• Journal of Life Science
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• v.14 no.1
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• pp.26-31
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• 2004

Redox factor-1 (Ref-1), known as a redox regulator, controls the DNA binding of AP-1 and is activated in HT29 colon cancer cells by hypoxia in vitro. REF-1 also increases tile DNA binding affinity of Hypoxia-inducible Factor-lalpha$ (HIF-lalpha$), HIF-like Factor (HLF) and early growth response-1 (Egr-1) which induce expression of the genes involved in angiogenesis, so that we speculate that REF-1 may play a role in hypoxia-induced angiogenesis. In this research we tried to detect novel proteins interacting with REF-1 using Yeast two-hybrid system using full-length REF-1 cDNA as bait. As result of such screening we detected 3 positive clones. DNA sequencing and GeneBank search revealed that one of the clones contained the same sequences as M.musculus cDNA for tioredoxin.

• Bulletin of the Korean Chemical Society
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• v.20 no.12
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• pp.1457-1463
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• 1999

Structure and their redox property of the vanadium oxides prepared by decomposing NH₄VO₃ at various temperatures were studied by XRD, SEM, XPS, and temperature programmed reduction/temperature programmed oxidation (TPR/TPO) experiment. All TPR profiles have two sharp peaks in the temperature range 650-750℃, and the area ratio of the two sharp peaks changed from sample to sample. There were three redox steps in TPR/TPO profiles. The oxidation proceeded in the reverse order of the reduction process, and both the reactions proceeded via quite a stable intermediates. The changes of the morphological factor $(I_{(101)}/I_{(010)})$, the ratio of $O_{1S}$ peak area (O$_{1S}$( α)/O$_{1S}$( β)) in the XPS results, and the ratio of hydrogen consumption in TPR profiles with various vanadium oxides showed the distinct relationship between the structural property and their redox property of vanadium oxides. The change of the specific yield of phthalic anhydride with various vanadium oxides showed a very similar trend to those of the peak area ratio in TPR profiles, which meant that the first reduction step related to the partial oxidation of o-xylene on the vanadium oxide catalyst.

• Journal of Soil and Groundwater Environment
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• v.25 no.1
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• pp.25-36
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• 2020

In a redox transition zone, geochemical reactions are facilitated by active bacteria that mediate reactions involving electrons, and arsenic (As) and iron (Fe) cycles are the major electron transfer reactions occurring at such a site. In this study, the effect of repetitive redox changes on soil bacterial community in As-contaminated soil was investigated. The results revealed that bacterial community changed actively in response to redox changes, and bacterial diversity gradually decreased as the cycle repeated. Proportion of strict aerobes and anaerobes decreased, while microaerophilic species such as Azospirillum oryzae group became the predominant species, accounting for 72.7% of the total counts after four weeks of incubation. Bacterial species capable of reducing Fe or As (e.g., Clostridium, Desulfitobacterium) belonging to diverse phylogenetic groups were detected. Indices representing richness (i.e., Chao 1) and phylogenetic diversity decreased from 1,868 and 1,926 to 848 and 1,121, respectively. Principle component analysis suggests that repetitive redox fluctuation, rather than oxic or anoxic status itself, is an important factor in determining the change of soil bacterial community, which in turn affects the cycling of As and Fe in redox transition zones.

• 대한약리학회:학술대회논문집
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• 2006.10a
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• pp.112.2-112.2
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• 2006

• Proceedings of the PSK Conference
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• 2001.10a
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• pp.217.1-217.1
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• 2001

• Animal Bioscience
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• v.34 no.4
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• pp.652-661
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• 2021

Objective: Wooden breast (WB) is a novel myopathy affecting modern broiler chickens, which causes substantial economic losses in the poultry industry. The objective of this study was to evaluate the effect of WB abnormality on meat quality, redox status, as well as the expression of genes of the nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway. Methods: A total of 80 broilers (Ross 308, 42 days of age, about 2.6 kg body weight) raised at Jiujin farm (Suqian, Jiangsu, China) were used. Twelve unaffected (no detectable hardness of the breast area) and twelve WB-affected (diffuse remarkable hardness in the breast muscle) birds were selected from the commercial broiler farm according to the criteria proposed by previous studies. Results: The results indicated that WB showed histological lesions characterized by fiber degeneration and fibrosis, along with an increase of muscle fiber diameter (p<0.05). Moreover, higher pH value, lightness, yellowness, drip loss and cooking loss were observed in the WB group (p<0.05). Compared with the normal breast (NOR) group, the WB group showed higher formation of reactive oxygen species (p<0.05), increased level of oxidation products and antioxidant activities (p<0.05), accompanied with mitochondrial damages and lower mitochondrial membrane potential (p<0.05). Meanwhile, the relative mRNA expressions of Nrf2 and its downstream antioxidant genes including heme oxygenase-1, NAD(P)H qui none dehydrogenase 1, glutathione peroxidase, superoxide dismutase, and glutamate-cysteine ligase were higher than those of the NOR group (p<0.05). Conclusion: In conclusion, WB myopathy impairs meat quality by causing oxidative damages and mitochondrial dysfunction in broilers, even though the activated Nrf2/antioxidant response element pathway provides protection for the birds.

• 순환기질환의공학회:학술대회논문집
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• 2003.11a
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• pp.2-3
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• 2003

• Molecules and Cells
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• v.39 no.1
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• pp.65-71
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• 2016

A challenge in the redox field is the elucidation of the molecular mechanisms, by which $H_2O_2$ mediates signal transduction in cells. This is relevant since redox pathways are disturbed in some pathologies. The transcription factor OxyR is the $H_2O_2$ sensor in bacteria, whereas Cys-based peroxidases are involved in the perception of this oxidant in eukaryotic cells. Three possible mechanisms may be involved in $H_2O_2$ signaling that are not mutually exclusive. In the simplest pathway, $H_2O_2$ signals through direct oxidation of the signaling protein, such as a phosphatase or a transcription factor. Although signaling proteins are frequently observed in the oxidized state in biological systems, in most cases their direct oxidation by $H_2O_2$ is too slow ($10^1M^{-1}s^{-1}$ range) to outcompete Cys-based peroxidases and glutathione. In some particular cellular compartments (such as vicinity of NADPH oxidases), it is possible that a signaling protein faces extremely high $H_2O_2$ concentrations, making the direct oxidation feasible. Alternatively, high $H_2O_2$ levels can hyperoxidize peroxiredoxins leading to local building up of $H_2O_2$ that then could oxidize a signaling protein (floodgate hypothesis). In a second model, $H_2O_2$ oxidizes Cys-based peroxidases that then through thiol-disulfide reshuffling would transmit the oxidized equivalents to the signaling protein. The third model of signaling is centered on the reducing substrate of Cys-based peroxidases that in most cases is thioredoxin. Is this model, peroxiredoxins would signal by modulating the thioredoxin redox status. More kinetic data is required to allow the identification of the complex network of thiol switches.

• Bulletin of the Korean Chemical Society
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• v.28 no.9
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• pp.1455-1456
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• 2007

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.3
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• pp.139-144
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• 2010

In this study, we evaluated the role of apurinic/apyrimidinic endonuclease1/redox factor-1 (Ref-1) on the tumor necrosis factor-$\alpha$ (TNF-$\alpha$) induced cyclooxygenase-2 (COX-2) expression using A549 lung adenocarcinoma cells. TNF-$\alpha$ induced the expression of COX-2 in A549 cells, but did not induce BEAS-2B expression. The expression of COX-2 in A549 cells was TNF-$\alpha$ dose-dependent (5~100 ng/ml). TNF-$\alpha$-stimulated A549 cells evidenced increased Ref-1 expression in a dose-dependent manner. The adenoviral transfection of cells with AdRef-1 inhibited TNF-$\alpha$-induced COX-2 expression relative to that seen in the control cells ($Ad{\beta}gal$). Pretreatment with $10\;{\mu}M$ of SB203580 suppressed TNF-$\alpha$-induced COX-2 expression, thereby suggesting that p38 MAPK might be involved in COX-2 expression in A549 cells. The phosphorylation of p38 MAPK was increased significantly after 5 minutes of treatment with TNF-$\alpha$, reaching a maximum level at 10 min which persisted for up to 60 min. However, p38MAPK phosphorylation was markedly suppressed in the Ref-1-overexpressed A549 cells. Taken together, our results appear to indicate that Ref-1 negatively regulates COX-2 expression in response to cytokine stimulation via the inhibition of p38 MAPK phosphorylation. In the lung cancer cell lines, Ref-1 may be involved as an important negative regulator of inflammatory gene expression.