Survivin enhances Aurora-B kinase activity and localizes Aurora-B in human cells

被引:110
作者
Chen, J [1 ]
Jin, S [1 ]
Tahir, SK [1 ]
Zhang, HC [1 ]
Liu, XS [1 ]
Sarthy, AV [1 ]
McGonigal, TP [1 ]
Liu, ZH [1 ]
Rosenberg, SH [1 ]
Ng, SC [1 ]
机构
[1] Abbott Labs, Canc Res, Abbott Pk, IL 60064 USA
关键词
D O I
10.1074/jbc.M211119200
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Survivin, one of the most tumor-specific gene products, has been implicated in both anti-apoptosis and cytokinesis. However, the mechanism by which survivin regulates these two different processes is still elusive. Here, we show that survivin binds to the catalytic domain of Aurora-B. We demonstrate that in the presence of survivin, Aurora-B phosphorylates histone H3 much more efficiently than in the absence of survivin in a cell-free system. Furthermore, we confirm that cells lacking survivin due to survivin antisense oligonucleotide-treatment have lower Aurora-B kinase activity, whereas cells overexpressing survivin have higher Aurora-B kinase activity. We also provide evidence that depletion of survivin by survivin antisense oligonucleotide treatment causes significant reduction of endogenous phosphorylated histone H3 and mislocalization of Aurora-B. These results indicate that survivin stimulates Aurora-B kinase activity and helps correctly target Aurora-B to its substrates during the cell cycle, thus providing a mechanism as to how survivin exerts its function in human cells.
引用
收藏
页码:486 / 490
页数:5
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