Andrew R. Tee

Co-discovered that the TSC1–TSC2 complex acts as a GTPase-activating protein for Rheb

PhD, University of Dundee (Christopher G. Proud lab) · postdoc, Harvard Medical School (John Blenis lab) · independent investigator, University of Dundee (Grahame Hardie lab) · Professor of Cancer Cell Biology, Cardiff University (since 2007)

Faculty profile, Cardiff University ↗

Portrait: Cardiff University

In 2003, Andrew Tee's group and Kun-Liang Guan's group, working independently, showed that the TSC1–TSC2 complex acts directly as a GTPase-activating protein (GAP) for the small GTPase Rheb — the physical mechanism that explains why mutations in TSC1 or TSC2, which cause the genetic disorder Tuberous Sclerosis Complex, lead to unchecked mTORC1 activity and the disease's characteristic benign tumours.

Tee trained with Christopher Proud at Dundee on translational control, then did postdoctoral work with John Blenis at Harvard, before returning to Dundee as an independent investigator in Grahame Hardie's lab — the lab that discovered AMPK — placing him at the intersection of two of the pathway's foundational research groups before he established his own lab at Cardiff University in 2007.

His Cardiff group continues to use inherited tumour-suppressor syndromes — TSC, Birt-Hogg-Dubé, Cowden syndrome — as natural models for dissecting mTOR signalling in cancer, alongside advisory roles for several Tuberous Sclerosis and LAM patient foundations.

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