• BMB Reports
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• v.35 no.1
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• pp.106-115
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• 2002

The serine/threonine kinase Akt has been intensely studied for its role in growth factor-mediated cell survival for the past 5 years. On the other hand, the ongoing research effort has recently uncovered novel regulatory mechanisms and downstream effectors of Akt that demonstrate the involvement of Akt in other cellular functions such as cell cycle progression, angiogenesis, and cancer cell invasion/metastasis. Furthermore, recent studies using whole model organisms suggest additional roles for Akt in important diseases such as aging and diabetes. The following review addresses these recent advances in the understanding of Akt function.

• IMMUNE NETWORK
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• v.11 no.4
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• pp.223-226
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• 2011

Although exercise-induced growth factors such as Insulin-like growth factor-I (IGF-I) are known to affect various aspects of physiology in skeletal muscle cells, the molecular mechanism by which IGF-I modulates anti-inflammatory effects in these cells is presently unknown. Here, we showed that IGF-I stimulation suppresses the expression of toll-like receptor 4 (TLR4), a key innate immune receptor. A pharmacological inhibitor study further showed that PI3K/Akt signaling pathway is required for IGF-I-mediated negative regulation of TLR4 expression. Furthermore, IGF-I treatment reduced the expression of various NF-${\kappa}B$-target genes such as TNF-${\alpha}$ and IL-6. Taken together, these findings indicate that the anti-inflammatory effect of exercise may be due, at least in part, to IGF-I-induced suppression of TLR4 and subsequent downregulation of the TLR4-dependent inflammatory signaling pathway.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.4
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• pp.1425-1430
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• 2012

Cyclin L2 is a novel member of the cyclin family, recently implicated in the regulation of cell cycle progression and/or transcriptional regulation. The present study was undertaken to investigate the effects of overexpression on tumor cell growth and chemosensitivity in human gastric cells in vitro. Cyclin L2 was transfected into human gastric cancer cell line BCG823 and expressed with a mammalian expression vector pcDNA3.1. The effects and mechanisms of cyclin L2 on cell growth, cell cycling and apoptosis were studied. Compared to control vectors, overexpression of cyclin L2 inhibited the growth of BCG823 cells and enhance their chemosensitivity to fluorouracil, docetaxel and cisplatin. The anti-proliferative effects of cyclin L2 could be due to G0/G1 arrest and apoptosis. Cyclin L2 induced G0/G1 arrest and apoptosis involved upregulation of caspase-3 and down regulation Bcl-2 and survivin. The results indicated that overexpression of cyclin L2 protein may promote efficient growth inhibition and enhance chemosensitivity to chemotherapeutic agents in human gastric cancer cells by inducing G0/G1 cell cycle arrest and apoptosis.

• Journal of Microbiology and Biotechnology
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• v.23 no.11
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• pp.1586-1597
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• 2013

Energy-efficient metabolic responses were often noted in high-productive cultures. To better understand these metabolic responses, an investigation into the relationship between metabolic responses and energy regulation was conducted via a comparative analysis among cultures with different energy source supplies. Both glycolysis and glutaminolysis were studied through the kinetic analyses of major extracellular metabolites concerning the fast and slow cell growth stages, respectively, as well as the time-course profiles of intracellular metabolites. In three cultures showing distinct antibody productivities, the amino acid metabolism and energy state were further examined. Both the transition of lactate from production to consumption and steady intracellular pools of pyruvate and lactate were observed to be correlated with efficient energy regulation. In addition, an efficient utilization of amino acids as the replenishment for the TCA cycle was also found in the cultures with upregulated energy metabolism. It was further revealed that the inefficient energy regulation would cause low cell productivity based on the comparative analysis of cell growth and productivity in cultures having distinct energy regulation.

• Journal of Digital Convergence
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• v.11 no.2
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• pp.59-70
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• 2013

The arcade game market is 2nd big market in the world following console game market. It is a driving force of growth for game industry but its Korean case was decreasing growth of game industry by various kinds of factors. Therefore, it is placed too much emphasis on online game industry and it lost industry growth power. The characteristics of arcade game are spatiality, expandability of device, rewardability, amusemenability. The importance of arcade game are development of new device and freedom of application it but it is restricted by prior deliberation and regulation of industry in korea. Many problems arise from classifying speculation device to arcade game and relaxation of regulation. In this paper, we analyze effectiveness from policy change in Arcade game industry, especially we focused on regulation policy. Also, we found problems and suggested alternatives by comparision on policy of foreign country.

• Molecules and Cells
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• v.37 no.6
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• pp.487-496
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• 2014

Angiotensinogen (AGT), the precursor of angiotensin I, is known to be involved in tumor angiogenesis and associated with the pathogenesis of coronary atherosclerosis. This study was undertaken to determine the role played by AGT in endothelial progenitor cells (EPCs) in tumor progression and metastasis. It was found that the number of EPC colonies formed by AGT heterozygous knockout ($AGT^{+/-}$) cells was less than that formed by wild-type (WT) cells, and that the migration and tube formation abilities of $AGT^{+/-}$ EPCs were significantly lower than those of WT EPCs. In addition, the gene expressions of vascular endothelial growth factor (VEGF), Flk1, angiopoietin (Ang)-1, Ang-2, Tie-2, stromal derived factor (SDF)-1, C-X-C chemokine receptor type 4 (CXCR4), and of endothelial nitric oxide synthase (eNOS) were suppressed in $AGT^{+/-}$ EPCs. Furthermore, the expressions of hypoxia-inducible factor (HIF)-$1{\alpha}$and $-2{\alpha}$ were downregulated in $AGT^{+/-}$ early EPCs under hypoxic conditions, suggesting a blunting of response to hypoxia. Moreover, the activation of Akt/eNOS signaling pathways induced by VEGF, epithelial growth factor (EGF), or SDF-$1{\alpha}$ were suppressed in $AGT^{+/-}$ EPCs. In $AGT^{+/-}$ mice, the incorporation of EPCs into the tumor vasculature was significantly reduced, and lung tumor growth and melanoma metastasis were attenuated. In conclusion, AGT is required for hypoxia-induced vasculogenesis.

• International Commerce and Information Review
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• v.9 no.1
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• pp.277-295
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• 2007

This paper presents the ODR phenomenon with a specific focus on regulatory problems. It argues that the current regulatory framework for online dispute resolution is, to a large extent, defective. Existing deficiencies result not only from a lack of comprehensive ODR law, but also from the weakness of the other modalities of regulation : norms and market. The current today's approach to regulating ODR has been unsuccessful, and it is time to re-examine that position. I would like to say that suggesting details of the optimal ODR regulatory framework is beyond the scope of this paper. From a broader perspective, the field of ODR seems to be not sufficiently regulated. Neither by law, nor by the restrains set by other norms or market. Given the current weakness of the modalities of regulation, online dispute resolution requires greater institutional and international support. It appears that adoption of internationally harmonized ODR law would not hamper the development of norms and market, but rather support their proper growth. As a result, the co-regulation approach recommended in this paper is different from both traditional state-oriented models of regulation and self-regulatory systems. Arguably, this co-regulation approach is the optimal model for regulation of online dispute resolution under current circumstances.

• The Korean Journal of Zoology
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• v.35 no.2
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• pp.161-172
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• 1992

In the short-term treahent of 12-0-tetradecanoylphorbol-13-acetate (TPA) or platelet-derived growth factor (PDGF), the'Wh and PDGF induced the Protein Kinase C (PKC) activation and migration from the cytoplasm to the peripheral nulcear membrane. And the activated PKC which was directly or indirectly stimulated by TPA or PDGF Phosphorylated many kinds of PKC's targeting proteins and induces various biological responses. Especially, the cytoplasmic PKC was phosphorylated within 1 hr and 10 min by TPA-and PDGF-treahent respectivelv. In the long-term treatment of TPA or PDGF, both of them induced the down-regulation and translocation of PKC in the mvoblasts. The down-regulation of PKC isozyrnes, the pattern of PKC I and ll was similar to the PKC 111 isozpnes in the cytoplasm. But in the nucleolus, the TPA did not induce and down-regulation or the inhibition of the immunoreactivity of PKC III antibody. This investigation indicates that each isozvmes of PKC mal be performed the different effects to the down-regulation of the cytoplasm or nucleolus. And douvn-regulated myoblasts contained low immunoreactivity of PKC antibodies.

• KOREAN JOURNAL OF CROP SCIENCE
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• v.34 no.s01
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• pp.1-3
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• 1989

• Proceedings of the Botanical Society of Korea Conference
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• 1993.07a
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• pp.89-106
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• 1993