• Proceedings of the Korean Society of Potoscience Conference
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• spring
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• pp.97-103
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• 2003

Phytochrome controls diverse aspects of plant development in response to the ambient light conditions. HFRl, a basic helix-loop-helix protein, is required for a subset of phytochrome A (phy A)-mediated photo-responses in Arabidopsis. Here, we show that overexpression of HFR1-N105, but not the one of the full-length HFR1, confers exaggerated photo-responses. The transgenic plants overexpressing HFR1- N105 exhibited light-independence in a subset of photo-responses, including germination, de-etiolation, gravitropic hypocotyl growth, and blocking of greening. Overexpression of HFR1-N105 also caused constitutive light-responses in the expression of some light-regulated genes. In addition, the HFR1-N105 overexpressor showed hypersensitive responses under R and FR light, dependently on phyB and phyA, respectively. End-of-day far-red light response and petiole elongation were suppressed in the HFR1-N105 overexpressor plants. Together these results imply that overexpression of HFR1-N105 activated a branch of light signaling, supporting the hypothesis that transcriptional regulation in the nucleus would be the primary mechanism of light signaling in Arabidopsis. We discuss the biotechnological potential of the mutant bHLH protein, HFR1-N105 in regard to suppressed shade avoidance syndrome.

• Parasites, Hosts and Diseases
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• v.59 no.5
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• pp.501-505
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• 2021

The pathogenic free-living amoeba Naegleria fowleri causes primary amoebic meningoencephalitis, a fatal infection, by penetrating the nasal mucosa and migrating to the brain via the olfactory nerves. N. fowleri can induce host cell death via lytic necrosis. Similar to phosphorylation, O-linked β-N-acetylglucosamine (O-GlcNAc) glycosylation (O-GlcNAcylation) is involved in various cell-signaling processes, including apoptosis and proliferation, with O-GlcNAc addition and removal regulated by O-GlcNAc transferase and O-GlcNAcase (OGA), respectively. However, the detailed mechanism of host cell death induced by N. fowleri is unknown. In this study, we investigated whether N. fowleri can induce the modulation of O-GlcNAcylated proteins during cell death in Jurkat T cells. Co-incubation with live N. fowleri trophozoites increased DNA fragmentation. In addition, incubation with N. fowleri induced a dramatic reduction in O-GlcNAcylated protein levels in 30 min. Moreover, pretreatment of Jurkat T cells with the OGA inhibitor PUGNAc prevented N. fowleri-induced O-deGlcNAcylation and DNA fragmentation. These results suggest that O-deGlcNAcylation is an important signaling process that occurs during Jurkat T cell death induced by N. fowleri.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.3
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• pp.327-334
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• 2017

Epidemiologic interest in particulate matter (PM) is growing particularly because of its impact of respiratory health. It has been elucidated that PM evoked inflammatory signal in pulmonary epithelia. However, it has not been established $Ca^{2+}$ signaling mechanisms involved in acute PM-derived signaling in pulmonary fibroblasts. In the present study, we explored dust particles PM modulated intracellular $Ca^{2+}$ signaling and sought to provide a therapeutic strategy by antagonizing PM-induced intracellular $Ca^{2+}$ signaling in human lung fibroblasts MRC5 cells. We demonstrated that PM10, less than $10{\mu}m$, induced intracellular $Ca^{2+}$ signaling, which was mediated by extracellular $Ca^{2+}$. The PM10-mediated intracellular $Ca^{2+}$ signaling was attenuated by antioxidants, phospholipase blockers, polyADPR polymerase 1 inhibitor, and transient receptor potential melastatin 2 (TRPM2) inhibitors. In addition, PM-mediated increases in reactive oxygen species were attenuated by TRPM2 blockers, clotrimazole (CLZ) and N-(p-amylcinnamoyl) anthranilic acid (ACA). Our results showed that PM10 enhanced reactive oxygen species signal by measuring DCF fluorescence and the DCF signal attenuated by both TRPM2 blockers CLZ and ACA. Here, we suggest functional inhibition of TRPM2 channels as a potential therapeutic strategy for modulation of dust particle-mediated signaling and oxidative stress accompanying lung diseases.

• Bulletin of the Korean Chemical Society
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• v.31 no.5
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• pp.1309-1313
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• 2010

The effects of boronic acid on the fluoride-selective chemosignaling behavior of a merocyanine dye were investigated. In the presence of phenylboronic acid (PBA), N-methylquinolinium-based merocyanine dye displayed fluoride-selective chromogenic signaling behavior over other commonly coexisting anions in the micromolar concentration range. Signaling is produced by a fluoride-induced displacement of the dye from its complex with PBA, resulting in a significant chromogenic signal for the fluoride ion. This signaling was successfully analyzed using a ratiometric analysis of the UV-vis absorption in response to changes in fluoride ion concentration. A PBA substituted with an electron withdrawing group was found to exhibit a more pronounced signal. Polymer-bound PBA also exhibited useful fluoride-selective signaling behavior.

• Journal of Korean Neurosurgical Society
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• v.42 no.6
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• pp.470-474
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• 2007

Objective : The brain is dependent on glucose as an energy source. Intricate homeostatic mechanisms have been implicated in maintaining the blood glucose concentration in the brain. The aim of this study is to find the way to identify the metabolic proteins regulating the glucose in rat hypothalamus. Methods : In this study, we analysed the secretome from rat hypothalamus in vivo. We introduced 500 nM of insulin into the rat hypothalamus. The chromatographic patterns of the secretome were identified, after which Mass Spectrometry-Mass Spectrometry (MS-MS) analysis was performed. Results : In Liquid Chromatography-Mass Spectrometry (LC-MS) analysis, 60 proteins were identified in the secretome. Among them, 8 novel proteins were unveiled and were associated with the energy metabolism of insulin signaling in mitochondria of rat hypothalamic neuron. Nineteen other proteins have unknown functions. These ligands were confirmed to be secreting from the rat hypothalmus on insulin signaling by western blotting. Conclusion : The hypothalamus is the master endocrine gland responsible for the regulation of various physiological and metabolic processes. Proteomics using LC-MS analysis offer a efficient means for generating a comprehensive analysis of hypothalamic protein expression by insulin signaling.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.8
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• pp.4775-4778
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• 2013

The key signaling networks regulating cancer cell proliferation remain to be defined. The leucine-rich repeat containing G-protein coupled receptor 48 (GPR48) plays an important role in multiple organ development. In the present study, we investigated whether GPR48 functions in cancer cells using MCF-7, HepG2, NCI-N87 and PC-3 cells. We found that GPR48 overexpression promotes while its knockdown using small interfering RNA oligos inhibits cell proliferation. In addition, Wnt/${\beta}$-catenin signaling was activated in cells overexpressing GPR48. Therefore, our results indicated that GPR48 activates Wnt/${\beta}$-catenin signaling to regulate cancer cell proliferation.

• Journal of applied mathematics & informatics
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• v.12 no.1_2
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• pp.395-408
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• 2003

Common Channel Signaling(CCS) networks need special controls to avoid overload of signaling networks and degradation of call process-ing rate, since they play an important role of controlling communication transfer networks. Congestion control and flow control mechanisms are well described in ITU-T recommendation on Signaling System No.7(SS7). For the practical provisions, however, we need an analysis on the relation among service objects, system requirements and implementation of congestion control algorithms. SS7 provides several options for controlling link congestion in CCS networks. In this paper we give a general queueing model of congestion control algorithm which covers both the international and national options. From the queuing model, we obtain the performance parameters such as throughput, message loss rate and mean delay for the international option. To show the performance of the algorithm, some numerical results are also given.

• Molecules and Cells
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• v.23 no.2
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• pp.123-131
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• 2007

Extracellular stresses induce heat shock response and render cells resistant to lethal stresses. Heat shock response involves induction of heat shock proteins (Hsps). Recently the roles of Hsps in neurodegenerative diseases and cancer are attracting increasing attention and have accelerated the study of heat shock response mechanism. This review focuses on the stress sensing steps, molecules involved in Hsps production, diseases related to Hsp malfunctions, and the potential of proteomics as a tool for understanding the complex signaling pathways relevant to these events.

• Proceedings of the KIEE Conference
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• 1999.07a
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• pp.492-494
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• 1999

To improve safety operation of urban transit, compatible design of signaling system is most important factor at future train operation and management. Therefore, signaling system should be designed compatible transport demand of target year. In addition, signaling system should be designed improved train safety, based fail-safe principle. Most of all, to solve passenger concentration, high density and to improve efficiency of train operation. Headway improvement of train is most important. Train organization length of new urban transit as light rail is generally shorter than EMU. Therefore, to increase passenger service and operation efficiency, minimum headway of one minute in this system should be important required.

• Molecules and Cells
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• v.26 no.4
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• pp.350-355
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• 2008

Chk2 is a well characterized protein kinase with key roles in the DNA damage response. Chk2 is activated by phosphorylation following DNA damage, and relays that signal to various substrate proteins to induce cell cycle arrest, DNA repair, and apoptosis. In order to identify novel components of the Chk2 signaling pathway in Drosophila, we screened 2,240 EP misexpression lines for dominant modifiers of an adult rough eye phenotype caused by Chk2 overexpression in postmitotic cells of the eye imaginal disc. The rough eye phenotype was suppressed by mutation of the ATM kinase, a well-described activator of Chk2. Twenty-five EP modifiers were identified (three enhancers and 22 suppressors), none of which correspond to previously known components of Chk2 signaling. Three EPs caused defects in G2 arrest after irradiation with incomplete penetrance when homozygous, and are likely directly involved in the response to DNA damage. Possible roles for these modifiers in the DNA damage response and Chk2 signaling are discussed.