SUNGKYUNKWAN UNIVERSITY SCHOOL OF MEDICINE
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Hyun-Jin Kim
Hyun-Jin Kim PhD
| Graduate Program | Neuroscience |
| Research Area | TRP(transient receptor potential) channel, Autophagy |
| Laboratory | Molecular Neurophysiology Lab Laboratory |
| kimhyunjin@skku.edu | |
| Tel | +82-31-299-6105 |
Education & Careers
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2010 ~ Present Assistant, Associate Professor, Professor Sungkyunkwan University School of Medicine, Suwon, Korea
2006 -2010 Post-doc, University of Texas Southwestern Medical Center at Dallas, TX, USA
2001 -2006 PhD, Department of Physiology, Seoul National University College of Medicine, Seoul, Korea
1994 -2000 MD, Seoul National University College of Medicine, Seoul, Korea
Research Interest
1) Ion channels
Ion channels are pore-forming membrane proteins that allow ions to pass through the channel pore. Their functions include establishing a resting membrane potential, shaping action potentials and other electrical signals by gating the flow of ions across the cell membrane, controlling the flow of ions across secretory and epithelial cells, and regulating cell volume. Ion channels are present in the membranes of all cells. We are now interested in understanding function of Transient Receptor Potential (TRP) channels which have been implicated in a diverse range of cellular processes.
2) Autophagy
Autophagy is the natural, regulated mechanism of the cell that removes unnecessary or dysfunctional components. It allows the orderly degradation and recycling of cellular components. Defects in autophagy have been linked to various human diseases, including neurodegeneration and cancer, and interest in modulating autophagy as a potential treatment for these diseases has grown rapidly. Our research focuses on the regulation of autophagy by one of TRP channels in mammalian cells.
Ion channels are pore-forming membrane proteins that allow ions to pass through the channel pore. Their functions include establishing a resting membrane potential, shaping action potentials and other electrical signals by gating the flow of ions across the cell membrane, controlling the flow of ions across secretory and epithelial cells, and regulating cell volume. Ion channels are present in the membranes of all cells. We are now interested in understanding function of Transient Receptor Potential (TRP) channels which have been implicated in a diverse range of cellular processes.
2) Autophagy
Autophagy is the natural, regulated mechanism of the cell that removes unnecessary or dysfunctional components. It allows the orderly degradation and recycling of cellular components. Defects in autophagy have been linked to various human diseases, including neurodegeneration and cancer, and interest in modulating autophagy as a potential treatment for these diseases has grown rapidly. Our research focuses on the regulation of autophagy by one of TRP channels in mammalian cells.
Representative Research Achievements
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1. Hahn S, Um KB, Kim SW, Kim HJ*, Park MK. Proximal dendritic localization of NALCN channels underlies tonic and burst firing in nigral dopaminergic neurons. J Physiol. (2023) Jan601(1):171-193.
2. Kim SW, Kim MK, Hong S, Choi A, Choi JH, Muallem S, So I, Yang D, Kim HJ*. The intracellular Ca2+ channel TRPML3 is a PI3P effector that regulates autophagosome biogenesis. Proc Natl Acad Sci U S A. (2022) Oct 25119(43):e2200085119.
3. Um KB, Hahn S, Kim SW, Lee YJ, Birnbaumer L, Kim HJ*, Park MK. TRPC3 and NALCN channels drive pacemaking in substantia nigra dopaminergic neurons. Elife. (2021) Aug 1910:e70920.
4. Hahn S, Kim SW, Um KB, Kim HJ*, Park MK. N-benzhydryl quinuclidine compounds are a potent and Src kinase-independent inhibitor of NALCN channels. Br J Pharmacol. (2020) Aug177(16):3795-3810.
5. Kim SW, Kim DH, Park KS, Kim MK, Park YM, Muallem S, So I, Kim HJ*. Palmitoylation controls trafficking of the intracellular Ca2+ channel MCOLN3/TRPML3 to regulate autophagy. Autophagy. (2019) Feb15(2):327-340.
6. Myeong J, Ko J, Kwak M, Kim J, Woo J, Ha K, Hong C, Yang D, Kim HJ*, Jeon JH, So I. Dual action of the Gαq-PLCβ-PI(4,5)P2 pathway on TRPC1/4 and TRPC1/5 heterotetramers. Sci Rep. (2018) Aug 148(1):12117.