• Animal cells and systems
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• v.12 no.1
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• pp.1-9
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• 2008

In the developing limb, chondrogenesis is an important prerequisite for the formation of cartilage whose template is required for bone formation. Chondrogenesis is a tightly regulated multi-step process, including mesenchymal cell recruitment/migration, prechondrogenic condensation of the mesenchymal cells, commitment to the chondrogenic lineage, and differentiation into chondrocytes. This process is controlled exquisitely by cellular interactions with the surrounding matrix and regulating factors that initiate or suppress cellular signaling pathways and transcription of specific genes in a temporal-spatial manner. Understanding the cellular and molecular mechanisms of chondrogenesis is important not only in the context of establishing basic principle of developmental biology but also in providing research direction toward preventive and/or regenerative medicine. Here, I will overview the current understanding of cellular and molecular mechanisms contributing to prechondrogenic condensation processes, the crucial steps for chondrogenesis, focusing on cell-cell and cell-matrix interactions.

• BMB Reports
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• v.35 no.1
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• pp.67-86
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• 2002

Three routes have been identified triggering neuronal death under physiological and pathological conditions. Excess activation of ionotropic glutamate receptors cause influx and accumulation of $Ca^{2+}$ and $Na^+$ that result in rapid swelling and subsequent neuronal death within a few hours. The second route is caused by oxidative stress due to accumulation of reactive oxygen and nitrogen species. Apoptosis or programmed cell death that often occurs during developmental process has been coined as additional route to pathological neuronal death in the mature nervous system. Evidence is being accumulated that excitotoxicity, oxidative stress, and apoptosis propagate through distinctive and mutually exclusive signal transduction pathway and contribute to neuronal loss following hypoxic-ischemic brain injury. Thus, the therapeutic intervention of hypoxic-ischemic neuronal injury should be aimed to prevent excitotoxicity, oxidative stress, and apoptosis in a concerted way.

• BMB Reports
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• v.51 no.10
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• pp.486-492
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• 2018

The CCN protein family is composed of six matricellular proteins, which serve regulatory roles rather than structural roles in the extracellular matrix. First identified as secreted proteins which are induced by oncogenes, the acronym CCN came from the names of the first three members: CYR61, CTGF, and NOV. All six members of the CCN family consist of four cysteine-rich modular domains. CCN proteins are known to regulate cell adhesion, proliferation, differentiation, and apoptosis. In addition, CCN proteins are associated with cardiovascular and skeletal development, injury repair, inflammation, and cancer. They function either through binding to integrin receptors or by regulating the expression and activity of growth factors and cytokines. Given their diverse roles related to the pathology of certain diseases such as fibrosis, arthritis, atherosclerosis, diabetic nephropathy, retinopathy, and cancer, there are many emerging studies targeting CCN protein signaling pathways in attempts to elucidate their potentials as therapeutic targets.

• BMB Reports
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• v.35 no.6
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• pp.537-546
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• 2002

NF-${\kappa}B$/Rel transcription factor family participates in diverse biological processes including embryo development, hematopoiesis, immune regulation, as well as neuronal functions. In this review, the NF-${\kappa}B$/Rel signal transduction pathways and their important roles in the regulation of immune system will be discussed. NF-${\kappa}B$/Rel members execute distinct functions in multiple immune cell types via the regulation of target genes essential for cell proliferation, survival, effector functions, cell trafficking and communication, as well as the formation of lymphoid architecture. Consequently, proper activation of NF-${\kappa}B$/Rel during immune responses to allergens, auto-antigens, allo-antigens, and pathogenic infection is crucial for the integrity of host innate and adaptive immunity.

• Asian-Australasian Journal of Animal Sciences
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• v.30 no.3
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• pp.299-308
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• 2017

Oxidative stress suppresses animal health, performance, and production, subsequently impacting economic feasibility; hence, maintaining and improving oxidative status especially through natural nutrition strategy are essential for normal physiological process in animals. Phytochemicals are naturally occurring antioxidants that could be considered as one of the most promising materials used in animal diets in various forms. In this review, their antioxidant effects on animals are discussed as reflected by improved apparent performance, productivity, and the internal physiological changes. Moreover, the antioxidant actions toward animals further describe a molecular basis to elucidate their underlying mechanisms targeting signal transduction pathways, especially through the antioxidant response element/nuclear factor (erythroid-derived 2)-like 2 transcription system.

• Molecules and Cells
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• v.22 no.2
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• pp.133-140
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• 2006

Jun activation domain-binding protein 1 (Jab1) is involved in various cellular mechanisms including development in Drosophila and mouse, cell cycle control and signal transduction pathways. Recent studies also determined that Jab1 functions as a nuclear exporter and inducer of cytoplasmic degradation for several proteins including p53, p27, capsid of West Nile virus, and Smad4/7 proteins. In particular, p53 is shown to bind to and to be exported into the cytoplasm by Jab1, which helps to maintain low levels of p53 under normal conditions. This review was undertaken in an effort to understand the biological significance of the homeostasis of p53 as maintained in the presence of Jab1. Based on our observations, we have provided potential mechanistic hypotheses for the nuclear export of p53 in coordination with Jab1 and the role of other factors in these processes.

• Journal of Fisheries and Marine Sciences Education
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• v.28 no.5
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• pp.1266-1272
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• 2016

Phospholipase C is a key enzyme of signaling pathways hydrolyzed phosphatidylinositol 4,5-bisphosphate to generate 2 second messengers. Among the PLC, $PLC-{\beta}$ subfamily consisted of 4 isoforms, $PLC-{\beta}$ 1~4. Here, we studied the tissue specific expression of $PLC-{\beta}3$ in olive flounder (Paralichthys olivaceus) following external stimulation like lipopolysaccharide (LPS), concanavalin A (ConA) and environmental stress compared with the inflammatory cytokines IL-1b. $PoPLC-{\beta}3$ gene transcripts has the effect in stimulated tissue compared to control. These results provide what we sure to be a important role for $PLC-{\beta}3$ activity in tissue and verify $PLC-{\beta}3$ as potential immune enzyme for signal transduction.

• Genomics & Informatics
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• v.4 no.2
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• pp.57-64
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• 2006

We identified differentially expressed genes in RAW264.7 cells in response to single and double ligand treatments (LPS, $IFN{\gamma}$, 2MA, LPS plus $IFN{\gamma}$, and LPS plus 2MA). The majority of the regulated transcripts responded additively to dual ligand treatment. However, a significant fraction responded in a non-additive fashion. Several cytokines showing non-additive transcriptional responses to dual ligand treatment also showed non-additive protein production/secretion responses in separately performed experiments. Many of the genes with non-additive responses to LPS plus 2MA showed enhanced responses and encoded pro-inflammatory proteins. LPS plus $IFN{\gamma}$ appeared to induce both non-additive enhancement and non-additive attenuation of gene expression. The affected genes were associated with a variety of biological functions. These experiments reveal both dependent and independent regulatory pathways and point out the specific nature of the regulatory interactions.

• Genomics & Informatics
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• v.11 no.4
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• pp.224-229
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• 2013

Receptor for advanced glycation endproducts (RAGE) is a multi-ligand receptor that is able to bind several different ligands, including advanced glycation endproducts, high-mobility group protein (B)1 (HMGB1), S-100 calcium-binding protein, amyloid-${\beta}$-protein, Mac-1, and phosphatidylserine. Its interaction is engaged in critical cellular processes, such as inflammation, proliferation, apoptosis, autophagy, and migration, and dysregulation of RAGE and its ligands leads to the development of numerous human diseases. In this review, we summarize the signaling pathways regulated by RAGE and its ligands identified up to date and demonstrate the effects of hyper-activation of RAGE signals on human diseases, focused mainly on renal disorders. Finally, we propose that RAGE and its ligands are the potential targets for the diagnosis, monitoring, and treatment of numerous renal diseases.

• Genomics & Informatics
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• v.18 no.4
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• pp.39.1-39.8
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• 2020

Alzheimer's disease (AD) is a chronic, progressive brain disorder that slowly destroys affected individuals' memory and reasoning faculties, and consequently, their ability to perform the simplest tasks. This study investigated the hub genes of AD. Proteins interact with other proteins and non-protein molecules, and these interactions play an important role in understanding protein function. Computational methods are useful for understanding biological problems, in particular, network analyses of protein-protein interactions. Through a protein network analysis, we identified the following top 10 hub genes associated with AD: PTGER3, C3AR1, NPY, ADCY2, CXCL12, CCR5, MTNR1A, CNR2, GRM2, and CXCL8. Through gene enrichment, it was identified that most gene functions could be classified as integral to the plasma membrane, G-protein coupled receptor activity, and cell communication under gene ontology, as well as involvement in signal transduction pathways. Based on the convergent functional genomics ranking, the prioritized genes were NPY, CXCL12, CCR5, and CNR2.