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논문 기본 정보

자료유형
학술저널
저자정보
Im, Chang-Nim (Department of Biochemistry and Molecular Biology, College of Medicine, Seoul National University) Zheng, Ying (Department of Biochemistry and Molecular Biology, College of Medicine, Seoul National University) Kim, Sun Hye (Department of Biochemistry and Molecular Biology, College of Medicine, Seoul National University) Huang, Tai-Qin (Department of Biochemistry and Molecular Biology, College of Medicine, Seoul National University) Cho, Du-Hyong (Department of Neurology, Konkuk University Medical Center, Konkuk University) Seo, Jeong-Sun (Department of Biochemistry and Molecular Biology, College of Medicine, Seoul National University)
저널정보
한국생물정보시스템생물학회 Interdisciplinary Bio Central Interdisciplinary Bio Central 제5권 제4호
발행연도
2013.1
수록면
91 - 97 (7page)

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Introduction: Tumor necrosis factor receptor-associated protein 1 (TRAP1) is a mitochondrial heat shock protein (HSP), which belongs to HSP90 family. It plays important roles in regulating mitochondrial integrity, protecting against oxidative stress, and inhibiting cell death. Recent studies suggest that TRAP1 is linked to mitochondria and its metabolism. In this study, we established TRAP1 transgenic mice and performed partial hepatectomy (PH) on wild-type (WT) and TRAP1 transgenic mice to investigate the function of TRAP1 during liver regeneration. Results and Discussion: We found that TRAP1 was highly expressed in liver as well as kidney. In addition, liver regeneration slightly decreased together with increased fatty liver and inflammation at 72 hr after PH in TRAP1 transgenic mice compared with WT control group mice. Concomitantly, we observed decreased levels of p38 protein in TRAP1 transgenic mice compared with WT control group mice. These results suggest that TRAP1 plays a critical role in liver energy balance by regulating lipid accumulation during liver regeneration. Conclusions and Prospects: To our knowledge, we reported, for the first time, that liver regeneration slightly reduced together with increased fat accumulations after PH in TRAP1 transgenic mice compared with WT control group mice. Concomitantly, we observed decreased levels of p38 protein in TRAP1 transgenic mice compared with WT control group mice. Overexpression of TRAP1 might affect liver regeneration via disturbing mitochondrial function leading to fatty liver in vivo.

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