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450 West Drive
Chapel Hill, NC

University of North Carolina, Chapel Hill

The Emanuele Lab studies cell cycle regulation using systematic technologies and traditional cell, molecular and biochemical techniques.

News & Pics

Pomp and Circumstance for Allie Mills

Michael Emanuele

Allie attended the UNC Grad School Graduation Ceremony on Saturday May 12, 2018 in the Dean Smith Center. Also, it was Mike's first "hooding ceremony", evident in the poor job he did trying to "hood" Allie on stage! Congrats again Allie.

 Allie Mills and Mike Emanuele, UNC Graduation, May 2018

Allie Mills and Mike Emanuele, UNC Graduation, May 2018

Congrats Dr. Allie Mills!!

Michael Emanuele

Today was a big day in the lab. Our first graduate student, Allie Mills, successfully defended her dissertation to the Department of Pharmacology. She delivered a fantastic seminar to all of those in attendance. Congrats Allie and great job. 

 Allie and Mike, post-defense

Allie and Mike, post-defense

Congrats Raj!!

Michael Emanuele

Congratulations to Raj Choudhury on winning the UNC Lineberger Cancer Center Pagano Award in recognition of your paper describing a ubiquitin signaling circuit involved in regulation cell cycle entry. Read Raj's paper here.


 

 

Great job Raj on your new paper out in Cell Reports!

Michael Emanuele

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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Great work Xianxi on your paper out in MCB!

Michael Emanuele

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.

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