• Journal of Microbiology and Biotechnology
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• v.20 no.3
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• pp.558-562
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• 2010

SDS-PAGE of extracted surface-associated proteins of Lactobacillus rhamnosus strains E/N, Oxy, and Pen, was performed. The obtained protein patterns allowed differentiation of the examined strains, which was not accomplished by the commonly used RAPD genotypic method. The differentiation by the SDS-PAGE method proved to be a useful tool for strain-specific identification, which was further confirmed by 2DE analysis. Therefore, it can be used as an alternative or complementary method for both conventional and genotypic identification procedures, especially when closely related lactobacilli isolates are identified.

• Journal of Periodontal and Implant Science
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• v.35 no.3
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• pp.799-811
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• 2005

This study was carried out to examine the potency of the three surface compo- nents from Porphyromonas gingivalis to stimulate the murine macrophage cell line RAW264.7 to synthesize the pro-inflammatory cytokine tumor necrosis factor alpha($TNF-{\alpha}$) and nitric oxide (NO). Lipopolysaccharide(LPS). lipid A-associated proteins(LAP) and saline-extractable surface -associated material(SAM) were isolated from P. gingivalis 381. $TNF-{\alpha}$ release into culture supernatants was determined by two-site ELISA. NO production was assayed by measuring the accumulation of nitrite in culture supernatants. Western blot analysis of iNOS and analysis of reverse transcription(RT)-PCR products were carried out. The surface components extracted from this bacterium were almost equally potent in stimulating release of $TNF-{\alpha}$ and NO by RAW264.7 cells. $TNF-{\alpha}$ that was being measured immunologically was due to activation of $TNF-{\alpha}$ gene transcription. The present study clearly shows that P. gingivalis surface components fully induced iNOS expression in RAW264.7 cells in the absence of other stimuli. The ability of P. gingivalis surface components to promote the production of $TNF-{\alpha}$ and NO may be important in the pathogenesis of inflammatory periodontal disease.

• Applied Science and Convergence Technology
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• v.24 no.1
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• pp.1-8
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• 2015

Protein immobilization on a gold surface plays an important role in the usefulness of biosensors that utilize gold-coated surfaces such as surface plasmon resonance (SPR), quartz crystal microbalance (QCM), etc. For developing high performance biosensors, it is necessarily required that immobilized proteins must remain biologically active. Loss of protein activity and maintenance of its stability on transducer surfaces is directly associated with the choice of immobilization methods, affecting protein-protein interactions. During the past decade, a variety of strategies have been extensively developed for the effective immobilization of proteins in terms of the orientation, density, and stability of immobilized proteins on analytical devices operating on different principles. In this review, recent advances and novel strategies in protein immobilization technologies developed for biosensors are briefly discussed, thereby providing an useful information for the selection of appropriate immobilization approach.

• Tuberculosis and Respiratory Diseases
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• v.38 no.3
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• pp.228-235
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• 1991

Pulmonary surfactant is a lipoprotein complex composed primarily of phospholipid and lungspecific apoproteins that reduces surface tension in the alveolus and maintains alveolar stability at low lung volume. Three families of lung-specific apoproteins have been described: SP-A, a glycoprotein with a reduced molecular weight of 28~36 KDa. SP-B a hydrophobic protein with a nonreduced molecular weight of 18 KDa, and SP-C a hydrophobic protein with a non-reduced molecular weight of 5~8 KDa. Surfactant proteins have important roles in regulating surfactant metabolism as well as in determining its physical properties. The synthesis of the active surfactant peptides appears to be modulated by system with considerable complexity, including numerous levels of regulation such as cell-specific, hormonal and developmental controls. Endotoxin appears to alter surfactant protein mRNAs differentially. It is hoped that the elucidation of the factors controlling the synthesis and metabolism of the surfactant proteins will aid in understanding the pathogenesis of hyaline membrane disease and offer new avenues for the therapy and diagnosis of ther pulmonary disorders as well.

• Molecules and Cells
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• v.45 no.6
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• pp.353-361
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• 2022

Chronic rhinosinusitis (CRS) is a multifactorial, heterogeneous disease characterized by persistent inflammation of the sinonasal mucosa and tissue remodeling, which can include basal/progenitor cell hyperplasia, goblet cell hyperplasia, squamous cell metaplasia, loss or dysfunction of ciliated cells, and increased matrix deposition. Repeated injuries can stimulate airway epithelial cells to produce inflammatory mediators that activate epithelial cells, immune cells, or the epithelial-mesenchymal trophic unit. This persistent inflammation can consequently induce aberrant tissue remodeling. However, the molecular mechanisms driving disease within the different molecular CRS subtypes remain inadequately characterized. Numerous secreted and cell surface proteins relevant to airway inflammation and remodeling are initially synthesized as inactive precursor proteins, including growth/differentiation factors and their associated receptors, enzymes, adhesion molecules, neuropeptides, and peptide hormones. Therefore, these precursor proteins require post-translational cleavage by proprotein convertases (PCs) to become fully functional. In this review, we summarize the roles of PCs in CRS-associated tissue remodeling and discuss the therapeutic potential of targeting PCs for CRS treatment.

• The Korean Journal of Zoology
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• v.26 no.4
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• pp.235-251
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• 1983

Several approaches have been made to access the mechanism of fusion in chick myoblast in vitro. Lactoperoxidase-catalyzed iodination was applied to labell cell surface proteins during myogenesis. Quantitative as well as qualitative changes were observed in $^131$I surface components of prefusion and postfusion cells. Two proteins with a molecular weight of 165K and 93K daltons were observed to appear at the onset of fusion as compared to prefusion stage. At the same time, 245K dalton protein decreased whereas the low molecular weight proteins increased consistently. The decrease of high molecular weight proteins appears to be associated with the cell cycle of myoblast during differentiation. The increased appearance of low molecular weight proteins might be due to the proteolytic cleavage of the high molecular weight proteins. Examination of intracellulr cAMP levels during fusion has revealed that a large but transient increase in cAMP occurs before the onset of fusion. This result suggests a causal relationship between the increase of cAMP and the onset of fusion, and further, that differentiating myoblasts are synthronized to a high degree. During the course of myoblast differentiation, at least four lowe molecular weight proteins, which different from major surface proteins iodinated, were identifiable in the culture medium. These proteins could be ascribed to be released from the membrane by proteolytic cleavage of surface proteins in the course of myoblast fusion. The significance of cell surface alterations and the released proteins during the fusion, the involvement of cAMP in the onset of fusion and the possibility that fusion is promoted by external factor(s) are discussed.

• BMB Reports
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• v.44 no.6
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• pp.369-374
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• 2011

MHC-I molecules play a critical role in immune surveillance against viruses by presenting peptides to cytotoxic T lymphocytes. Although the mechanisms by which MHC-I molecules assemble and acquire peptides in the ER are well characterized, how MHC-I molecules traffic to the cell surface remains poorly understood. To identify novel proteins that regulate the intracellular transport of MHC-I molecules, MHC-I-interacting proteins were isolated by affinity purification, and their identity was determined by mass spectrometry. Among the identified MHC-I-associated proteins was Tmp21, the human ortholog of yeast Emp24p, which mediates the ER-Golgi trafficking of a subset of proteins. Here, we show that Tmp21 binds to human classical and non-classical MHC-I molecules. The Tmp21-MHC-I complex lacks ${\beta}_2$-microglobulin, and the number of the complexes is increased when free MHC-I heavy chains are more abundant. Taken together, these results suggest that Tmp21 is a novel protein that preferentially binds to ${\beta}_2$-microglobulin-free MHC-I heavy chains.

• Journal of Microbiology and Biotechnology
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• v.17 no.6
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• pp.993-1001
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• 2007

The technique of serological analysis of antigens by recombinant cDNA expression library (SEREX) uses autologous patient sera as a screening probe to isolate tumor-associated antigens for various tumor types. Isolation of tumor-associated antigens that are specifically reactive with patient sera, but not with normal sera, is important to avoid false-positive and autoimmunogenic antigens for the cancer immunotherapy. Here, we describe a selection methodology to isolate patient sera-specific antigens from a yeast surface-expressed cDNA library constructed from 15 patient lung tissues with non-small cell lung cancer (NSCLC). Several rounds of positive selection using patient sera alone as a screening probe isolated clones exhibiting comparable reactivity with both patient and normal sera. However, the combination of negative selection with allogeneic normal sera to remove antigens reactive with normal sera and subsequent positive selection with patient sera efficiently enriched patient sera-specific antigens. Using the selection methodology described here, we isolated 3 known and 5 unknown proteins, which have not been isolated previously, but and potentially associated with NSCLC.

• BMB Reports
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• v.35 no.1
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• pp.61-66
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• 2002

The TNF receptor-associated factor (TRAF) family is a group of adapter proteins that link a wide variety of cell surface receptors. Including the TNF and IL-1 receptor superfamily to diverse signaling cascades, which lead to the activation of NF-${\kappa}B$ and mitogen-activated protein kinases. In addition, TRAFs interact with a variety of proteins that regulate receptor-induced cell death or survival. Thus, TRAF-mediated signals may directly induce cell survival or interfere with the death receptor-induced apoptosis.

• Biomolecules & Therapeutics
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• v.12 no.3
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• pp.145-150
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• 2004

Inflammation is a frequent radiation-induced reaction following therapeutic irradiation. Treatment of human umbilical endothelial cells (HUVEC) with ${\gamma}$-irradiation (${\gamma}$IR) induces the expression of adhesion proteins such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Since the upregulation of these proteins on endothelial cell Surface has been known to be associated with inflammation, interfering with the expression of adhesion molecules is an important therapeutic target. In the present study, we demonstrate that vitamin C inhibits ${\gamma}$IR induced expression of ICAM-1, VCAM-1, and E-selectin on HUVEC in a dose- and time dependent manner. Vitamin C a1so inhibited the production of Nitric oxide (NO) induced by ${\gamma}$IR. These data suggest that vitamin C has therapeutic potential for the treatment of various inflammatory disorder associated with an increase of endothelial leukocyte adhesion molecules.