Cdc20 turnover rate: A key determinant in cancer patient response to anti-mitotic therapies?

BioEssays

Volumn 35, Issue 9, 2013, Pages 762-762

  Fry, Andrew M ^a  

^a UNIVERSITY OF LEICESTER   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

ANTINEOPLASTIC AGENT; CELL CYCLE PROTEIN 20; CYCLIN B;

ARTICLE; CANCER PATIENT; HUMAN; M PHASE CELL CYCLE CHECKPOINT; MITOSIS; TREATMENT RESPONSE;

APOPTOSIS; CDC20 PROTEINS; CELL CYCLE CHECKPOINTS; HUMANS; MITOSIS; NEOPLASMS;

EID: 84881611353     PISSN: 02659247     EISSN: 15211878     Source Type: Journal    
DOI: 10.1002/bies.201300053     Document Type: Article

References (4)

1. Nilsson J. 2011. Cdc20 control of cell fate during prolonged mitotic arrest: Do Cdc20 protein levels affect cell fate in response to antimitotic compounds? BioEssays 33: 903-9.
2. Mansfield J, Collin P, Collins MO, Choudhary JS, et al. 2011. APC15 drives the turnover of MCC-CDC20 to make the spindle assembly checkpoint responsive to kinetochore attachment. Nat Cell Biol 13: 1234-43.
3. Uzunova K, Dye BT, Schutz H, Ladurner R, et al. 2012. APC15 mediates CDC20 autoubiquitylation by APC/C(MCC) and disassembly of the mitotic checkpoint complex. Nat Struct Mol Biol 19: 1116-23.
4. Foster SA, Morgan DO. 2012. The APC/C subunit Mnd2/Apc15 promotes Cdc20 autoubiquitination and spindle assembly checkpoint inactivation. Mol Cell 47: 921-32.