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Transglutaminase 2 regulates redox homeostasis by inhibiting NRF2 degradation in keratinocytes : NRF2 degradation 억제를 통한 트랜스글루타미네이즈 2의 레독스 항상성 조절
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- Authors
- Advisor
- 김인규
- Major
- 의과대학 의과학과
- Issue Date
- 2018-02
- Publisher
- 서울대학교 대학원
- Keywords
- Transglutaminase 2 ; Reactive oxygen species ; Glutathione ; Nrf2
- Description
- 학위논문 (석사)-- 서울대학교 대학원 : 의과대학 의과학과, 2018. 2. 김인규.
- Abstract
- Unbalanced antioxidant homeostasis results in overproduction of reactive oxygen species (ROS) triggering cellular damage and apoptosis. We have reported that Transglutaminase 2 (TG2) is activated by ROS, and TG2 has an anti-apoptotic effect against ROS. However, the molecular mechanism of TG2 in redox regulation is unknown. To examine whether TG2 is required for antioxidative defense system, we established a TG2 deficient keratinocyte HaCaT cell lines and tested the effects upon ROS homeostasis. As a result, TG2 deficient HaCaT cells exposed to tert-butyl hydroperoxide (tBHP), showed high levels of intracellular ROS. In addition, TG2 deficient HaCaT cells showed reduced total GSH levels, a GSH reduction capacity, and reduced protein levels of its glutamate cysteine ligase catalytic subunit (Gclc) that was caused by increased proteasomal degradation of Nuclear factor-erythroid 2 p45-related factor 2 (Nrf2). Collectively, our observations indicate that TG2 in keratinocytes increases antioxidative signaling pathways and its ability to regulate redox homeostasis. This suggests that TG2 may function to ensure cell survival under oxidative stress conditions.
- Language
- English
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