A long standing question is how the oncogenic kinase AKT promotes cell cycle progression. This study shows that Cyclin F, a non-canonical Cyclin, and substrate receptor for the SCF family of ubiquitin ligases, is a bona fide AKT substrate. This connects oncogenic AKT signaling, which is recurrently activated in many cancers, to control of the core cell cycle oscillator. This study was a collaboration with out colleagues at UNC in the Liu lab. Read about it here
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This paper describes a paradoxical relationship between the cell cycle transcription factor FoxM1 and a Cul4-based ubiquitin ligase. FoxM1 is recurrently activated in aggressive breast and ovarian cancers, and this study shows that VprBP, a substrate receptor for Cul4, controls both the degradation and activation of FoxM1. Moreover, we showed that VprBP is overexpressed in high-grade serous ovarian tumors, potentially contributing to FoxM1 activation in malignancy. This study was a collaborative efforts with our colleauges at UNC, in the Bowers and Bae-Jump labs. Read more here.
Raj just accepted a position at Glaxo-Smith Kline in the Philadelphia area. We will miss you. Good luck. Enjoy the cheesesteaks and pretzels!
This paper describes a feedback circuit that controls cell cycle entry. It centers on two crucial cell cycle ubiquitin ligases, the SCF and APC/C and shows that they coordinately control each other during progression through the cell cycle. Read more here