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Catalytic Assembly of the Mitotic Checkpoint Inhibitor BubR1-Cdc20 by a Mad2-Induced Functional Switch in Cdc20.

Mol Cell.. 2013-07;  51(1):92-104
Han JS, Holland AJ, Fachinetti D, Kulukian A, Cetin B, Cleveland DW. 1 Ludwig Institute for Cancer Research, University of California at San Diego, La Jolla, CA 92093, USA2 Department of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, CA 92093, USA3 Department of Biology, University of California at San Diego, La Jolla, CA 92093, USA4 Laboratory of Mammalian Cell Biology and Development, The Rockefeller University, New York, NY 10065, USA
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摘要

SummaryThe mitotic checkpoint acts to maintain chromosome content by generation of a diffusible anaphase inhibitor. Unattached kinetochores catalyze a conformational shift in Mad2, converting an inactive open form into a closed form that can capture Cdc20, the mitotic activator of the APC/C ubiquitin ligase. Mad2 binding is now shown to promote a functional switch in Cdc20, exposing a previously inaccessible site for binding to BubR1’s conserved Mad3 homology domain. BubR1, but not Mad2, binding to APC/CCdc20 is demonstrated to inhibit ubiquitination of cyclin B. Closed Mad2 is further shown to catalytically amplify production of BubR1-Cdc20 without necessarily being part of the complex. Thus, the mi... More

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