Shomit Sengupta
Showed that mTORC1 controls whether the liver makes ketone bodies during fasting, and now leads biology for drug discovery at a metabolic-disease biotech
SVP, Head of Biology, Atavistik Bio · Associate Director, Agios · Lead Biologist, Navitor Pharmaceuticals · Broad Institute CDoT · Catabasis Pharmaceuticals · postdoc, Brugge Lab, Harvard Medical School · PhD, Whitehead/MIT (Sabatini Lab)
Atavistik Bio (Boston, Massachusetts, USA) ↗ Lab lineagetrained under David M. Sabatini →
Portrait: Atavistik Bio
Showed (SEN2010) that during fasting the liver must switch mTORC1 off to make ketones — losing TSC1 locked the pathway on and blocked ketogenesis via PPARα/NCoR1; aged livers show chronically elevated mTORC1 and a similar ketogenesis defect.
Moved through Catabasis, Broad CDoT, Navitor (built on Sabatini-lab amino-acid-sensing biology), Agios, now heading biology at Atavistik Bio's metabolism pipeline.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2006 | M | Prolonged rapamycin treatment inhibits mTORC2 assembly and Akt/PKB SAR2006 Co-author: prolonged rapamycin treatment blocks mTORC2 assembly and Akt/PKB signalling in many cell types (later linked in mice to rapamycin's insulin resistance, LAM2012). |
| 2010 | M | mTORC1 controls fasting-induced ketogenesis and its modulation by ageing SEN2010 mTORC1 suppresses fasting-induced hepatic ketogenesis via PPARα; suppression worsens with age. |
| 2012 | M | mTORC1 in the Paneth cell niche couples intestinal stem-cell function to calorie intake YIL2012 Co-author: calorie restriction lowers mTORC1 in Paneth cells, which then support more intestinal stem cells through the enzyme Bst1 (mice). |
Co-authors in the Atlas 10
People with a profile here who share at least one study with Shomit Sengupta.
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- David M. Sabatini 3 shared studies Identified mTOR (as RAFT1) in 1994. His lab then mapped much of the machinery around it: raptor and rictor at the core of mTORC1 and mTORC2, the Rag–Ragulator system that docks mTORC1 on the lysosome, and the sensors that detect leucine, arginine and SAM
- Andrew L. Markhard Contributed, as a Sabatini-lab researcher, to the discovery that Ragulator docks mTORC1 on the lysosome, and now studies metabolite signals that tell the body it has eaten
- Dos D. Sarbassov Discovered rictor as a Sabatini-lab postdoc, in parallel with Michael Hall's lab, defining mTOR Complex 2, and showed that this complex is the long-sought kinase that phosphorylates Akt on serine 473. He also found that prolonged rapamycin treatment can block mTORC2 assembly
- Dudley W. Lamming Showed as a postdoc that rapamycin's harm to glucose metabolism comes largely from its effect on mTORC2, while the lifespan benefit tracks mTORC1. His Wisconsin lab studies intermittent rapamycin dosing and how restricting dietary protein or single amino acids affects metabolism and ageing
- Kivanç Birsoy Cancer metabolism researcher who trained with Jeffrey Friedman and David Sabatini and now heads the Laboratory of Metabolic Regulation and Genetics at The Rockefeller University, using genetic screens to find how cancer cells rewire their metabolism
- Mathieu Laplante Co-wrote with David Sabatini one of the field's most cited reviews of mTOR in growth and disease, and his Laval lab studies how mTORC1 and DEPTOR control fat tissue and metabolism
- Ömer H. Yilmaz Pathologist and stem-cell biologist who studies how diet and nutrient sensing control intestinal stem cells; as a postdoc with David Sabatini he showed that calorie restriction acts on the stem-cell niche through mTORC1 in Paneth cells
- Peggy P. Hsu Identified, in parallel with Yonghao Yu's group, Grb10 as an mTORC1 substrate that feeds back to dampen insulin and growth-factor signalling, and now studies the earliest steps of lung cancer as a physician-scientist
- Siraj M. Ali Worked in the Sabatini lab on the papers that discovered raptor, mLST8 and rictor, and on the finding that the rictor-mTOR complex phosphorylates Akt. He later moved into cancer genomics and clinical diagnostics
- Timothy R. Peterson Discovered DEPTOR, an inhibitor that binds mTOR in both complexes and is overexpressed in some multiple myelomas. He also showed that mTORC1 controls fat synthesis by regulating where the enzyme lipin 1 sits in the cell, and through it the SREBP pathway
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