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Thrap3 promotes nonalcoholic fatty liver disease by suppressing AMPK-mediated autophagy
Jang Hyun-Jun,Lee Yo Han,Dao Tam,Jo Yunju,Khim Keon Woo,Eom Hye-jin,Lee Ju Eun,Song Yi Jin,Choi Sun Sil,Park Kieun,Ji Haneul,Chae Young Chan,Myung Kyungjae,Kim Hongtae,Ryu Dongryeol,Park Neung Hwa,Par 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Autophagy functions in cellular quality control and metabolic regulation. Dysregulation of autophagy is one of the major pathogenic factors contributing to the progression of nonalcoholic fatty liver disease (NAFLD). Autophagy is involved in the breakdown of intracellular lipids and the maintenance of healthy mitochondria in NAFLD. However, the mechanisms underlying autophagy dysregulation in NAFLD remain unclear. Here, we demonstrate that the hepatic expression level of Thrap3 was significantly increased in NAFLD conditions. Liver-specific Thrap3 knockout improved lipid accumulation and metabolic properties in a high-fat diet (HFD)-induced NAFLD model. Furthermore, Thrap3 deficiency enhanced autophagy and mitochondrial function. Interestingly, Thrap3 knockout increased the cytosolic translocation of AMPK from the nucleus and enhanced its activation through physical interaction. The translocation of AMPK was regulated by direct binding with AMPK and the C-terminal domain of Thrap3. Our results indicate a role for Thrap3 in NAFLD progression and suggest that Thrap3 is a potential target for NAFLD treatment.
Precision Targeting Tumor Cells Using Cancer-specific InDel Mutations with CRISPR-Cas9
Taejoon Kwon,Jae Sun Ra,Soyoung Lee,In-Joon Baek,Keon Woo Khim,Eun A Lee,Eun Kyung Song,Daniyar Otarbayev,Woojae Jung,Yong Hwan Park,Minwoo Wie,Juyoung Bae,Himchan Cheng,Jun Hong Park,Namwoo Kim,Yuri 한국고분자학회 2024 한국고분자학회 학술대회 연구논문 초록집 Vol.49 No.1