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
University of Michigan · postdoc, Vander Heiden Lab, MIT · oncology fellowship, Dana-Farber & MGH · residency, Brigham and Women's · MD, Harvard · PhD, MIT (Sabatini Lab) · BA, Princeton
Hsu Lab, University of Michigan Rogel Cancer Center (Ann Arbor, Michigan, USA) ↗ Lab lineagetrained under David M. Sabatini → Bluesky@peggyphsu.bsky.social ↗
Portrait: American Society for Clinical Investigation (ASCI)
Used quantitative phosphoproteomics (HSU2011) to map mTOR's substrates directly, identifying Grb10 — mTORC1 phosphorylates/stabilizes it, and Grb10 suppresses PI3K/growth-factor signaling, explaining mTORC1-hyperactivation-causes-insulin-resistance. (Reported in parallel, in the same issue of Science, by Yonghao Yu and John Blenis.)
Physician-scientist path through MIT/Harvard/Dana-Farber/MGH; now thoracic oncologist and stem cell biologist studying how airway basal cells give rise to never-smoking, ALK-fusion lung cancer. NCI K08, Burroughs Wellcome Fund Career Award (2025), 2026 ASCI Young Physician-Scientist.
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). |
| 2011 | M | The mTOR-regulated phosphoproteome reveals a mechanism of mTORC1-mediated inhibition of growth factor signaling HSU2011 Mapped the mTOR phosphoproteome, identifying Grb10 as a direct mTORC1 substrate feeding back on PI3K. |
Co-authors in the Atlas 10
People with a profile here who share at least one study with Peggy P. Hsu.
ShowHide
- David M. Sabatini 2 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
- Kathleen Ottina Researcher in David Sabatini's lab at the Whitehead Institute and HHMI at MIT who contributed to studies of the GATOR1 amino acid off-switch, mTORC1 feedback on growth-factor signalling, and cancer drug resistance
- Michael B. Yaffe Cancer biologist and physician-scientist known for working out how phosphorylation creates binding sites on proteins, including the 14-3-3 family of phosphoserine/threonine-binding proteins, and how kinases choose their targets.
- Nathanael S. Gray Medicinal chemist whose lab designed Torin1, an ATP-competitive mTOR inhibitor that blocks functions of mTORC1 that rapamycin misses. His lab is also known for covalent kinase inhibitors and targeted protein degraders
- Seong A. Kang Contributed to the Sabatini-lab studies that identified PRAS40 and DEPTOR, two of the cell's own mTOR inhibitors, and to the first characterisation of the mTOR inhibitor Torin1
- 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
- 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
Every researcher with a profile →
Thank you. That helps us know which pages have been read by someone who knows the work.
Thank you. We will check it and correct the page.
Thank you. Your answer was counted anonymously.