TDAG51 deficiency promotes oxidative stress-induced apoptosis through the generation of reactive oxygen species in mouse embryonic fibroblasts |
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Authors: | Eui-Soon Park Juhyeok Kim Tae-uk Ha Jong-Soon Choi Kwan Soo Hong Jaerang Rho |
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Affiliation: | 1.Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon, Korea;2.Division of Life Science, Korea Basic Science Institute, Daejeon, Korea;3.Graduate School of Analytical Science and Technology, Chungnam National University, Daejeon, Korea;4.Division of MR Research, Korea Basic Science Institute, Daejeon, Korea |
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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. |
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Keywords: | apoptosis oxidative stress ROS TDAG51 |
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