SCFCyclin F controls centrosome homeostasis and mitotic fidelity through CP110 degradation

Vincenzo D’Angiolella, Valerio Donato, Sangeetha Vijayakumar, Anita Saraf, Laurence Florens, Michael P. Washburn, Brian Dynlacht and Michele Pagano ()
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Vincenzo D’Angiolella: NYU Cancer Institute, New York University School of Medicine, 522 First Avenue, SRB 1107, New York, New York 10016, USA
Valerio Donato: NYU Cancer Institute, New York University School of Medicine, 522 First Avenue, SRB 1107, New York, New York 10016, USA
Sangeetha Vijayakumar: NYU Cancer Institute, New York University School of Medicine, 522 First Avenue, SRB 1107, New York, New York 10016, USA
Anita Saraf: The Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA
Laurence Florens: The Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA
Michael P. Washburn: The Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA
Brian Dynlacht: NYU Cancer Institute, New York University School of Medicine, 522 First Avenue, SRB 1107, New York, New York 10016, USA
Michele Pagano: NYU Cancer Institute, New York University School of Medicine, 522 First Avenue, SRB 1107, New York, New York 10016, USA

Nature, 2010, vol. 466, issue 7302, 138-142

Abstract: A role for Cyclin F Cyclin F is the founding member of the F-box protein family but its functions are unknown. In contrast to most cyclins, it does not bind or activate cyclin-dependent kinases (CDKs). Here, a protein essential for centrosome duplication, CP110, is identified as a substrate of Cyclin F. CP110 and Cyclin F associate on centrioles during the cell cycle, and Cyclin F is proposed to limit centrosome duplication by targeting CP110 for degradation.

Date: 2010
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DOI: 10.1038/nature09140

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