Oliver's mTOR Atlas Evidence Platform
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Steven D. Cappell

Studies how single cells commit to dividing; showed that mTOR briefly switches off the APC/C to give cells a pulse of glycolysis at cell cycle entry

Stadtman Investigator, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute · PhD, University of North Carolina at Chapel Hill

Cappell Lab, Laboratory of Cancer Biology and Genetics, NCI (Bethesda, Maryland, USA) ↗

Steven D. Cappell Portrait: NIH Intramural Research Program

Steven Cappell did his PhD at the University of North Carolina at Chapel Hill in the lab of Henrik Dohlman and was a Damon Runyon postdoctoral fellow with Tobias Meyer at Stanford University. He joined the National Cancer Institute in 2017, where his lab studies how individual cells decide to enter the cell cycle.

In 2025 his group showed that, right after growth-factor stimulation, mTOR phosphorylates CDH1 and briefly inactivates the APC/C, letting the glycolytic enzyme PFKFB3 build up until a slower phosphatase restores APC/C activity. The result is a short, timed pulse of glycolysis that cells need to enter the cycle — a case where the timing of an mTOR-driven signal, not only its size, does the work.

Milestones in the Atlas

YearEvidenceStudy
2025 M Transient APC/C inactivation by mTOR boosts glycolysis during cell cycle entry PAU2025 Senior author: transient mTOR-driven APC/C inactivation creates the pulse of glycolysis required for cell cycle entry.

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