So Woon Kim
Sungkyunkwan University
6 Papers
9 Citations
So Woon Kim is an academic researcher from Sungkyunkwan University. The author has contributed to research in topics: Autophagosome & Chemistry. The author has an hindex of 2, co-authored 5 publications.
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Papers
Palmitoylation controls trafficking of the intracellular Ca2+ channel MCOLN3/TRPML3 to regulate autophagy.
So Woon Kim,Donghyun Kim,Kyoung Sun Park,Mi Kyung Kim,Yun Min Park,Shmuel Muallem,Insuk So,Hyunjin Kim +7 more
TL;DR: The results suggest that trafficking and channel function of MCOLN3/TRPML3 are regulated in the context of autophagy, and palmitoylation is a prerequisite for the function of the channel as a Ca2+ channel in autophagosome formation by controlling its trafficking between subcellular compartments.
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TRPC3 and NALCN channels drive pacemaking in substantia nigra dopaminergic neurons
Ki Bum Um,Suyun Hahn,So Woon Kim,Yoon Je Lee,Lutz Birnbaumer,Hyunjin Kim,Hyunjin Kim,Myoung Kyu Park,Myoung Kyu Park +8 more
TL;DR: In this paper, the authors show that TRPC3 and NALCN channels together form sustained inward currents responsible for the slow depolarization of midbrain dopamine (DA) neurons, and they conclude that these channels are two major leak channels that drive robust pacemaking in nigral DA neurons.
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N-benzhydryl quinuclidine compounds are a potent and Src kinase-independent inhibitor of NALCN channels.
TL;DR: NALCN is a Na+ leak, GPCR‐activated channel that regulates the resting membrane potential and neuronal excitability and lack of specific blockers hampers further investigation.
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The intracellular Ca2+ channel TRPML3 is a PI3P effector that regulates autophagosome biogenesis
So Woon Kim,Mi Kyung Kim,Seokwoo Hong,Areum Choi,J.-H. Choi,Shmuel Muallem,Insuk So,Dongki Yang,Hyun-Jin Kim +8 more
TL;DR: It is shown that lipid-regulated TRPML3 is the Ca2+ release channel in the phagophore that provides the Ca1+ necessary for autophagy progress, and phosphatidylinositol-3-phosphate (PI3P), an essential lipid for Autophagosome formation, is a selective regulator of TRP ML3.
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TRPC3 and NALCN channels drive pacemaking in substantia nigra dopaminergic neurons
Ki Bum Um,Suyun Hahn,So Woon Kim,Yoon Je Lee,Lutz Birnbaumer,Lutz Birnbaumer,Hyunjin Kim,Hyunjin Kim,Myoung Kyu Park,Myoung Kyu Park +9 more
TL;DR: In this article, the authors show that TRPC3 and NALCN channels together form sustained inward currents responsible for the slow depolarization of midbrain dopamine (DA) neurons, and they conclude that these channels are two major leak channels that drive robust pacemaking in nigral DA neurons.
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