Andrew L. Markhard
Pinpoints the lysosomal switch that turns mTORC1 on and now traces metabolite signals that tell the body when it has eaten
Research staff, Sabatini Lab, Whitehead/MIT · Lab Manager, Mootha Lab, Broad/MGH (2012–2022) · Research Scientist, Long Lab, Stanford · now Ph.D. student, NYU Grossman School of Medicine
Long Lab, Stanford (formerly Mootha Lab, Broad/MGH) ↗
Portrait: Long Lab, Stanford University
Part of team showing (SAR2006) prolonged rapamycin also disassembles mTORC2, root of insulin-resistance side effect. Part of team (SAN2010) showing Ragulator recruits Rag GTPases to the lysosomal surface, docking mTORC1 next to Rheb.
Decade as Mootha-lab manager mapping mitochondrial proteins, then Stanford metabolomics (2024 Nature: enzyme PTER/taurine; 2026 Nature Metabolism: python-derived gut-brain feeding signal). Now pursuing a PhD at NYU.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2006 | M | Prolonged rapamycin treatment inhibits mTORC2 assembly and Akt/PKB SAR2006 Co-authored: prolonged rapamycin disassembles mTORC2, explaining the insulin-resistance side effect. |
| 2010 | M | Ragulator-Rag complex targets mTORC1 to the lysosomal surface and is necessary for its activation by amino acids SAN2010 Helped show Ragulator recruits Rag GTPases to the lysosomal surface, docking mTORC1 next to Rheb. |