Andrew R. Tee
First author of one of several 2003 papers showing that the TSC1–TSC2 complex acts as a GTPase-activating protein for Rheb
Professor of Cancer Cell Biology, Cardiff University (at Cardiff since 2007; Professor since 2019) · independent investigator, University of Dundee (Grahame Hardie lab) · postdoc, Harvard Medical School (John Blenis lab) · PhD, University of Dundee (Christopher G. Proud lab)
Faculty profile, Cardiff University (Cardiff, Wales, United Kingdom) ↗ Lab lineagetrained under John Blenis →
Portrait: Cardiff University
In 2003, as a postdoc in John Blenis's lab working with Lewis Cantley's group, Andrew Tee led one of several independent studies (alongside those from Kun-Liang Guan's, George Thomas's and other groups) showing 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 — a leading AMPK lab — 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.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2002 | M | Tuberous sclerosis complex-1 and -2 gene products function together to inhibit mammalian target of rapamycin (mTOR)-mediated downstream signaling TEE2002 First author: the TSC1–TSC2 complex inhibits mTOR signalling to 4E-BP1 and S6K1, and a patient-derived TSC2 mutant fails to do so. |
| 2002 | M | Identification of the tuberous sclerosis complex-2 tumor suppressor gene product tuberin as a target of the phosphoinositide 3-kinase/akt pathway MAN2002 Co-author of the study identifying tuberin (TSC2) as a direct Akt substrate, tying PI3K–Akt signalling to S6K1 activation. |
| 2003 | M | Tuberous sclerosis complex gene products, Tuberin and Hamartin, control mTOR signaling by acting as a GTPase-activating protein complex toward Rheb TEE2003 Shows TSC1/TSC2 acts as a GAP for Rheb — the mechanism explaining how TSC-complex mutations cause the pathway's overactivation. |
Co-authors in the Atlas 5
People with a profile here who share at least one study with Andrew R. Tee.
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- Brendan D. Manning 3 shared studies Was among the groups that in 2002 identified TSC2 as a direct target of Akt (MAN2002), linking insulin and PI3K signalling to mTORC1, and later found TBC1D7 as the third subunit of the TSC complex. His lab has shown how mTORC1 turns growth signals into the synthesis of lipids and nucleotides
- John Blenis 3 shared studies Showed early on that rapamycin blocks S6 kinase, then worked out how mTORC1 drives cell growth through its two main translation targets, S6K1 and 4E-BP1. His lab also found, in parallel with the Sabatini lab, that mTORC1 phosphorylates Grb10, a feedback brake on insulin signalling
- Lewis C. Cantley 3 shared studies Co-discovered PI3K, the pathway that feeds into mTOR from growth factors
- David J. Kwiatkowski Geneticist and physician who studies tuberous sclerosis complex (TSC) and the TSC1/TSC2 genes that restrain mTORC1.
- Diane C. Fingar Studies how mTORC1 and mTORC2 are regulated, especially through site-specific phosphorylation
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