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Cell 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)
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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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