Kun-Liang Guan
Showed how growth-factor and energy signals reach mTORC1 through TSC2 and Rheb, and, in parallel with the Sabatini lab, that the Rag GTPases carry the amino-acid signal. His lab also found that AMPK and mTORC1 control autophagy by phosphorylating the kinase ULK1 at different sites
Westlake University · UC San Diego · University of Michigan · MacArthur Fellow (1998) · Born 1963, Zhejiang, China
Guan Lab, Westlake University (Hangzhou, Zhejiang, China) ↗ Lab lineagetrained under Jack E. Dixon → ORCID0000-0003-1892-0174 ↗
Kun-Liang Guan grew up in Zhejiang, China, studied biology at Hangzhou University, and earned his PhD at Purdue. He won a MacArthur 'genius' Fellowship in 1998 and built his career at the University of Michigan and UC San Diego before returning to China to lead a lab at Westlake University.
Guan's lab worked out how signals reach mTOR from above. They showed that the tumour-suppressor complex TSC1/TSC2 acts as an off-switch by shutting down the small GTPase Rheb, and that the cellular energy sensor AMPK feeds into this control — explaining how growth factors, energy levels and stress all converge on mTOR. His team also helped define how amino acids and the Rag GTPases switch mTORC1 on. Separately, Guan is a leader of the Hippo pathway field, which controls organ size.
The timeline below follows Guan's mTOR-related discoveries collected in this Atlas.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2002 | M | TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling INO2002 Shows, in parallel with other groups, that TSC2 is switched off by Akt — wiring insulin and growth-factor signals into the control of mTOR. |
| 2003 | M | Rheb GTPase is a direct target of TSC2 GAP activity and regulates mTOR signaling INOK2003 One of several 2003 studies identifying Rheb as the direct target of TSC2's GAP activity and a key activator of mTOR. |
| 2003 | M | TSC2 mediates cellular energy response to control cell growth and survival INO2003 Links cellular energy status, via AMPK, to TSC2 and the control of cell growth and survival. |
| 2004 | M | Regulation of the TSC pathway by LKB1: evidence of a molecular link between tuberous sclerosis complex and Peutz-Jeghers syndrome COR2004 Shows LKB1 acts upstream of TSC2 through AMPK to restrain mTOR signalling, linking tuberous sclerosis and Peutz-Jeghers syndrome (senior author; cells). |
| 2006 | M | Identification of Sin1 as an essential TORC2 component required for complex formation and kinase activity YAN2006 Identified Sin1 as an essential TORC2 component required for Akt phosphorylation. |
| 2006 | M | TSC2 integrates Wnt and energy signals via a coordinated phosphorylation by AMPK and GSK3 to regulate cell growth INO2006 TSC2 integrates Wnt and energy signals through coordinated AMPK and GSK3 phosphorylation. |
| 2008 | M | Regulation of TORC1 by Rag GTPases in nutrient response KIM2008 Shows the Rag GTPases regulate TORC1 in response to nutrients. |
| 2008 | A | TSC-mTOR maintains quiescence and function of hematopoietic stem cells by repressing mitochondrial biogenesis and reactive oxygen species CHE2008 Showed why blood stem cells must keep mTOR LOW. Deleting TSC1 (which unleashes mTOR) drove resting stem cells into rapid division, flooded them with reactive oxygen species, and burned out their ability to self-renew. An antioxidant rescued them. A key link between mTOR, stem-cell exhaustion, and tissue aging. |
| 2010 | M | ATM signals to TSC2 in the cytoplasm to regulate mTORC1 in response to ROS ALE2010 Co-authors a study showing that ATM, in response to ROS, activates TSC2 in the cytoplasm through LKB1 and AMPK to repress mTORC1. |
| 2011 | M | AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1 KIM2011 Revealed the tug-of-war over ULK1: the energy sensor AMPK phosphorylates ULK1 at activating sites to turn autophagy ON when energy is low, while mTORC1 phosphorylates a different site (Ser757) to keep it OFF and even blocks AMPK from reaching ULK1. Two opposing kinases wired to the same switch. |
| 2013 | M | ULK1 induces autophagy by phosphorylating Beclin-1 and activating VPS34 lipid kinase RUS2013 Shows ULK1 phosphorylates Beclin-1 to activate the ATG14L–VPS34 lipid kinase complex and start autophagy when mTORC1 is off (senior author; cells and worms). |
| 2014 | M | Sestrins inhibit mTORC1 kinase activation through the GATOR complex PAR2014 Sestrins inhibit mTORC1 activation through the GATOR2 complex. |
| 2015 | M | Metabolism. Differential regulation of mTORC1 by leucine and glutamine JEW2015 Glutamine activates mTORC1 via a Rag-independent, Arf1-dependent route distinct from leucine. |
| 2019 | R | mTOR as a central hub of nutrient signalling and cell growth KIM2019 Review: mTOR as a central hub of nutrient signalling and cell growth. |
Co-authors in the Atlas 20
People with a profile here who share at least one study with Kun-Liang Guan.
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- Ken Inoki 7 shared studies Showed as a postdoc in Kun-Liang Guan's lab that Akt switches off TSC2, that TSC2 is the off-switch (GAP) for the small GTPase Rheb, and that AMPK and GSK3 feed energy and Wnt signals into the same brake. His Michigan lab studies mTOR signalling in metabolism and kidney disease
- Joungmok Kim 3 shared studies Showed as a Guan-lab postdoc that AMPK and mTORC1 control autophagy by phosphorylating ULK1 at different sites, with mTORC1's mark on Ser757 blocking activation by AMPK
- 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
- Angela Alexander First author of the study showing that the DNA-damage kinase ATM also works in the cytoplasm, where it switches on TSC2 in response to reactive oxygen species and so turns mTORC1 down
- Anita Parmigiani Molecular biologist who worked in Andrei Budanov's lab at Virginia Commonwealth University on Sestrins, stress-induced proteins that hold back mTORC1
- Benoit Viollet Showed that metformin still lowers liver glucose production without AMPK or LKB1, pointing instead to a drop in cellular energy charge
- Eunjung Kim Showed as first author, in Kun-Liang Guan's lab, that the Rag GTPases relay amino-acid availability to TORC1, in parallel with the Sabatini lab's discovery
- Hyun Woo Park Biochemist at Yonsei University who trained with Kun-Liang Guan on the Hippo-YAP/TAZ growth pathway and now studies how cancer cells change their signalling and metabolism to spread
- Cheryl Lyn Walker Cancer biologist and toxicologist who studies how environmental exposures reprogram the epigenome and target tumour suppressor genes; senior author of the study linking ATM to TSC2 and mTORC1 in the response to oxidative stress
- Chong Chen Showed that blood stem cells need TSC to keep mTOR in check in order to stay dormant and self-renew, and that rapamycin restores the function of aged blood stem cells in mice
- Jenna L. Jewell Studies how cells sense nutrients such as amino acids to control growth and metabolism through mTORC1
- 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.
- Michael N. Corradetti As an MD-PhD student at the University of Michigan, was first author on the 2004 study linking the LKB1 tumour suppressor to TSC2 through AMPK. He is now a radiation oncologist
- Mondira Kundu Physician-scientist who works out what the autophagy-initiating kinases ULK1 and ULK2 actually do when a cell runs short of fuel
- Pan Zheng Showed as senior author that blood stem cells need TSC to keep mTOR in check in order to stay dormant, and that rapamycin restores the function of aged blood stem cells in mice
- Qian Yang Researcher in Kun-Liang Guan's Michigan lab and first author of the 2006 study that identified Sin1 as an essential part of mTOR complex 2
- Ryan C. Russell Studies how the nutrient-sensing kinases mTORC1, ULK1 and AMPK control the autophagy machinery; as a postdoc with Kun-Liang Guan he showed that ULK1 phosphorylates Beclin-1 to switch on the autophagy-specific VPS34 complex.
- Tsuneo Ikenoue Gastroenterologist and cancer researcher at the University of Tokyo who trained in Kun-Liang Guan's mTOR lab and now builds mouse models of liver, bile duct and pancreatic cancer driven by the PI3K-Akt-mTOR pathway
- Young Chul Kim Cell biologist who studied mTOR and autophagy in Kun-Liang Guan's lab at UC San Diego and later moved to kidney research in Volker Vallon's group
- Yu Liu Cancer biologist working on how tumour-suppressor loss and epigenetic state decide whether a cell stays differentiated
Every researcher with a profile →
On the programme
Meetings in the Atlas calendar where Kun-Liang Guan is listed among the speakers or organisers.
- past FASEB SRC: Hippo Pathway in Biology and Disease 2026 (2nd) ↗ 1–4 Sep 2026 ·
Winnipeg, Canada · ★★★
All meetings in the calendar →
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