Defective mitochondrial COX1 translation due to loss of COX14 function triggers ROS-induced inflammation in mouse liver.

doi:10.1038/s41467-024-51109-y

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Article

Defective mitochondrial COX1 translation due to loss of COX14 function triggers ROS-induced inflammation in mouse liver.

Nature communications - 12 Aug 2024

Aich Abhishek, Boshnakovska Angela, Witte Steffen, Gall Tanja, Unthan-Fechner Kerstin, Yousefi Roya, Chowdhury Arpita, Dahal Drishan, Methi Aditi, Kaufmann Svenja, Silbern Ivan, Prochazka Jan, Nichtova Zuzana, Palkova Marcela, Raishbrook Miles, Koubkova Gizela, Sedlacek Radislav, Tröder Simon E, Zevnik Branko, Riedel Dietmar, Michanski Susann, Möbius Wiebke, Ströbel Philipp, Lüchtenborg Christian, Giavalisco Patrick, Urlaub Henning, Fischer Andre, Brügger Britta, Jakobs Stefan, Rehling Peter

Abstract excerpt

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...

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PMID: 39134548
DOI: 10.1038/s41467-024-51109-y
PMCID: PMC11319346

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COX14

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