Madi Y. Cissé
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.
Research Associate, Manning Lab, Department of Molecular Metabolism, Harvard T.H. Chan School of Public Health · previously at the Institut de Recherche en Cancérologie de Montpellier (Le Cam and Linares team, per PubMed affiliations)
Portrait: Harvard T.H. Chan School of Public Health (Manning Lab)
Madi Cissé is a co-author on both Manning lab studies that used AKT-resistant TSC2 mice to separate feeding signals. In liver, insulin acts through AKT–TSC2, but the after-meal rise in mTORC1 depends on dietary protein (KAL2026). In muscle, feeding-induced mTORC1 drives postprandial protein synthesis but is not needed to keep muscle size (LAP2026).
Before Harvard he worked at the Institut de Recherche en Cancérologie de Montpellier on p53-independent roles of MDM2 in serine metabolism and mitochondrial respiration (Molecular Cell 2016 and 2018). The Manning lab describes his research as how cancer cells regulate their metabolism through these signalling mechanisms.
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 Co-author: dietary protein, not insulin–AKT–TSC2 signalling, drives postprandial hepatic mTORC1. |
| 2026 | A | Feeding-Induced Muscle mTORC1 Signaling Regulates Postprandial Protein Synthesis and Endurance but Not Muscle Size LAP2026 Co-author: muscle mTORC1 activated by feeding controls postprandial protein synthesis and endurance, not muscle size. |
Co-authors in the Atlas
People with a profile here who share at least one study with Madi Y. Cissé.
- 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
- 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.
- Yann Cormerais 2 shared studies 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.
- 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
Every researcher with a profile →
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