Human homologue of S. pombe Rad9 interacts with BCL-2/BCL-X(L) and promotes apoptosis

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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123 Scopus citations


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 antiapoptotic Bcl-2-family proteins BCL-2 and BCL-x(L), 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-x(L). 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.

Original languageEnglish (US)
Pages (from-to)1-6
Number of pages6
JournalNature Cell Biology
Issue number1
StatePublished - 2000

All Science Journal Classification (ASJC) codes

  • Cell Biology


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