Seoul National University · Neuroscience
Professor Won-Kyung Ho's research lab specializes in cellular and molecular mechanisms underlying ion channel regulation, with a primary focus on potassium channels in cardiac and neuronal tissues. The lab investigates how cellular signaling pathways, including AMP-activated protein kinase (AMPK) and phosphoinositide metabolism, modulate ion channel trafficking and function in response to metabolic and physiological cues. Key research directions include the regulation of HERG and other voltage-gated K+ channels by intracellular second messengers, pharmacological agents, and ion concentrations, with implications for arrhythmia and drug-induced cardiotoxicity. The lab also explores lipid-protein interactions, particularly the role of phosphoinositides in subcellular targeting and functional regulation of ion channels and transporters.
Figures are computed from collected data and may differ slightly.
K(ATP) channel trafficking is regulated by energy status via AMPK, and this mechanism may play a key role in inhibiting insulin secretion under low energy status.
1. Amitriptyline has been known to induce QT prolongation and torsades de pointes which causes sudden death. We studied the effects of amitriptyline on the human ether-a-go-go-related gene (HERG) channel expressed in Xenopus oocytes and on the rapidly activating delayed rectifier K(+) current (I(Kr)) in rat atrial myocytes. 2. The amplitudes of steady-state currents and tail currents of HERG were decreased by amitriptyline dose-dependently. The decrease became more pronounced at more positive po
1. We expressed the human eag-related gene (HERG), which is known to encode the delayed rectifier K+ current (IKr) in cardiac muscle, in Xenopus oocytes. Using a two-microelectrode voltage clamp technique, the effect of external Ca2+ and Mg2+ on the HERG current (IHERG) was investigated. 2. When [Ca2+]o was increased, the amplitude of outward IHERG elicited by depolarization decreased, and the rate of current onset slowed. The rate of current decay observed on repolarization was greatly accelera
1. We have investigated the effect of U73122, a specific inhibitor of phospholipase C (PLC), on acetylcholine-activated K(+) currents (I(KACh)) in mouse atrial myocytes. 2. In perforated patch clamp mode, I(KACh) was activated by 10 microM acetylcholine. When atrial myocytes were pretreated with U73122 or U73343, I(KACh) was inhibited dose-dependently (half-maximal inhibition at 0.12+/-0.0085 and 0.16+/-0.0176 microM, respectively). The current-voltage relationships for I(KACh) in the absence an
Phosphoinositides are critical regulators of ion channel and transporter activity. There are multiple isomers of biologically active phosphoinositides in the plasma membrane and the different lipid species are non-randomly distributed. However, the mechanism by which cells impose selectivity and directionality on lipid movements and so generate a non-random lipid distribution remains unclear. In the present study we investigated which structural elements of phosphoinositides are responsible for
1. The properties of the delayed rectifier K+ current (IK) of rabbit isolated sino-atrial node cells were investigated in high (140 mM) [K+]o using the whole-cell-clamp technique. 2. Hyperpolarizing clamp pulses from 0 mV induced an instantaneous current jump (I-V relation linear) followed by a time-dependent increase in inward current to a peak, whereas depolarizing clamp pulses induced little outward current. The peak I-V relation showed a strong inward rectification. The inwardly rectifying c
Dendritic Na<sup>+</sup> channels in pyramidal neurons are known to amplify synaptic signals, thereby facilitating action potential (AP) generation. However, the mechanisms that modulate dendritic Na<sup>+</sup> channels have remained largely uncharacterized. Here, we report a new form of short-term plasticity in which proximal excitatory synaptic inputs to hippocampal CA1 pyramidal neurons transiently elevate dendritic excitability. High-frequency stimulations (HFS) to the Schaffer collateral (
Insulin secretion from pancreatic β cells in response to high glucose (HG) critically depends on the inhibition of K<sub>ATP</sub> channel activity in HG. It is generally believed that HG-induced effects are mediated by the increase in intracellular ATP, but here, we showed that, in INS-1 cells, endocytosis of K<sub>ATP</sub> channel plays a major role. Upon HG stimulation, resting membrane potential depolarized by 30.6 mV (from -69.2 to -38.6 mV) and K<sub>ATP</sub> conductance decreased by 91%
Here, we discovered a novel autoimmune encephalitis associated with anti-Ca<sub>V</sub> α2δ antibody. Further analysis of the antibody in autoimmune encephalitis might promote early diagnosis and treatment. ANN NEUROL 2021;89:740-752.
Dopaminergic projection to the hippocampus from the ventral tegmental area or locus ceruleus has been considered to play an essential role in the acquisition of novel information. Hence, the dopaminergic modulation of synaptic plasticity in the hippocampus has been widely studied. We examined how the D1 and D2 receptors influenced the mGluR5-mediated synaptic plasticity of the temporoammonic-CA1 synapses and showed that the dopaminergic modulation of the temporoammonic-CA1 synapses was expressed
We investigated the permeability of Cs+ and Na+ through various ion channels in rat atrial myocytes using the whole-cell voltage-clamp technique. With isotonic CsCl (140 mM) on both sides of the membrane and nominally [Ca2+]o-free conditions, depolarising clamp pulses induced an increase of outward currents which showed a biphasic time course. Repolarisation to the holding potential induced inward tail currents. With isotonic NaCl, depolarisation also induced outward currents which showed a mono
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