Do-Hyung Kim
Co-discovered raptor, the defining subunit of mTORC1
Postdoc, Whitehead Institute/MIT (Sabatini lab) · Professor, Metabolic & Systems Biology, University of Minnesota
Kim Lab, University of Minnesota ↗
Portrait: University of Minnesota College of Biological Sciences
Do-Hyung Kim did his postdoctoral work in David Sabatini's lab at the Whitehead Institute, where in 2002 he identified raptor, the partner protein that binds mTOR and makes the resulting complex — now called mTORC1 — sensitive to nutrients. The discovery gave the field its first molecular handle on what would become mTOR's two distinct complexes.
Kim went on to identify GbetaL (mLST8), a second core component shared by both mTOR complexes, and later helped characterize PRAS40 and other regulators that tune mTORC1 activity in response to insulin and amino acids. He now runs his own lab at the University of Minnesota, studying the wider mTOR signalling network in growth control and disease.
The timeline below follows Kim's contributions gathered in this Atlas.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2002 | M | mTOR interacts with raptor to form a nutrient-sensitive complex that signals to the cell growth machinery KIM2002 Identifies raptor, the defining partner protein that makes mTOR nutrient-sensitive and founds mTOR Complex 1. |
| 2003 | M | GbetaL, a positive regulator of the rapamycin-sensitive pathway required for the nutrient-sensitive interaction between raptor and mTOR KIM2003 Identifies GbetaL (mLST8), a positive regulator shared by both mTOR complexes. |
| 2004 | M | Rictor, a novel binding partner of mTOR, defines a rapamycin-insensitive and raptor-independent pathway that regulates the cytoskeleton SAR2004 Discovery of Rictor and the SECOND mTOR complex, mTORC2. Crucially showed this complex is NOT blocked by rapamycin and does not use Raptor - it controls the cytoskeleton via PKC. This is the paper that split mTOR biology into 'two faces' at the molecular level. |
| 2007 | M | Insulin signalling to mTOR mediated by the Akt/PKB substrate PRAS40 VAN2007 Insulin signals to mTORC1 through Akt phosphorylation of the inhibitor PRAS40. |
| 2012 | M | SH3BP4 is a negative regulator of amino acid-Rag GTPase-mTORC1 signaling KIM2012 Identifies SH3BP4 as a negative regulator that restrains Rag-GTPase signalling to mTORC1. |