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NTIS 바로가기Cell death & disease, v.8 no.12, 2017년, pp.3218 -
Nishi, Kensuke (Department of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, 814-0180 Japan) , Iwaihara, Yuri (Department of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, 814-0180 Japan) , Tsunoda, Toshiyuki (Department of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, 814-0180 Japan) , Doi, Keiko (Department of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, 814-0180 Japan) , Sakata, Toshifumi (Department of Otorhinolaryngology, Faculty of Medicine, Fukuoka University, Fukuoka, 814-0180 Japan) , Shirasawa, Senji (Department of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, 814-0180 Japan) , Ishikura, Shuhei (Department of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, 814-0180 Japan)
Excess production of reactive oxygen species (ROS) is known to cause apoptotic cell death. However, the molecular mechanisms whereby ROS induce apoptosis remain elusive. Here we show that the NHL-repeat-containing protein 2 (NHLRC2) thioredoxin-like domain protein is cleaved by caspase-8 in ROS-indu...
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