Korea University · 生化学・遺伝学・分子生物学
Professor Eun Mi Hwang's research lab focuses on ion channel biology, particularly the molecular mechanisms underlying cellular ion homeostasis and their roles in disease. The lab investigates the regulation of ion channel trafficking and function, with a strong emphasis on TRPM4 and volume-regulated anion channels (VRACs), linking these channels to neuronal cell death and cancer progression. Using molecular, cellular, and pharmacological approaches, the lab explores how ion channel dysfunction contributes to pathological conditions and identifies novel therapeutic targets. Their work also delves into epigenetic regulation of ion channel expression, as seen in the role of histone deacetylase inhibitors in restoring channel function in drug-resistant cancer cells.
Figures are computed from collected data and may differ slightly.
These results showed that the cell surface expression of TRPM4 channels is mediated by 14-3-3γ binding, and the specific inhibition of this trafficking process can be a potential therapeutic target for glutamate-induced neuronal cell death.
Volume-regulated anion channels (VRACs) are involved in cellular functions such as regulation of cell volume, proliferation, migration, and cell death. Although leucine-rich repeat-containing 8A (LRRC8A) has been characterized as a molecular component of VRACs, here we show that Drosophila melanogaster tweety homologue 1 and 2 (TTYH1 and TTYH2) are critical for VRAC currents in cancer cells. LRRC8A-independent VRAC currents were present in the gastric cancer cell line SNU-601, but almost complet
Astrocytes, the most abundant cell type in the brain, are non-excitable cells and play critical roles in brain function. Mature astrocytes typically exhibit a linear current-voltage relationship termed passive conductance, which is believed to enable astrocytes to maintain potassium homeostasis in the brain. We previously demonstrated that TWIK-1/TREK-1 heterodimeric channels mainly contribute to astrocytic passive conductance. However, the molecular identity of astrocytic passive conductance is
ANO1, a Ca<sup>2+</sup>-activated chloride channel, is highly expressed in glioblastoma cells and its surface expression is involved in their migration and invasion. However, the regulation of ANO1 surface expression in glioblastoma cells is largely unknown. In this study, we found that Ca<sup>2+</sup>/Calmodulin-dependent protein kinase II (CaMKII) β specifically enhances the surface expression and channel activity of ANO1 in U251 glioblastoma cells. When KN-93, a CaMKII inhibitor, was used to
TREK-1 (TWIK-related K+ channel), a member of the two-pore domain K+ (K2P) channel family, is highly expressed in astrocytes, where it plays a key role in glutamate release and passive conductance. In addition, TREK-1 is induced to protect neurons under pathological conditions such as hypoxia. However, the upstream regulation of TREK-1 remains poorly understood. In this study, we found that AEG-1 (astrocyte elevated gene-1) regulates the expression of astrocytic TREK-1 under hypoxic conditions.
Two-pore domain K⁺ (K2P) channels play essential roles in regulating resting membrane potential and cellular excitability. Although TWIK-1 (TWIK-tandem of pore domains in a weak inward rectifying K<b>⁺</b> channel) was the first identified member of the K2P channel family, it is only in recent years that the physiological roles of TWIK-1 have been studied in depth. A series of reports suggest that TWIK-1 may underlie diverse functions, such as intrinsic excitability of neurons, astrocytic passiv
Astrocytes play an important role in increasing synaptic plasticity, regulating endogenous homeostasis, and contributing to neuroprotection but become overactivated or apoptotic in persistent neuroinflammatory responses or pathological conditions. Although gliogenesis under these conditions may be essential for neuronal protection, much remains unknown. Here, we generated new conditional transgenic mice (cTg) that can induce apoptosis via Cre-dependent active caspase-3 (taCasp3-2A-TEVp) without
The combination of idiopathic thrombocytopenic purpura (ITP) and chronic renal failure (CRF) is uncommon. This report highlights a case of renal transplantation in a patient with ITP. A 35-year-old man with ITP was admitted with uremic symptoms. A renal transplant and splenectomy was simultaneously performed. A prophylactic pneumococcous vaccination was performed and intravenous immunoglobulin (1 g/kg) was administered before and after the operation. The patient's platelet count increased gradua
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