Daniel F. Egan
Finds two separate molecular switches AMPK uses to shut down mTOR and turn on autophagy when cells run low on energy
BA, Colby College · PhD, UCSD/Salk (Reuben Shaw lab, 2008–2014) · postdoc, Harvard Medical School (2014–2018) · industry: Casma Therapeutics → ReNAgade Therapeutics → Orna Therapeutics → now Director, Eli Lilly
Shaw Lab, Salk Institute (where this work was done) ↗
Co-author (GWI2008): AMPK directly phosphorylates Raptor, a second route (beyond TSC2) to shut mTORC1 down during energy stress. First author (EGA2010): AMPK directly phosphorylates ULK1, connecting energy sensing to mitophagy.
Moved from Salk PhD through Harvard postdoc into a string of Boston biotechs, now a director at Eli Lilly — an academic-to-industry path shaping AMPK/autophagy drug discovery.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2008 | M | AMPK phosphorylation of raptor mediates a metabolic checkpoint GWI2008 AMPK directly phosphorylates Raptor, a second route to shut down mTORC1 during energy stress. |
| 2010 | M | Phosphorylation of ULK1 (hATG1) by AMP-activated protein kinase connects energy sensing to mitophagy EGA2010 AMPK directly phosphorylates ULK1, linking energy sensing to mitophagy. |