• Journal of Life Science
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• v.19 no.10
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• pp.1346-1351
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• 2009

Recent evidence has shown that many pluripotetic neural crest cells are fate-restricted and that different fate-restricted crest cells emigrate from the neural tube at different times. Jin et al. (2001) identified the expression patterns of Wnts and its antagonists at the time that neural crest cells were being specified and suggested that Wnt signaling was involved in the segregation/differentiation of neural crest cells in the trunk in vitro. In this study, we evaluated the effects of Wnt signaling in avian neural crest lineage segregation. To accomplish this, Wnt signaling was disturbed at the time of neural crest segregation and differentiation by grafting Wnt-3a expressing cells and conducting dominant negative glycogen synthase kinase (dnGSK) electroporation. Stimulation of Wnt signaling induced neural crest lineage segregation and melanoblast specification, and increased the expression levels of genes known to be involved in neural crest development such as cadherin 7 and Slug, which suggests that they are involved in Wnt-induced neural crest lineage differentiation into melanoblasts.

• The Korean Journal of Physiology and Pharmacology
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• v.11 no.2
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• pp.57-64
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• 2007

Ischemic preconditioning (IPC) is known to protect the heart against ischemia/reperfusion (IR)-induced injuries, and regional differences in the mitochondrial antioxidant state during IR or IPC may promote the death or survival of viable and infarcted cardiac tissues under oxidative stress. To date, however, the interplay between the mitochondrial antioxidant enzyme system and the level of reactive oxygen species (ROS) in the body has not yet been resolved. In the present study, we examined the effects of IR- and IPC-induced oxidative stresses on mitochondrial function in viable and infarcted cardiac tissues. Our results showed that the mitochondria from viable areas in the IR-induced group were swollen and fused, whereas those in the infarcted area were heavily damaged. IPC protected the mitochondria, thus reducing cardiac injury. We also found that the activity of the mitochondrial antioxidant enzyme system, which includes manganese superoxide dismutase (Mn-SOD), was enhanced in the viable areas compared to the infarcted areas in proportion with decreasing levels of ROS and mitochondrial DNA (mtDNA) damage. These changes were also present between the IPC and IR groups. Regional differences in Mn-SOD expression were shown to be related to a reduction in mtDNA damage as well as to the release of mitochondrial cytochrome c (Cyt c). To the best of our knowledge, this might be the first study to explore the regional mitochondrial changes during IPC. The present findings are expected to help elucidate the molecular mechanism involved in IPC and helpful in the development of new clinical strategies against ischemic heart disease.

• Journal of Life Science
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• v.30 no.4
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• pp.402-409
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• 2020

Nervous necrosis virus (NNV) contains a bi-segmented viral genome, RNA1 (3.4 kb, RdRp), and RNA2 (1.4 kb, capsid protein) in a small particle (25 nm). Despite its extremely compact size, NNV has caused serious damage by infecting approximately 120 fish species worldwide since it was first reported in the late 1980s. In order to minimize the damage caused by NNV infection and develop effective vaccines, it is necessary to understand the intra cellular signaling system according to NNV infection. NNV infection induces cell cycle arrest at the G1 phase via the p53-dependent pathway to use the cellular system for its replication. Otherwise, host cells recognize NNV infection through the RIG-1-like receptor (RLR) signaling pathway to control the virus and infected cells, and then ISGs required for antiviral action are activated via the IFN signaling pathway. Moreover, apoptosis of infected cells is triggered by the unfolded protein response (UPR) through ER stress and mitochondria-mediated cell death. Cell signaling studies on the NNV infection mechanisms are still at an early stage and many pathways have yet to be identified. Understanding the various disease-specific cellular signaling systems associated with NNV infection is essential for rapid and accurate diagnosis and vaccine development.

• Proceedings of the KIEE Conference
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• 2005.07b
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• pp.1592-1594
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• 2005

This paper presents a method to construct a supervisory monitoring system for railway signaling devices which can provide the real-time operation information of signalling devices to several maintenance depots. Spying technique has been applied to acquire the real-time data transmitted among railway signaling devices without interfering the railway signalling system function.

• BMB Reports
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• v.49 no.5
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• pp.255-262
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• 2016

The disease known as cerebral cavernous malformations mostly occurs in the central nervous system, and their typical histological presentations are multiple lumen formation and vascular leakage at the brain capillary level, resulting in disruption of the blood-brain barrier. These abnormalities result in severe neurological symptoms such as seizures, focal neurological deficits and hemorrhagic strokes. CCM research has identified 'loss of function' mutations of three ccm genes responsible for the disease and also complex regulation of multiple signaling pathways including the WNT/β-catenin pathway, TGF-β and Notch signaling by the ccm genes. Although CCM research is a relatively new and small scientific field, as CCM research has the potential to regulate systemic blood vessel permeability and angiogenesis including that of the blood-brain barrier, this field is growing rapidly. In this review, I will provide a brief overview of CCM pathogenesis and function of ccm genes based on recent progress in CCM research.

• Journal of the Korea Society of Computer and Information
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• v.14 no.5
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• pp.175-182
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• 2009

We extracted protein signal delivery path from protein interaction data, using location information and weight of protein. We obtained the protein interaction data by experimenting in two-hybrid system using Yeast. We simulated function's data of Hypotonic Shock comparing to signal delivery path provided in KEGG from the results. We measured process running period as well. In future, this research can be key to discover the origin of various genetic diseases and develop treatment.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2023.04a
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• pp.45-45
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• 2023

Autophagy contributes to enhancing the immune system (innate and adaptive immune system) against foreign pathogens. Autophagy of macrophages is used as a major indicator for developing vaccine adjuvants to increase the adaptive immune response. In this study, RAL increased the production of immunostimulatory mediators and phagocytotic activity in RAW264.7 cells. RAL increased p62/SQSTM1 expression. Inhibition of TLR4, JNK, and PI3K/AKT blocked RAL-mediated increase of p62/SQSTM1. RAL activated JNK and PI3K/AKT signaling. RAL-mediated activation of JNK and PI3K/AKT signaling was reversed by TLR4 inhibition. Taken together, it is believed that RAL-mediated autophagy may be dependent on activating via TLR4-dependent activation of JNK and PI3K/AKT signaling in macrophages.

• Journal of the Korean Society for Railway
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• v.18 no.5
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• pp.426-438
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• 2015

Train speed controlling systems are now changing from wayside systems to onboard signaling systems. Locomotive engineers refer to wayside markers to decide on a braking point when the train speed appears to be lower than the current speed. However, in the onboard signaling systems that have been installed recently, the braking point is not determined by the wayside signal but by an onboard value. In this paper, we studied braking points and methods for deciding on such points by engineers using the onboard systems. An optimized braking point is proposed via simulation of decelerating velocity to control the velocity in the signaling system through a predefined point; Gaussian distributions are used to simulate the actual situation. We estimated and demonstrated how to obtain braking parameters in order to satisfy the interval of permitted error.

• BMB Reports
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• v.48 no.6
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• pp.301-302
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• 2015

Hypoxia is associated with many pathological conditions as well as the normal physiology of metazoans. We identified a lactate-dependent signaling pathway in hypoxia, mediated by the oxygen- and lactate-regulated protein NDRG family member 3 (NDRG3). Oxygen negatively regulates NDRG3 expression at the protein level via the PHD2/VHL system, whereas lactate, produced in excess under prolonged hypoxia, blocks its proteasomal degradation by binding to NDRG3. We also found that the stabilized NDRG3 protein promotes angiogenesis and cell growth under hypoxia by activating the Raf-ERK pathway. Inhibiting cellular lactate production abolishes NDRG3-mediated hypoxia responses. The NDRG3-Raf-ERK axis therefore provides the genetic basis for lactate-induced hypoxia signaling, which can be exploited for the development of therapies targeting hypoxia-induced diseases in addition to advancing our understanding of the normal physiology of hypoxia responses. [BMB Reports 2015; 48(6): 301-302]

• Proceedings of the KSR Conference
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• 2004.06a
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• pp.1495-1500
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• 2004

The interface link for railway signaling systems is generally point-to-point communication scheme, but there have been several efforts to apply the network technology to these interface link in overseas country. However general Ethernet scheme has several drawbacks, so this scheme cannot meet the very high reliability, safety and real-time properties. To overcome these drawbacks, there have been studies reduction and modeling of data collision probability for this ethernet at the industrial and academic world. Therefore, in this paper we analyzed describe a interface trend using network technology between railway signaling equipments and will describe a major technology and framework of a network for railway signaling system.