Jun Hee Lee
Physiologist at the University of Michigan who first showed in flies that Sestrin is a feedback brake on TOR that protects against age-related decline, and has since studied Sestrins as stress-induced regulators of mTORC1
Department of Molecular and Integrative Physiology, University of Michigan Medical School (papers 2016–2022) · Laboratory of Gene Regulation and Signal Transduction, University of California San Diego (Michael Karin lab, 2010 paper)
Jun Hee Lee is first author of LEE2010, a Science paper from Michael Karin's laboratory at the University of California San Diego. In fruit flies, the team found that Sestrin levels rise when TOR stays active, and that Sestrin then pushes TOR back down by switching on AMPK, the cell's energy sensor. This makes Sestrin a feedback brake. Flies without Sestrin built up fat and developed mitochondrial damage, muscle weakness and heart problems that looked like early ageing. Treating them with rapamycin or with an AMPK activator prevented these problems.
The paper put Sestrins on the map of ageing research. Later work by other groups showed that in mammals Sestrin2 binds the amino acid leucine and passes that signal to mTORC1 through the GATOR2 complex, so Sestrins are now seen as both stress sensors and nutrient sensors for mTORC1.
Lee moved to the University of Michigan, where PubMed lists the Department of Molecular and Integrative Physiology of the Medical School. Lee's group there continued the Sestrin work, including a 2016 review on the biochemical basis of Sestrin activity, which describes Sestrins as stress-induced proteins that hold down both reactive oxygen species and mTORC1, and a 2022 commentary with Robert Wessells on how Sestrin links exercise to body temperature control. No profile page was opened, so the current title is not confirmed.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2010 | A | Sestrin as a feedback inhibitor of TOR that prevents age-related pathologies LEE2010 First author: showed in fruit flies that Sestrin acts as a feedback inhibitor of TOR and that its loss causes age-like fat, mitochondrial, muscle and heart defects that TOR inhibition prevents. |
Co-authors in the Atlas 2
People with a profile here who share at least one study with Jun Hee Lee.
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- Andrei V. Budanov Helped identify the Sestrins as stress-induced proteins and was among the groups that showed they inhibit mTORC1 through the GATOR complex, a brake that protects against age-related disease
- Michael Karin Cell biologist best known for discovering AP-1 and JNK signaling and the IKK-NF-kB inflammation pathway, whose lab also co-led the study of Sestrin as a feedback inhibitor of TOR.
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