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• W2010506957 abstract "Apoptosis has an important role in maintaining tissue homeostasis in cellular stress responses such as inflammation, endoplasmic reticulum stress, and oxidative stress. T-cell death-associated gene 51 (TDAG51) is a member of the pleckstrin homology-like domain family and was first identified as a pro-apoptotic gene in T-cell receptor-mediated cell death. However, its pro-apoptotic function remains controversial. In this study, we investigated the role of TDAG51 in oxidative stress-induced apoptotic cell death in mouse embryonic fibroblasts (MEFs). TDAG51 expression was highly increased by oxidative stress responses. In response to oxidative stress, the production of intracellular reactive oxygen species was significantly enhanced in TDAG51-deficient MEFs, resulting in the activation of caspase-3. Thus, TDAG51 deficiency promotes apoptotic cell death in MEFs, and these results indicate that TDAG51 has a protective role in oxidative stress-induced cell death in MEFs. Researchers in Korea have demonstrated how an enigmatic protein helps cells to survive stressful conditions. Cells produce chemicals known as reactive oxygen species (ROS) over the course of normal metabolism as well as in response to certain environmental triggers. Accumulation of ROS molecules is toxic, however, and can ultimately lead to cell death via a process called apoptosis. Previous studies have yielded findings suggesting that TDAG51 can either promote or prevent apoptosis. Jaerang Rho's group at Chungnam National University showed that the T cell death-associated gene 51 (TDAG51) protein helps to fight cellular stress by reducing ROS levels. They demonstrated that TDAG51-deficient cells produced greater levels of ROS and were more likely to subsequently undergo apoptosis than normal cells under stressful conditions. These results therefore suggest a protective role for TDAG51." @default.
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• W2010506957 date "2013-08-01" @default.
• W2010506957 modified "2023-10-12" @default.
• W2010506957 title "TDAG51 deficiency promotes oxidative stress-induced apoptosis through the generation of reactive oxygen species in mouse embryonic fibroblasts" @default.
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• W2010506957 doi "https://doi.org/10.1038/emm.2013.67" @default.
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