)1110006 / I:(DE-2719)1140001},
      pnm          = {341 - Molecular Signaling (POF3-341) / 342 - Disease
                      Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-341 / G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:23453807},
      doi          = {10.1016/j.molcel.2013.01.036},
      url          = {https://pub.dzne.de/record/136839},
}