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• W2016695100 abstract "Reactive oxygen species (ROS) produced by tumor necrosis factor-alpha (TNF-alpha) have an important function in cell death by activating c-Jun N-terminal kinase. However, the exact mechanism of mitochondrial ROS production, after TNF-alpha stimulation, is not clearly understood. In this study, we determined that ROS modulator 1 (Romo1) and B-cell lymphoma-extra large (Bcl-X(L)) are directly associated with TNF-alpha-induced ROS production. In response to TNF-alpha, TNF complex II, which consists of receptor-interacting protein 1, TNF receptor-associated protein with death domain, TNF receptor-associated factor 2, Fas-associated death domain protein, and pro-caspase-8, binds to the C-terminus of Romo1 located in the mitochondria. Concurrently, Romo1 recruits Bcl-X(L) to reduce the mitochondrial membrane potential, resulting in ROS production and apoptotic cell death. On the basis of these results, we suggest that Romo1 is a molecular bridge between TNF-alpha signaling and the mitochondria for ROS production that triggers TNF-alpha-mediated apoptosis, as well as a novel target in the development of anti-inflammatory agents that block the origin of ROS production." @default.
• W2016695100 created "2016-06-24" @default.
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• W2016695100 date "2010-03-05" @default.
• W2016695100 modified "2023-10-16" @default.
• W2016695100 title "TNF-α-induced ROS production triggering apoptosis is directly linked to Romo1 and Bcl-XL" @default.
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• W2016695100 doi "https://doi.org/10.1038/cdd.2010.19" @default.
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