Tsvetkov, Peter; Coy, Shannon; Petrova, Boryana; Dreishpoon, Margaret; Verma, Ana; Abdusamad, Mai; Rossen, Jordan; Joesch-Cohen, Lena; Humeidi, Ranad; Spangler, Ryan D.; Eaton, John K.; Frenkel, Evgeni; Kocak, Mustafa; Corsello, Steven M.; Lutsenko, Svetlana; Kanarek, Naama; Santagata, Sandro; Golub, Todd R. published the artcile< Copper induces cell death by targeting lipoylated TCA cycle proteins>, COA of Formula: C15H22N2O2, the main research area is copper cell death TCA cycle mitochondrial respiration homeostasis PDHA1.
Copper is an essential cofactor for all organisms, and yet it becomes toxic if concentrations exceed a threshold maintained by evolutionarily conserved homeostatic mechanisms. How excess copper induces cell death, however, is unknown. Here, we show in human cells that copper-dependent, regulated cell death is distinct from known death mechanisms and is dependent on mitochondrial respiration. We show that copper-dependent death occurs by means of direct binding of copper to lipoylated components of the tricarboxylic acid (TCA) cycle. This results in lipoylated protein aggregation and subsequent iron-sulfur cluster protein loss, which leads to proteotoxic stress and ultimately cell death. These findings may explain the need for ancient copper homeostatic mechanisms.
Science (Washington, DC, United States) published new progress about Animal gene Role: BSU (Biological Study, Unclassified), BIOL (Biological Study) (DBT). 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, COA of Formula: C15H22N2O2.
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