Human homologue of S. pombe Rad9 interacts with BCL-2/BCL-xL and promotes apoptosis.

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-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.
Mesh Terms:
Animals, Apoptosis, Cell Cycle Proteins, Cell Nucleus, Cell Survival, Flow Cytometry, Humans, Indicators and Reagents, Mammals, Molecular Sequence Data, Plasmids, Propidium, Proto-Oncogene Proteins c-bcl-2, RNA, Antisense, Schizosaccharomyces, Sequence Homology, Amino Acid, Signal Transduction, Transfection, Two-Hybrid System Techniques, bcl-X Protein
Nat. Cell Biol.
Date: Jan. 01, 2000
Download Curated Data For This Publication
4858
Switch View:
  • Interactions 9