TNF-alpha- induced ROS production triggering apoptosis is directly linked to Romo1 and Bcl-X-L
- Authors
- Kim, J. J.; Lee, S. B.; Park, J. K.; Yoo, Y. D.
- Issue Date
- 9월-2010
- Publisher
- NATURE PUBLISHING GROUP
- Keywords
- TNF-alpha; ROS; apoptosis; mitochondria; Romo1; Bcl-X-L
- Citation
- CELL DEATH AND DIFFERENTIATION, v.17, no.9, pp.1420 - 1434
- Indexed
- SCIE
SCOPUS
- Journal Title
- CELL DEATH AND DIFFERENTIATION
- Volume
- 17
- Number
- 9
- Start Page
- 1420
- End Page
- 1434
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/115791
- DOI
- 10.1038/cdd.2010.19
- ISSN
- 1350-9047
- Abstract
- Reactive oxygen species (ROS) produced by tumor necrosis factor-a (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. Cell Death and Differentiation (2010) 17, 1420-1434; doi:10.1038/cdd.2010.19; published online 5 March 2010
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