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@MISC{Aich:280737,
      author       = {Aich, Abhishek and Patrick, Giavalisco and Rehling, Peter},
      othercontributors = {Aich, Abhishek and Boshnakovska, Angela and Witte, Steffen
                          and Gall, Tanja and Unthan-Fechner, Kerstin and Yousefi,
                          Roya and Chowdhury, Arpita and Dahal, Drishan and Methi,
                          Aditi and Kaufmann, Svenja and Silbern, Ivan and Prochazka,
                          Jan and Nichtova, Zusana and Palkova, Marcela and
                          Raishbrook, Miles and Koublova, Gizela and Sedlacek,
                          Radislav and Tröder, Simon E. and Zevnik, Branko and
                          Riedel, Dietmar and Michanski, Susann and Möbius, Wiebke
                          and Ströbel, Philipp and Lüchtenborg, Christian and
                          Giavalisco, Patrick and Urlaub, Henning and Fischer, Andre
                          and Brügger, Britta and Jakobs, Stefan and Rehling, Peter},
      title        = {{D}ataset: {D}efective mitochondrial {COX}1 translation due
                      to loss of {COX}14 function triggers {ROS}-induced
                      inflammation in liver},
      publisher    = {Zenodo},
      reportid     = {DZNE-2025-00958},
      year         = {2024},
      abstract     = {Data Content In this data repository Ultra High-Performance
                      Chromatography (UPLC) and Ion Chromatography (IC)- high
                      resolution mass spectrometry (HRMS) metabolomic data is
                      provided. The data consists of all analyzed raw files and
                      the associated peak picking files (TraceFinder 5.1, Thermo
                      Fisher Scientific). The data with the abreviation
                      $'Bz_QE_Plus'$ contains the UPLC-MS data of bezoylchloride
                      derivatized amines, phenols, thiols, and some alcohols
                      measured on a Q-Exactive Plus mass spectrometer), while the
                      files with the abbreviation $'IC_HF_TF'$ contain the anion
                      chromatographic data measured on a Q-Exactive Plus coupled
                      to an Integrion ion chroatograph. The provided data is
                      associated to an article submitted to Nature Communications
                      (“Defective mitochondrial COX1 translation due to loss of
                      COX14 function triggers ROS-induced inflammation in
                      liver”), describing the analysis of COX14 and COA3 mutants
                      (see abstract below). The sample and data analysis section,
                      which is also provided in the supplementary section of the
                      above mentioned article, are also attached as, doc files to
                      the deposited data.Abstract of the article Mitochondrial
                      oxidative phosphorylation (OXPHOS) fuels cellular ATP
                      demands. OXPHOS defects lead to severe human disorders with
                      unexplained tissue specific pathologies. Mitochondrial gene
                      expression is essential for OXPHOS biogenesis since core
                      subunits of the complexes are mitochondrial-encoded. COX14
                      is required for translation of COX1, the central
                      mitochondrial-encoded subunit of complex IV. Here we
                      generated a COX14 mutant mouse corresponding to a patient
                      with complex IV deficiency. COX14M19I mice display broad
                      tissue-specific pathologies. A hallmark phenotype is severe
                      liver inflammation linked to release of mitochondrial RNA
                      into the cytosol sensed by RIG-1 pathway. We find that
                      mitochondrial RNA release is triggered by increased reactive
                      oxygen species production in the deficiency of complex IV.
                      Additionally, we generated a COA3Y72C mouse, affected in an
                      assembly factor in early COX1 biogenesis, which displayed a
                      similar yet milder inflammatory phenotype. Our study
                      provides mechanistic insight into how defective
                      mitochondrial gene expression causes tissue-specific
                      inflammation.},
      cin          = {AG Fischer},
      cid          = {I:(DE-2719)1410002},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)32},
      doi          = {10.5281/zenodo.10640935},
      url          = {https://pub.dzne.de/record/280737},
}