Laboratory of Cellular Stress, Aging, and Human Diseases(스트레스 및 노화 질환 연구실)

Youngdae Gwon

스트레스 및 노화 질환 연구실
Membrane organelles are well-known examples of lipid bilayer-based compartmentalization.
Biomolecular condensates, on the other hand, are structures formed through liquid-liquid phase separation that are physically, structurally, and functionally distinct from their surroundings.
This is a relatively new research area but it is gaining a lot of attention because genetic risks linked to many human diseases such as amyotrophic lateral sclerosis, frontotemporal dementia, Paget disease of bone, Alzheimers disease alter the properties of biomolecular condensates.

Our laboratorys research theme is to investigate the transformation of representative biomolecular condensates such as stress granules, nucleolus, and RNA transport granules triggered by stress and aging using cell biology, biophysics, and systems biology approaches.

Specific research topics are as follows:
1. Measuring the physical properties of biomolecular condensates under various physiologic and pathologic contexts
2. Finding genetic/pharmacologic regulators of biomolecular condensates
3. Developing tools to observe biomolecular condensates in higher order systems than cells
Major Publications

1. Ubiquitination of G3BP1 mediates stress granule disassembly in a context-specific manner. Y Gwon, BA Maxwell, RM Kolaitis, P Zhang, HJ Kim, JP Taylor. Science (2021) 372(6549), eabf6548.
2. Ubiquitination is essential for recovery of cellular activities after heat shock. BA Maxwell, Y Gwon , A Mishra, J Peng, H Nakamura, K Zhang, HJ Kim, JP Taylor. Science (2021) 372(6549), eabc3593.
3. Amelioration of amyloid β-FcγRIIb neurotoxicity and tau pathologies by targeting LYN. Y Gwon, SH Kim, HT Kim, TI Kam, J Park, B Lim, H Cha, HJ Chang, YR Hong, YK Jung. The FASEB Journal (2019) 33(3), 4300-4313.
4. TOM1 regulates neuronal accumulation of amyloid-β oligomers by FcγRIIb2 variant in Alzheimers disease. Y Gwon*, TI Kam*, SH Kim, S Song, H Park, B Lim, H Lee, W Lee, DG Jo, YK Jung. Journal of Neuroscience (2018) 38(42), 9001-9018.&160(* equal contribution)
5. FcγRIIb-SHIP2 axis links Aβ to tau pathology by disrupting phosphoinositide metabolism in Alzheimers disease model. TI Kam*, H Park*, Y Gwon*, S Song, SH Kim, SW Moon, DG Jo, YK Jung. Elife (2016) 5, e18691. (* equal contribution)

(Tel) +82-31-299-6164,  (Email)