Ku70 suppresses the apoptotic translocation of bax to mitochondria

Motoshi Sawada, Weiyong Sun, Paulette Hayes, Konstantin Leskov, David A. Boothman, Shigemi Matsuyama

Research output: Contribution to journalArticlepeer-review

319 Scopus citations


Bax induces mitochondrial-dependent cell death signals in mammalian cells. However, the mechanism of how Bax is kept inactive has remained unclear. Yeast-based functional screening of Bax inhibitors from mammalian cDNA libraries identified Ku70 as a new Bax suppressor. Bax-mediated apoptosis was suppressed by overexpression of Ku70 in mammalian cells, but enhanced by downregulation of Ku70. We found that Ku70 interacts with Bax, and that the carboxyl terminus of Ku70 and the amino terminus of Bax are required for this interaction. Bax is known to translocate from the cytosol to mitochondria when cells receive apoptotic stimuli. We found that Ku70 blocks the mitochondrial translocation of Bax. These results suggest that in addition to its previously recognized DNA repair activity in the nucleus, Ku70 has a cytoprotective function in the cytosol that controls the localization of Bax.

Original languageEnglish (US)
Pages (from-to)320-329
Number of pages10
JournalNature cell biology
Issue number4
StatePublished - Apr 1 2003

ASJC Scopus subject areas

  • Cell Biology


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