RETRACTED: Ku70 suppresses the apoptotic translocation of Bax to mitochondria (Retracted article. See vol 9, pg 480, 2007)

被引:294
作者
Sawada, M
Sun, WY
Hayes, P
Leskov, K
Boothman, DA
Matsuyama, S
机构
[1] Blood Ctr SE Wisconsin Inc, Blood Res Inst, Milwaukee, WI 53226 USA
[2] Med Coll Wisconsin, Dept Biochem, Milwaukee, WI 53226 USA
[3] Case Western Reserve Univ, Dept Radiat Oncol, Cleveland, OH 44106 USA
[4] Case Western Reserve Univ, Dept Pharmacol, Cleveland, OH 44106 USA
[5] Univ Hosp Cleveland, Cleveland, OH 44106 USA
关键词
D O I
10.1038/ncb950
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:320 / 329
页数:10
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