Journal
CELL REPORTS
Volume 24, Issue 13, Pages 3404-3412Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.08.076
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Funding
- Medical Research Council (MRC) [MC_UU_00001/7]
- NIH [R01-CA076584, R01-GM057587]
- Cancer Research UK (CRUK) through the Cancer Research UK Oxford Centre [C5255/A18085]
- John Fell grant [133/075]
- Wellcome Trust [097813/Z/11/Z]
- Royal Dutch Academy of Arts and Sciences (KNAW)
- Dutch Cancer Society (KWF) [HUBR 2014-6806]
- MRC [MC_UU_00001/7] Funding Source: UKRI
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Orderly progressions of events in the cell division cycle are necessary to ensure the replication of DNA and cell division. Checkpoint systems allow the accurate execution of each cell-cycle phase. The precise regulation of the levels of cyclin proteins is fundamental to coordinate cell division with checkpoints, avoiding genome instability. Cyclin F has important functions in regulating the cell cycle during the G2 checkpoint; however, the mechanisms underlying the regulation of cyclin F are poorly understood. Here, we observe that cyclin F is regulated by proteolysis through beta-TrCP. beta-TrCP recognizes cyclin F through a non-canonical degron site (TSGXXS) after its phosphorylation by casein kinase II. The degradation of cyclin F mediated by beta-TrCP occurs at the G2/M transition. This event is required to promote mitotic progression and favors the activation of a transcriptional program required for mitosis.
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