Yann Cormerais
Research scientist in the Manning lab who works on how PI3K–AKT–TSC2 signalling controls mTORC1 in living tissues, using mouse models in which TSC2 cannot be phosphorylated by AKT.
Research Scientist, Manning Lab, Department of Molecular Metabolism, Harvard T.H. Chan School of Public Health · PhD, Université de Nice (Nathalie Mazure and Jacques Pouysségur, 2016)
Portrait: Harvard T.H. Chan School of Public Health (Manning Lab)
Yann Cormerais is second author on the liver study showing that insulin activates hepatic mTORC1 mainly through AKT phosphorylation of TSC2, but that the rise in mTORC1 after a meal depends on dietary protein (KAL2026). He is also a co-author on the companion muscle study, where the same TSC2 phospho-mutant blocked feeding-induced mTORC1 and protein synthesis without shrinking muscle (LAP2026). He was first author of the 2024 preprint that introduced the TSC2-5A mouse used in both studies.
His PhD thesis at the Université de Nice (2016), supervised by Nathalie Mazure and Jacques Pouysségur, studied the amino acid transporter LAT1 as a requirement for mTORC1 activity and tumor growth. In the Manning lab his stated interest is the in vivo role of PI3K–mTORC1 signalling in mammalian growth and metabolism.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2026 | A | Dietary protein governs the role of insulin signaling in the postprandial regulation of hepatic mTORC1. KAL2026 Second author: AKT–TSC2 phosphorylation drives insulin-induced hepatic mTORC1, but feeding-induced activation needs dietary protein. |
| 2026 | A | Feeding-Induced Muscle mTORC1 Signaling Regulates Postprandial Protein Synthesis and Endurance but Not Muscle Size LAP2026 Co-author: feeding-induced muscle mTORC1 drives postprandial protein synthesis but is not needed for muscle size. |
Co-authors in the Atlas
People with a profile here who share at least one study with Yann Cormerais.
- Brendan D. Manning 2 shared studies Was among the groups that in 2002 identified TSC2 as a direct target of Akt, 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
- Karen E. Inouye 2 shared studies Metabolic physiologist who runs the Hotamışlıgil lab’s physiology facility, which specialises in glucose clamps, and co-authored two 2026 mouse studies on how feeding controls mTORC1 in liver and muscle.
- Krystle C. Kalafut 2 shared studies Hepatic mTORC1 and nutrient signalling
- Madi Y. Cissé 2 shared studies Research associate in the Manning lab and co-author on the two 2026 mouse studies showing which feeding signals switch on mTORC1 in liver and in skeletal muscle.
- Samuel C. Lapp 2 shared studies First author of the muscle study showing that feeding-induced mTORC1 activation through AKT–TSC2 drives postprandial protein synthesis but is not needed to build or keep muscle mass.
- Gökhan S. Hotamışlıgil Leads a Harvard laboratory on metabolic disease and was elected to the US National Academy of Sciences in 2026 for achievements in metabolic research
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