Deficiency in the membrane protein Tmbim3a/Grinaa initiates cold-induced ER stress and cell death by activating an intrinsic apoptotic pathway in zebrafish.

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第一作者： Kai,Chen

第一单位： State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Hubei, Wuhan 430072, China.

作者： Kai,Chen ^[1] ; Xixi,Li ^[2] ; Guili,Song ^[1] ; Tong,Zhou ^[2] ; Yong,Long ^[1] ; Qing,Li ^[1] ; Shan,Zhong ^[2] ; Zongbin,Cui ^[1]

作者单位： State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Hubei, Wuhan 430072, China. ^[1] University of Chinese Academy of Sciences, Beijing 100049, China. ^[2] Department of Genetics, Wuhan University, Wuhan, Hubei 430071, China. ^[3] State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Hubei, Wuhan 430072, China zbcui@ihb.ac.cn. ^[4] Innovative Academy of Seed Design, Chinese Academy of Sciences, Beijing 100101, China. ^[5]

关键词 Grinaa apoptosis calcium homeostasis calcium intracellular release cell death cold exposure endoplasmic reticulum stress endoplasmic reticulum stress (ER stress)stress response transmembrane BAX inhibitor motif (TMBIM)unfolded protein response (UPR)zebrafish