Joungmok Kim
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
Professor, Dept. of Oral Biochemistry and Molecular Biology, Kyung Hee University, Seoul · training/postdoc in Kun-Liang Guan's lab, Univ. of Michigan Life Sciences Institute → UC San Diego
Kyung Hee University (Seoul, South Korea) ↗
Portrait: Kyung Hee University
First author (KIM2011): AMPK directly phosphorylates ULK1 at activating sites, mTORC1 phosphorylates Ser757 to keep it off and block AMPK access — the tug-of-war deciding autophagy on/off. Co-authored with Guan an influential 2019 review (KIM2019) reframing mTOR as the central hub of nutrient signaling.
Long apprenticeship in Guan's lab (Michigan → UCSD). Now Professor at Kyung Hee dental school, Seoul — extending AMPK/mTOR/autophagy biology into oral/dental contexts, retains UCSD Pharmacology affiliation.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2011 | M | AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1 KIM2011 First author: mTORC1 phosphorylates ULK1 at Ser757 to keep autophagy off and block AMPK's activating site. |
| 2013 | M | ULK1 induces autophagy by phosphorylating Beclin-1 and activating VPS34 lipid kinase RUS2013 Co-author: ULK1 phosphorylates Beclin-1 to activate the ATG14L–VPS34 complex and induce autophagy. |
| 2019 | R | mTOR as a central hub of nutrient signalling and cell growth KIM2019 Co-authors influential review reframing mTOR as the central hub integrating nutrient signals with cell growth. |
Co-authors in the Atlas 4
People with a profile here who share at least one study with Joungmok Kim.
ShowHide
- Kun-Liang Guan 3 shared studies 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
- Benoit Viollet Showed that metformin still lowers liver glucose production without AMPK or LKB1, pointing instead to a drop in cellular energy charge
- Mondira Kundu Physician-scientist who works out what the autophagy-initiating kinases ULK1 and ULK2 actually do when a cell runs short of fuel
- 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.
Every researcher with a profile →
Thank you. That helps us know which pages have been read by someone who knows the work.
Thank you. We will check it and correct the page.
Thank you. Your answer was counted anonymously.