Daniel F. Egan
Showed as first author that AMPK directly phosphorylates ULK1, linking low cellular energy to autophagy and mitophagy, and contributed to the finding that AMPK brakes mTORC1 by phosphorylating raptor
Director, Eli Lilly · industry: Orna Therapeutics, ReNAgade Therapeutics, Casma Therapeutics · postdoc, Harvard Medical School (2014–2018) · PhD, UCSD/Salk (Reuben Shaw lab, 2008–2014) · BA, Colby College
Shaw Lab, Salk Institute (where this work was done) (La Jolla, California, USA) ↗ Lab lineagetrained under Reuben J. Shaw →
Portrait: Spiegelman Lab, Dana-Farber Cancer Institute
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 that began with AMPK/autophagy biology.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| 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. |
Co-authors in the Atlas 9
People with a profile here who share at least one study with Daniel F. Egan.
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- Dana M. Gwinn 2 shared studies First author of the 2008 study showing that the energy sensor AMPK switches off mTORC1 by phosphorylating raptor
- David B. Shackelford 2 shared studies Cancer biologist at UCLA who studies lung tumours that have lost the LKB1 tumour suppressor, the upstream activator of AMPK, and who trained in Reuben Shaw's lab at the Salk Institute
- Maria M. Mihaylova 2 shared studies Studies how intestinal stem cells change with age and how diet shapes their metabolism
- Reuben J. Shaw 2 shared studies Showed, in parallel with two other groups, that the tumour suppressor LKB1 directly activates AMPK, and that AMPK brakes mTORC1 by phosphorylating raptor. His Salk lab also linked AMPK to autophagy through ULK1 and helped explain how metformin acts in the liver
- Benjamin E. Turk Kinase biochemist who studies how protein kinases choose their substrates; co-author on the discovery that AMPK phosphorylates raptor and on the study showing that mTORC1 sites differ in intrinsic substrate quality.
- Benoit Viollet Showed that metformin still lowers liver glucose production without AMPK or LKB1, pointing instead to a drop in cellular energy charge
- John M. Asara Mass-spectrometry specialist whose core facility supplied metabolomics and proteomics for several mTOR studies, including measurements of purine, pyrimidine and SAM metabolism downstream of mTORC1.
- Malene Hansen Showed in worms, alongside a 2007 report from Beth Levine's laboratory, that autophagy is required for dietary restriction to extend lifespan
- Mondira Kundu Physician-scientist who works out what the autophagy-initiating kinases ULK1 and ULK2 actually do when a cell runs short of fuel
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