Attila Garami
First author of the 2003 study, from George Thomas's group at the Friedrich Miescher Institute, showing that insulin switches on Rheb and that the TSC1-TSC2 complex switches it off
Friedrich Miescher Institute for Biomedical Research, Basel (at the time of the study, 2003)
Attila Garami was first author of a 2003 Molecular Cell paper (GAR2003) that helped fix the order of steps above mTOR. Rheb is a small GTPase, a molecular switch that is on when it holds GTP and off when it holds GDP. The study showed that insulin raises the amount of active, GTP-loaded Rheb. The tumour-suppressor proteins TSC1 and TSC2 work together as Rheb's GAP, an enzyme that makes Rheb burn its GTP and so turns it off. Active Rheb in turn drives the signals that mTOR sends to S6K and 4E-BP, the proteins that boost protein synthesis.
Put together, this placed Rheb directly upstream of mTOR and directly downstream of TSC1-TSC2. It explained why losing TSC1 or TSC2, as in the disease tuberous sclerosis complex, leaves mTOR stuck on. The work used cultured cells and fruit-fly genetics.
The paper came from the Friedrich Miescher Institute in Basel, where Garami worked in George Thomas's group. A current position could not be confirmed from an official source, so the affiliation shown is the one on the Atlas paper.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2003 | M | Insulin activation of Rheb, a mediator of mTOR/S6K/4E-BP signaling, is inhibited by TSC1 and 2 GAR2003 First author: showed that insulin activates Rheb and that TSC1-TSC2 acts as Rheb's off-switch, placing Rheb directly upstream of mTOR. |
Co-authors in the Atlas 5
People with a profile here who share at least one study with Attila Garami.
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- Ernst Hafen Developmental geneticist who used Drosophila to work out how insulin and TOR signalling control cell and body size, including the role of Rheb.
- George Thomas Purified and cloned S6K1, the kinase that became the classic readout of mTORC1 activity. His lab later showed that mice lacking S6K1 resist diet-induced obesity, and that amino acids signal to mTORC1 through the lipid kinase hVps34 (GUL2008)
- Johannes L. (Hans) Bos Cancer biologist known for work on Ras mutations and for the small GTPase Rap1 and its activator Epac, a cAMP-regulated switch for cell adhesion
- Sara C. Kozma Studies the S6K/mTOR pathway and how it controls cell growth, ribosome production, diabetes and cancer, including mTOR signalling in liver cancer.
- Takahiro Nobukuni Showed as first author that amino acids activate mTOR through the lipid kinase hVps34, by a route separate from insulin signalling through TSC, in parallel with a study from Jonathan Backer's laboratory
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