Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2052689 | FEBS Letters | 2005 | 7 Pages |
Abstract
We investigated why treatment of cells with dual aurora A and B kinase inhibitors produces phenotypes identical to inactivation of aurora B. We found that dual aurora kinase inhibitors in fact potently inhibit cellular activities of both kinases, indicating that inactivation of aurora B bypasses aurora A in mitosis. RNAi experiments further established that inactivation of aurora B indeed bypasses the requirement for aurora A and leads to polyploidy. Inactivation of aurora A activates checkpoint kinase BubR1 in an aurora B-dependent manner. Our results thus show that aurora B is responsible for mitotic arrest in the absence of aurora A.
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Authors
Hui Yang, Teresa Burke, Jack Dempsey, Bruce Diaz, Elizabeth Collins, John Toth, Richard Beckmann, Xiang Ye,