Author: ["Kiyoshi Komatsu","Toshiyuki Miyashita","Haiying Hang","Kevin M. Hopkins","Wei Zheng","Sandy Cuddeback","Masao Yamada","Howard B. Lieberman","Hong-Gang Wang"]
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Abstract
DNA damage induces apoptosis through a signalling pathway that can be suppressed by the BCL-2 protein, but the mechanism by which DNA damage does this is unknown. Here, using yeast two-hybrid and co-immunoprecipitation studies, we show that RAD9, a human protein involved in the control of a cell-cycle checkpoint, interacts with the anti-apoptotic Bcl-2-family proteins BCL-2 and BCL-xL, but not with the pro-apoptotic BAX and BAD. When overexpressed in mammalian cells, RAD9 induces apoptosis that can be blocked by BCL-2 or BCL-xL. Conversely, antisense RAD9 RNA suppresses cell death induced by methyl methanesulphonate. These findings indicate that RAD9 may have a new role in regulating apoptosis after DNA damage, in addition to its previously described checkpoint-control and other radioresistance-promoting functions. Cite this article
Komatsu, K., Miyashita, T., Hang, H. et al. Human homologue of S. pombe Rad9 interacts with BCL-2/BCL-xL and promotes apoptosis. Nat Cell Biol 2, 1–6 (2000). https://doi.org/10.1038/71316 