Yasemin Sancak
Showed as a Sabatini-lab graduate student, in parallel with Kun-Liang Guan's lab, that the Rag GTPases relay amino-acid signals to mTORC1, and that Ragulator anchors them to the lysosome where mTORC1 is switched on. She also identified PRAS40 as an insulin-regulated inhibitor of mTORC1
Associate Professor of Pharmacology, University of Washington · Pew Biomedical Scholar · postdoc, Vamsi Mootha lab, Massachusetts General Hospital & Broad Institute · PhD, Sabatini lab, Whitehead Institute/MIT
Sancak Lab, University of Washington (Seattle, Washington, USA) ↗ Lab lineagetrained under David M. Sabatini → Bluesky@yasesancak.bsky.social ↗
Portrait: UW Dept. of Pharmacology
Yasemin Sancak trained in David Sabatini's lab, where she identified, in parallel with Kun-Liang Guan's lab, the Rag GTPases as the long-sought link between amino acids and mTORC1: when nutrients are present, the Rags bind raptor and pull mTORC1 to the surface of the lysosome, its site of activation. She went on to show that the Ragulator complex anchors the Rags there and is itself required for amino-acid signalling.
Sancak also helped characterize PRAS40 as an insulin-regulated inhibitor of mTORC1 and DEPTOR as an mTOR-binding inhibitor overexpressed in some cancers. She now runs her own lab in the Department of Pharmacology at the University of Washington, where her focus has shifted to how mitochondria are regulated by calcium signalling.
The timeline below follows Sancak's mTOR-related discoveries gathered in this Atlas.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2007 | M | PRAS40 is an insulin-regulated inhibitor of the mTORC1 protein kinase SAN2007 Identifies PRAS40 as an insulin-regulated inhibitor of the mTORC1 kinase. |
| 2008 | M | The Rag GTPases bind raptor and mediate amino acid signaling to mTORC1 SAN2008 Discovers, in parallel with Kun-Liang Guan's lab, that the Rag GTPases bind raptor and mediate amino-acid signalling to mTORC1. |
| 2009 | M | DEPTOR is an mTOR inhibitor frequently overexpressed in multiple myeloma cells and required for their survival PET2009 Identified DEPTOR as a built-in brake on BOTH mTOR complexes. The twist: in some multiple myelomas DEPTOR is overexpressed, which by relieving a feedback loop actually keeps pro-survival Akt signaling ON - a neat example of how an 'inhibitor' can be co-opted by cancer. |
| 2010 | M | Ragulator-Rag complex targets mTORC1 to the lysosomal surface and is necessary for its activation by amino acids SAN2010 Shows the Ragulator-Rag complex anchors mTORC1 to the lysosomal surface, required for its activation by amino acids. |
| 2011 | M | mTORC1 senses lysosomal amino acids through an inside-out mechanism that requires the vacuolar H(+)-ATPase ZON2011 Showed amino acid sensing starts INSIDE the lysosome: amino acids accumulate in the lumen and the v-ATPase relays that signal outward ('inside-out') to Ragulator-Rag. A surprising twist on where the cell measures its nutrient status. |
Co-authors in the Atlas 13
People with a profile here who share at least one study with Yasemin Sancak.
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- David M. Sabatini 5 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
- Carson C. Thoreen 3 shared studies Used Torin1, one of the first ATP-competitive mTOR inhibitors, to reveal functions of mTORC1 that rapamycin cannot block. He then showed that mTORC1 controls translation of mRNAs for the protein-making machinery mainly through the 4E-BP proteins
- Liron Bar-Peled 3 shared studies Showed as a Sabatini-lab graduate student that Ragulator switches the Rag GTPases on, acting as their GEF. He also discovered GATOR1 and GATOR2; GATOR1 switches the Rags off and its genes are mutated in some cancers
- Timothy R. Peterson 3 shared studies 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
- Robert A Lindquist 2 shared studies Researcher in David Sabatini's group at the Whitehead Institute who ran large image-based RNAi screens for regulators of TORC1 signaling and helped build the CellProfiler image-analysis software
- Roberto Zoncu 2 shared studies Showed as a postdoc that mTORC1 senses amino acids from inside the lysosome, through the v-ATPase and Ragulator. His Berkeley lab has since mapped how the Rag GTPases and the folliculin complex switch mTORC1 on, and how lysosomal cholesterol feeds into the same system
- Seong A. Kang 2 shared studies 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
- Alejo Efeyan Showed that the Rag GTPases, which relay amino-acid signals to mTORC1, are a life-or-death switch for newborn mice surviving the fast before their first feeding
- 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
- 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
- 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
- Shuyu Wang Co-discovered SLC38A9 as a Sabatini-lab MD-PhD student, a lysosomal amino-acid transporter that signals arginine sufficiency to mTORC1
- W. Michael Kuehl Physician-scientist who spent decades working out the genetic and molecular biology of multiple myeloma and its precursor condition MGUS.
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