Home > Publications Database > Defective mitochondrial COX1 translation due to loss of COX14 function triggers ROS-induced inflammation in mouse liver. > print

001     271329
005     20250127091623.0
024 7 _ |a pmc:PMC11319346
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024 7 _ |a 10.1038/s41467-024-51109-y
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024 7 _ |a pmid:39134548
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024 7 _ |a altmetric:166265533
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037 _ _ |a DZNE-2024-01031
041 _ _ |a English
082 _ _ |a 500
100 1 _ |a Aich, Abhishek
|0 0000-0001-8331-9874
|b 0
245 _ _ |a Defective mitochondrial COX1 translation due to loss of COX14 function triggers ROS-induced inflammation in mouse liver.
260 _ _ |a [London]
|c 2024
|b Nature Publishing Group UK
336 7 _ |a article
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336 7 _ |a Output Types/Journal article
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336 7 _ |a Journal Article
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|s 1723723581_26248
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a 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 describe 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 describe a COA3Y72C mouse, affected in an assembly factor that cooperates with COX14 in early COX1 biogenesis, which displays a similar yet milder inflammatory phenotype. Our study provides insight into a link between defective mitochondrial gene expression and tissue-specific inflammation.
536 _ _ |a 352 - Disease Mechanisms (POF4-352)
|0 G:(DE-HGF)POF4-352
|c POF4-352
|f POF IV
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
650 _ 7 |a Reactive Oxygen Species
|2 NLM Chemicals
650 _ 7 |a Electron Transport Complex IV
|0 EC 1.9.3.1
|2 NLM Chemicals
650 _ 7 |a Ddx58 protein, mouse
|0 EC 3.6.1.-
|2 NLM Chemicals
650 _ 7 |a RNA, Mitochondrial
|2 NLM Chemicals
650 _ 7 |a Ptgs1 protein, mouse
|0 EC 1.14.99.1
|2 NLM Chemicals
650 _ 7 |a Mitochondrial Proteins
|2 NLM Chemicals
650 _ 7 |a DEAD-box RNA Helicases
|0 EC 3.6.4.13
|2 NLM Chemicals
650 _ 7 |a DEAD Box Protein 58
|0 EC 3.6.4.13
|2 NLM Chemicals
650 _ 7 |a Membrane Proteins
|2 NLM Chemicals
650 _ 7 |a Cyclooxygenase 1
|0 EC 1.14.99.1
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Reactive Oxygen Species: metabolism
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Liver: metabolism
|2 MeSH
650 _ 2 |a Liver: pathology
|2 MeSH
650 _ 2 |a Inflammation: metabolism
|2 MeSH
650 _ 2 |a Inflammation: genetics
|2 MeSH
650 _ 2 |a Inflammation: pathology
|2 MeSH
650 _ 2 |a Electron Transport Complex IV: metabolism
|2 MeSH
650 _ 2 |a Electron Transport Complex IV: genetics
|2 MeSH
650 _ 2 |a Oxidative Phosphorylation
|2 MeSH
650 _ 2 |a Mitochondria: metabolism
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a RNA, Mitochondrial: genetics
|2 MeSH
650 _ 2 |a RNA, Mitochondrial: metabolism
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Mitochondrial Proteins: metabolism
|2 MeSH
650 _ 2 |a Mitochondrial Proteins: genetics
|2 MeSH
650 _ 2 |a Protein Biosynthesis
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a DEAD-box RNA Helicases: metabolism
|2 MeSH
650 _ 2 |a DEAD-box RNA Helicases: genetics
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Mutation
|2 MeSH
650 _ 2 |a DEAD Box Protein 58
|2 MeSH
650 _ 2 |a Membrane Proteins
|2 MeSH
650 _ 2 |a Cyclooxygenase 1
|2 MeSH
700 1 _ |a Boshnakovska, Angela
|0 0009-0008-3572-0223
|b 1
700 1 _ |a Witte, Steffen
|b 2
700 1 _ |a Gall, Tanja
|b 3
700 1 _ |a Unthan-Fechner, Kerstin
|b 4
700 1 _ |a Yousefi, Roya
|b 5
700 1 _ |a Chowdhury, Arpita
|0 0000-0001-5025-0268
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700 1 _ |a Dahal, Drishan
|b 7
700 1 _ |a Methi, Aditi
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700 1 _ |a Kaufmann, Svenja
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700 1 _ |a Silbern, Ivan
|0 0000-0001-8284-954X
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700 1 _ |a Prochazka, Jan
|0 0000-0003-4675-8995
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700 1 _ |a Nichtova, Zuzana
|0 0000-0001-7358-3268
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700 1 _ |a Palkova, Marcela
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700 1 _ |a Raishbrook, Miles
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700 1 _ |a Koubkova, Gizela
|0 0000-0001-6497-6094
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700 1 _ |a Sedlacek, Radislav
|0 0000-0002-3352-392X
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700 1 _ |a Tröder, Simon E
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700 1 _ |a Zevnik, Branko
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700 1 _ |a Riedel, Dietmar
|0 0000-0003-2970-6894
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700 1 _ |a Michanski, Susann
|b 20
700 1 _ |a Möbius, Wiebke
|0 0000-0002-2902-7165
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700 1 _ |a Ströbel, Philipp
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700 1 _ |a Lüchtenborg, Christian
|b 23
700 1 _ |a Giavalisco, Patrick
|0 0000-0002-4636-1827
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700 1 _ |a Urlaub, Henning
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700 1 _ |a Fischer, Andre
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700 1 _ |a Brügger, Britta
|0 0000-0002-3477-8270
|b 27
700 1 _ |a Jakobs, Stefan
|0 0000-0002-8028-3121
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700 1 _ |a Rehling, Peter
|0 0000-0001-5661-5272
|b 29
773 _ _ |a 10.1038/s41467-024-51109-y
|g Vol. 15, no. 1, p. 6914
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|p 6914
|t Nature Communications
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|y 2024
|x 2041-1723
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