Raffaele Nicastro
Cell biologist at the University of Fribourg who studies TORC1 signalling in yeast and mammals, and first author of the discovery that malonyl-CoA is a natural mTORC1 inhibitor
Department of Biology, University of Fribourg (papers 2016–2026, many with Claudio De Virgilio) · earlier papers with an affiliation in Milan, Italy (2014–2015)
Raffaele Nicastro is the first author of NIC2023, a Nature Cell Biology paper by groups at the University of Fribourg and Constantinos Demetriades's lab. mTOR is a kinase, an enzyme that uses ATP to tag other proteins. The study found that malonyl-CoA, a small molecule made on the way to building fatty acids, fits directly into the mTOR catalytic pocket and competes with ATP. It works like a natural version of the ATP-competitive mTOR drugs. When the fat-making enzyme fatty acid synthase is turned down, malonyl-CoA builds up and dampens mTORC1. This ties the cell's capacity to make fat to its overall growth output. The effect was seen in yeast and mammalian cells, which is why the paper calls it conserved.
Nicastro's PubMed record shows many papers from the University of Fribourg between 2016 and 2026 many of them with Claudio De Virgilio, whose group studies how TORC1 is controlled in yeast. Papers from 2014 and 2015 list an affiliation in Milan, Italy. No official profile was found, so the position shown is the affiliation 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 |
|---|---|---|
| 2023 | M | Malonyl-CoA is a conserved endogenous ATP-competitive mTORC1 inhibitor NIC2023 First author: showed that malonyl-CoA binds the mTOR catalytic pocket and acts as a conserved, ATP-competitive inhibitor of mTORC1. |
Co-authors in the Atlas 8
People with a profile here who share at least one study with Raffaele Nicastro.
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- Aurelio A. Teleman Uses fruit-fly genetics and human cells to study how growth signalling through TOR controls cell and body size. His lab showed that starvation and other stresses move TSC2 to the lysosome to switch mTORC1 off
- Claudio De Virgilio Yeast geneticist whose lab found the EGO/Rag GTPase complex that activates TORC1 and showed that the SEACIT complex (Iml1–Npr2–Npr3) switches TORC1 off by acting as a GAP for the Rag GTPase Gtr1.
- Constantinos Demetriades Showed as a postdoc in Aurelio Teleman's lab that starvation and other stresses pull TSC2 to the lysosome to switch mTORC1 off. His group, at the Max Planck Institute for Biology of Ageing in Cologne from 2017 and at ERIBA in Groningen since 2025, studies how cells sense nutrients and stress through mTORC1 and how this changes with age
- Gianluca Figlia Cell biologist who studied how mTORC1 senses nutrients in Aurelio Teleman's group at the German Cancer Research Center, including the finding that glutamine is sensed through the kinase GCN2, and who now works at the Institute of Neuropathology in Aachen
- Julian Nüchel Co-author on two Demetriades-lab mTORC1 papers from Cologne: the spatial split of mTORC1 signalling by amino acid source and malonyl-CoA as a direct mTORC1 inhibitor.
- Laura Brohée Cell biologist who studied how lipid metabolism and the lysosome feed into mTORC1, first at the University of Liège and then at the Max Planck Institute for Biology of Ageing in Cologne
- Peter Gollwitzer First author of the 'Rag dimer code' study showing that the four Rag GTPase paralogues are not interchangeable: RagC/D sets substrate choice and RagA/B sets the response to amino acid withdrawal.
- Stephanie A. Fernandes First author of the study showing that lysosomal and cytoplasmic pools of mTORC1 respond to different amino acid sources and phosphorylate different substrates.
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