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Search Results: 1 - 10 of 5002 matches for " Kyungsun Choi "
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Downregulation of OPA3 Is Responsible for Transforming Growth Factor-β-Induced Mitochondrial Elongation and F-Actin Rearrangement in Retinal Pigment Epithelial ARPE-19 Cells
Seung-Wook Ryu, Jonghee Yoon, Nambin Yim, Kyungsun Choi, Chulhee Choi
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0063495
Abstract: Transforming growth factor-β signaling is known to be a key signaling pathway in the induction of epithelial–mesenchymal transition. However, the mechanism of TGF-β signaling in the modulation of EMT remains unclear. In this study, we found that TGF-β treatment resulted in elongation of mitochondria accompanied by induction of N-cadherin, vimentin, and F-actin in retinal pigment epithelial cells. Moreover, OPA3, which plays a crucial role in mitochondrial dynamics, was downregulated following TGF-β treatment. Suppression of TGF-β signaling using Smad2 siRNA prevented loss of OPA3 induced by TGF-β. Knockdown of OPA3 by siRNA and inducible shRNA significantly increased stress fiber levels, cell length, cell migration and mitochondrial elongation. In contrast, forced expression of OPA3 in ARPE-19 cells inhibited F-actin rearrangement and induced mitochondrial fragmentation. We also showed that Drp1 depletion increased cell length and induced rearrangement of F-actin. Depletion of Mfn1 blocked the increase in cell length during TGF-β-mediated EMT. These results collectively substantiate the involvement of mitochondrial dynamics in TGF-β-induced EMT.
Mutant Ubiquitin Attenuates Interleukin-1β- and Tumor Necrosis Factor-α-Induced Pro-Inflammatory Signaling in Human Astrocytic Cells
Kyungsun Choi, Junseong Park, Jungsul Lee, Eun Chun Han, Chulhee Choi
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0067891
Abstract: A frameshift mutation of ubiquitin called ubiquitin+1 (UBB+1) was found in the aging and Alzheimer’s disease brains and thought to be associated with neuronal dysfuction and degeneration. Even though ubiquitylation has been known to regulate vital cellular functions mainly through proteasome-dependent degradation of polyubiquitinated substrates, proteolysis-independent roles of ubiquitylation have emerged as key mechanisms in various signaling cascades. In this study, we have investigated the effect of UBB+1 on proinflammatory signaling such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in human astrocytes. Treatment with TNF-α and IL-1β induced expression of CCL2 and CXCL8 by human astrocytic cells; while ectopic expression of UBB+1 significantly abrogated the proinflammatory cytokine-induced expression of chemokines. Ectopic expression of UBB+1 suppressed TNF-α- and IL-1β-induced activation of NF-κB and JNK signaling pathway. Furthermore, we have demonstrated that polyubiquitylation of TRAFs and subsequent phosphorylation of TAK1 were significantly inhibited by stable expression of UBB+1. Collectively, these results suggest that UBB+1 may affect proinflammatory signaling in the central nervous system via inhibitory mechanisms of ubiquitin-dependent signaling in human astrocytes.
Mutant Ubiquitin UBB+1 Induces Mitochondrial Fusion by Destabilizing Mitochondrial Fission-Specific Proteins and Confers Resistance to Oxidative Stress-Induced Cell Death in Astrocytic Cells
Nambin Yim, Seung-Wook Ryu, Eun Chun Han, Jonghee Yoon, Kyungsun Choi, Chulhee Choi
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0099937
Abstract: Mutant ubiquitin UBB+1 is observed in a variety of aging-related neurodegenerative diseases and acts as a potent inhibitor of the ubiquitin proteasome system (UPS). In the present study, we investigated the relationship between impaired UPS (using ectopic expression of UBB+1) and mitochondrial dynamics in astrocytes, which are the most abundant glial cells in the central nervous system. Immunocytochemistry and fluorescence recovery after photobleaching revealed that ectopic expression of UBB+1 induced mitochondrial elongation. We further demonstrated that overexpression of UBB+1 destabilized mitochondrial fission-specific proteins including Drp1, Fis1, and OPA3, but not the mitochondrial fusion-specific proteins Mfn1, Mfn2, and OPA1. The reduction in mitochondrial fission-specific proteins by UBB+1 was prevented by inhibiting the 26 S proteasome using chemical inhibitors, including MG132, lactacystin and epoxomicin. We then assessed the involvement of proteases that target mitochondrial proteins by using various protease inhibitors. Finally, we confirmed that either overexpression of UBB+1 or inhibiting the proteasome can protect astrocytic cells from H2O2-induced cell death compared with control cells. Our results suggest that UBB+1 destabilizes mitochondrial fission-specific proteins, leading to mitochondrial fusion and the subsequent resistance to oxidative stress. We therefore propose a protective role of UBB+1 overexpression or the proteasome inhibition in astrocytes in degenerative brains.
Phenotypic Modulation of Primary Vascular Smooth Muscle Cells by Short-Term Culture on Micropatterned Substrate
Soyoung Chang, Seungjeong Song, Jungsul Lee, Jonghee Yoon, Junseong Park, Sungyoung Choi, Je-Kyun Park, Kyungsun Choi, Chulhee Choi
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0088089
Abstract: Loss of contractility and acquisition of an epithelial phenotype of vascular smooth muscle cells (VSMCs) are key events in proliferative vascular pathologies such as atherosclerosis and post-angioplastic restenosis. There is no proper cell culture system allowing differentiation of VSMCs so that it is difficult to delineate the molecular mechanism responsible for proliferative vasculopathy. We investigated whether a micropatterned substrate could restore the contractile phenotype of VSMCs in vitro. To induce and maintain the differentiated VSMC phenotype in vitro, we introduced a micropatterned groove substrate to modulate the morphology and function of VSMCs. Later than 7th passage of VSMCs showed typical synthetic phenotype characterized by epithelial morphology, increased proliferation rates and corresponding gene expression profiles; while short-term culture of these cells on a micropatterned groove induced a change to an intermediate phenotype characterized by low proliferation rates, increased migration, a spindle-like morphology associated with cytoskeletal rearrangement and expression of muscle-specific genes. Microarray analysis showed preferential expression of contractile and smooth muscle cell-specific genes in cells cultured on the micropatterned groove. Culture on a patterned groove may provide a valuable model for the study the role of VSMCs in normal vascular physiology and a variety of proliferative vascular diseases.
Topological Excitations in Double-Layer Quantum Hall systems
Kyungsun Moon
Physics , 1996, DOI: 10.1103/PhysRevLett.78.3741
Abstract: Double-layer quantum Hall systems with spontaneous broken symmetry can exhibit a novel manybody quantum Hall effect due to the strong interlayer coherence. When the layer separation becomes close to the critical value, quantum fluctuations can destroy the interlayer coherence and the quantum Hall effect will disappear. We calculate the renormalized isospin stiffness $\rho_s$ due to quantum fluctuations within the Hartree-Fock-RPA formalism. The activation energy of the topological excitations thus obtained demonstrates a nice qualitative agreement with recent experiment.
Photon Number Splitting of Squeezed Light by a Single Qubit in Circuit QED
Kyungsun Moon
Physics , 2013, DOI: 10.1103/PhysRevA.88.043830
Abstract: We theoretically propose an efficient way to generate and detect squeezed light by a single qubit in circuit QED. By tuning the qubit energy splitting close to the fundamental frequency of the first harmonic mode (FHM) in a transmission line resonator and placing the qubit at the nodal point of the third harmonic mode, one can generate the resonantly enhanced squeezing of the FHM upon pumping with the second harmonic mode. In order to investigate the photon number splitting for the squeezed FHM, we have numerically calculated the qubit absorption spectrum, which exhibits regularly spaced peaks at frequencies separated by twice the effective dispersive shift. It is also shown that adding a small pump field for the FHM makes additional peaks develop in between the dominant ones as well.
Anisotropic Transport of Quantum Hall Meron-Pair Excitations
Kyungsun Moon,Kieran Mullen
Physics , 1997, DOI: 10.1103/PhysRevB.57.1378
Abstract: Double-layer quantum Hall systems at total filling factor $\nu_T=1$ can exhibit a commensurate-incommensurate phase transition driven by a magnetic field $B_{\parallel}$ oriented parallel to the layers. Within the commensurate phase, the lowest charge excitations are believed to be linearly-confined Meron pairs, which are energetically favored to align with $B_{\parallel}$. In order to investigate this interesting object, we propose a gated double-layer Hall bar experiment in which $B_{\parallel}$ can be rotated with respect to the direction of a constriction. We demonstrate the strong angle-dependent transport due to the anisotropic nature of linearly-confined Meron pairs and discuss how it would be manifested in experiment.
An accurate effective action for `baby' to `adult' skyrmions
Kyungsun Moon,Kieran Mullen
Physics , 1997, DOI: 10.1103/PhysRevB.57.14833
Abstract: Starting with a Chern-Simons theory, we derive an effective action for interacting quantum Hall skyrmions that takes into account both large-distance physics and short-distance details as well. We numerically calculate the classical static skyrmion profile from this action and find excellent agreement with other, microscopic calculations over a wide range of skyrmion sizes including the experimentally relevant one. This implies that the essential physics of this regime might be captured by a continuum classical model rather than resorting to more microscopic approaches. We also show that the skyrmion energy closely follows the formula suggested earlier by Sondhi et al. for a broad parameter range of interest as well.
Tunneling magnetoresistance in diluted magnetic semiconductor tunnel junctions
Pin Lyu,Kyungsun Moon
Physics , 2001, DOI: 10.1103/PhysRevB.64.035201
Abstract: Using the spin-polarized tunneling model and taking into account the basic physics of ferromagnetic semiconductors, we study the temperature dependence of the tunneling magnetoresistance (TMR) in the diluted magnetic semiconductor (DMS) trilayer heterostructure system (Ga,Mn)As/AlAs/(Ga,Mn)As. The experimentally observed TMR ratio is in reasonable agreement with our result based on the typical material parameters. It is also shown that the TMR ratio has a strong dependence on both the itinerant-carrier density and the magnetic ion density in the DMS electrodes. This can provide a potential way to achieve larger TMR ratio by optimally adjusting the material parameters.
Ferromagnetism in diluted magnetic semiconductor quantum dot arrays embedded in semiconductors
Pin Lyu,Kyungsun Moon
Physics , 2002, DOI: 10.1140/epjb/e2004-00009-1
Abstract: We present an Anderson-type model Hamiltonian with exchange coupling between the localized spins and the confined holes in the quantum dots to study the ferromagnetism in diluted magnetic semiconductor (DMS) quantum dot arrays embedded in semiconductors. The hybridization between the quantum-confined holes in the DMS quantum dots and the itinerant holes in the semiconductor valence band makes hole transfer between quantum dots, which can induce the long range ferromagnetic order of the localized spins. In addition, it makes the carrier spins both in the DMS quantum dots and in the semiconductors polarized. The spontaneous magnetization of the localized spins and the spin polarization of the holes are calculated using both the Weiss mean field approximation and the self-consistent spin wave approximation, which are developed for the present model.
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