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Yang, Kyeong Eun,Jang, Hyunx2010,Jin,Hwang, Inx2010,Hu,Chung, Youngx2010,Ho,Choi, Jongx2010,Soon,Lee, Taex2010,Hoon,Chung, Yunx2010,Jo,Lee, Minx2010,Seung,Lee, Mi Young,Yeo, Euix2010,J BLACKWELL PUBLISHING 2016 AGING CELL Vol.15 No.2
<P><B>Summary</B></P><P>Phenyl‐2‐pyridyl ketoxime (PPKO) was found to be one of the small molecules enriched in the extracellular matrix of near‐senescent human diploid fibroblasts (HDFs). Treatment of young HDFs with PPKO reduced the viability of young HDFs in a dose‐ and time‐dependent manner and resulted in senescence‐associated β‐galactosidase (SA‐β‐gal) staining and G2/M cell cycle arrest. In addition, the levels of some senescence‐associated proteins, such as phosphorylated ERK1/2, caveolin‐1, p53, p16<SUP>ink4a</SUP>, and p21<SUP>waf1</SUP>, were elevated in PPKO‐treated cells. To monitor the effect of PPKO on cell stress responses, reactive oxygen species (ROS) production was examined by flow cytometry. After PPKO treatment, ROS levels transiently increased at 30 min but then returned to baseline at 60 min. The levels of some antioxidant enzymes, such as catalase, peroxiredoxin II and glutathione peroxidase I, were transiently induced by PPKO treatment. SOD II levels increased gradually, whereas the SOD I and III levels were biphasic during the experimental periods after PPKO treatment. Cellular senescence induced by PPKO was suppressed by chemical antioxidants, such as N‐acetylcysteine, 2,2,6,6‐tetramethylpiperidinyloxy, and L‐buthionine‐(<I>S</I>,<I>R</I>)‐sulfoximine. Furthermore, PPKO increased nitric oxide (NO) production via inducible NO synthase (iNOS) in HDFs. In the presence of NOS inhibitors, such as L‐NG‐nitroarginine methyl ester and L‐NG‐monomethylarginine, PPKO‐induced transient NO production and SA‐β‐gal staining were abrogated. Taken together, these results suggest that PPKO induces cellular senescence in association with transient ROS and NO production and the subsequent induction of senescence‐associated proteins<B>.</B></P>
Hong, Mi Jeong,Yoo, Seung Soo,Choi, Jin Eun,Kang, Hyox2010,Gyoung,Do, Sook Kyung,Lee, Jang Hyuck,Lee, Won Kee,Lee, Jaehee,Lee, Shin Yup,Cha, Seung Ick,Kim, Chang Ho,Lee, Eung Bae,Cho, Sukki,Jheon, S John Wiley and Sons Inc. 2018 Cancer Science Vol.109 No.12
<P>RegulomeDB is a new tool that can predict the regulatory function of genetic variants. We applied RegulomeDB in selecting putative functional variants and evaluated the relationship between these variants and survival outcomes of surgically resected non‐small‐cell lung cancer. Among the 244 variants studied, 14 were associated with overall survival (<I>P </I><<I> </I>0.05) in the discovery cohort and one variant (rs2257609 C>T) was replicated in the validation cohort. In the combined analysis, rs2257609 C>T was significantly associated with worse overall and disease‐free survival under a dominant model (<I>P </I>=<I> </I>2 × 10<SUP>−5</SUP> and <I>P </I>=<I> </I>0.001, respectively). rs2257609 is located in the <I>SLC5A10</I> intron, but RegulomeDB predicted that this variant affected <I>DRG2</I>, not <I>SLC5A10</I> expression. The expression level of <I>SLC5A10</I> was not different with the rs2257609 genotype. However, <I>DRG2</I> expression was different according to the rs2257609 genotype (<I>P</I><SUB>trend</SUB><SUP> </SUP>= 0.03) and was significantly higher in tumor than in non‐malignant lung tissues (<I>P </I>=<I> </I>1 × 10<SUP>−5</SUP>). Luciferase assay also showed higher promoter activity of <I>DRG2</I> in samples with the rs2257609 T allele (<I>P </I><<I> </I>0.0001). rs2257609 C>T affected <I>DRG2</I> expression and, thus, influenced the prognosis of early‐stage non‐small‐cell lung cancer. This study was approved by the Institutional Review Broad of Kyungpook National University of Hospital (Approval No. KNUMC 2014‐04‐210‐003).</P>
Huy, Hangsak,Song, Hae Young,Kim, Mi Jeong,Kim, Won Sam,Kim, Dong Oh,Byun, Jaex2010,Eun,Lee, Jungwoon,Park, Youngx2010,Jun,Kim, Taex2010,Don,Yoon, Suk Ran,Choi, Eunx2010,Ji,Lee, Chulx2010,Ho John Wiley and Sons Inc. 2018 Aging cell Vol.17 No.6
<P><B>Abstract</B></P><P>Aging is associated with an inevitable and universal loss of cell homeostasis and restricts an organism's lifespan by an increased susceptibility to diseases and tissue degeneration. The glucose uptake associated with producing energy for cell survival is one of the major causes of ROS production under physiological conditions. However, the overall mechanisms by which glucose uptake results in cellular senescence remain mysterious. In this study, we found that TXNIP deficiency accelerated the senescent phenotypes of MEF cells under high glucose condition. TXNIP<SUP>‐/‐</SUP> MEF cells showed greater induced glucose uptake and ROS levels than wild‐type cells, and <I>N</I>‐acetylcysteine (NAC) treatment rescued the cellular senescence of TXNIP<SUP>‐/‐</SUP> MEF cells. Interestingly, TXNIP<SUP>‐/‐</SUP> MEF cells showed continuous activation of AKT during long‐term subculture, and AKT signaling inhibition completely blocked the cellular senescence of TXNIP<SUP>‐/‐</SUP> MEF cells. In addition, we found that TXNIP interacted with AKT via the PH domain of AKT, and their interaction was increased by high glucose or H<SUB>2</SUB>O<SUB>2</SUB> treatment. The inhibition of AKT activity by TXNIP was confirmed using western blotting and an in vitro kinase assay. TXNIP deficiency in type 1 diabetes mice (Akita) efficiently decreased the blood glucose levels and finally increased mouse survival. However, in normal mice, TXNIP deficiency induced metabolic aging of mice and cellular senescence of kidney cells by inducing AKT activity and aging‐associated gene expression. Altogether, these results suggest that TXNIP regulates cellular senescence by inhibiting AKT pathways via a direct interaction under conditions of glucose‐derived metabolic stress.</P>
Transfer‐Free Growth of Few‐Layer Graphene by Self‐Assembled Monolayers
Shin, Hyeonx2010,Jin,Choi, Won Mook,Yoon, Seonx2010,Mi,Han, Gang Hee,Woo, Yun Sung,Kim, Eun Sung,Chae, Seung Jin,Li, Xiangx2010,Shu,Benayad, Anass,Loc, Duong Dinh,Gunes, Fethullah,Lee, Young Hee WILEY‐VCH Verlag 2011 Advanced Materials Vol.23 No.38
<P><B>Graphene layers are directly synthesized</B> <B>on an oxide substrate</B> without transfer. The catalytic structure aids graphene formation without the vaporization of a self‐assembled monolayer (SAM) material and induces direct growth of graphene on the substrate. Film uniformity and the number of graphene layers are modulated. The catalytic structure and growth process provide a robust method for transfer‐free graphene growth with uniform thickness. </P>
Analysis of Protein Redox Modification by Hypoxia
Choi, Kyoungx2010,Soo,Park, Soox2010,Yeon,Baek, Sunx2010,Hee,Deyx2010,Rao, Rama,Park, Youngx2010,Mee,Zhang, Haitao,Ip, Clement,Park, Eunx2010,Mi,Hong Kim, Yeul,Park, Jong Hoon MARCEL DEKKER, INC 2006 PREPARATIVE BIOCHEMISTRY AND BIOTECHNOLOGY Vol.36 No.1
<P>We examined hypoxia-induced changes in global thiol proteome profile in human prostate cancer cells using a BIAM-based display method. We analyzed the kinetics of protein thiol modification by using a pattern recognition algorithm, self-organizing maps (SOM) clustering, and identified the BIAM-labeled proteins by MALDI-TOF and ESI-tandem mass spectrometry. We found 99 out of 215 of total BIAM-labeled proteins were affected by hypoxia treatment and, yet, with diverse patterns and kinetics of redox modification. Our study proved that proteomics analysis employing the BIAM-labeling method can provide valuable information pertaining to global changes in the redox status of proteins in response to hypoxia.</P>
β‐Catenin regulates melanocyte dendricity through the modulation of PKCζ and PKCδ
Kim, Jinx2010,Hwa,Sohn, Kyungx2010,Cheol,Choi, Taex2010,Young,Kim, Mi Yoon,Ando, Hideya,Choi, Sun Ja,Kim, Sooil,Lee, Young Ho,Lee, Jeungx2010,Hoon,Kim, Chang Deok,Yoon, Taex2010,Jin Blackwell Publishing Ltd 2010 Pigment cell & melanoma research Vol.23 No.3
<P><B>Summary</B></P><P>The Wnt/β‐catenin signaling pathway is involved in the melanocyte differentiation and melanoma development. However, the effect of β‐catenin for dendrite formation has not been clearly elucidated yet in normal human epidermal melanocytes (NHEM). To investigate the effect of β‐catenin, we transduced NHEM with recombinant adenovirus expressing β‐catenin. Forced expression of β‐catenin led to the dramatic morphological changes of NHEM, including the reduction of dendrite length and enlargement of cell body. Concomitantly with, the protein levels for dendrite formation‐related molecules, such as Rac1 and Cdc42, were markedly decreased. In addition, phosphorylation of p38 MAPK was significantly reduced by β‐catenin, potentiating its inhibitory role for dendrite formation. Interestingly, overexpression of β‐catenin led to the increase of protein kinase C ζ (PKCζ) level, while protein kinase C δ (PKCδ) was decreased by β‐catenin, suggesting that those PKCs were β‐catenin‐downstream modulators in NHMC. When PKCζ was overexpressed, dendrites were shortened, with the reduced protein levels for Rac1 and Cdc42. In contrast, PKCδ overexpression led to the elongation of dendrites, with the increased levels for Rac1 and Cdc42. These results suggest that β‐catenin play an inhibitory role for dendrite formation through the modulation of PKCζ and PKCδ.</P>
Hong, Mi Jeong,Lee, Shin Yup,Choi, Jin Eun,Kang, Hyox2010,Gyoung,Do, Sook Kyung,Lee, Jang Hyuck,Yoo, Seung Soo,Lee, Eung Bae,Seok, Yangki,Cho, Sukki,Jheon, Sanghoon,Lee, Jaehee,Cha, Seung Ick,Kim, C Wiley-Blackwells 2018 Thoracic cancer Vol.9 No.8
<P><B>Background</B></P><P>Genome‐wide association studies have indicated that most of the currently identified disease and trait‐associated single nucleotide polymorphisms (SNPs) are intronic or intergenic. RegulomeDB is a recently developed database that provides functional annotations for regulatory features of SNPs located in non‐coding regions. We evaluated the potential regulatory SNPs in the <I>EGFR</I> gene region using RegulomeDB and their associations with prognosis after surgery in non‐small cell lung cancer (NSCLC) patients.</P><P><B>Methods</B></P><P>A total of 698 patients with surgically resected NSCLC were enrolled and seven SNPs were selected based on the RegulomeDB database. All SNPs were genotyped using SEQUENOM MassARRAY iPLEX assay.</P><P><B>Results</B></P><P>Among the seven SNPs evaluated, rs9642391 (<I>EGFR</I> ivs19+2851C>G) was significantly associated with survival outcome (adjusted hazard ratio [HR] for overall survival = 0.70, 95% confidence interval [CI] 0.56–0.87, <I>P</I> = 0.001; adjusted HR for disease‐free survival = 0.82, 95% CI 0.70–0.97, <I>P</I> = 0.02; under a codominant model). According to RegulomeDB, rs9642391C>G, which is located in intron 19 of <I>EGFR</I>, was predicted to influence the expression of <I>GBAS</I> but not <I>EGFR</I>. As predicted, rs9642391C>G was associated with <I>GBAS</I> (<I>P</I> = 0.024) but not <I>EGFR</I> messenger RNA expression in tumor tissues.</P><P><B>Conclusion</B></P><P>In conclusion, our study provides evidence that rs9642391C>G in the intron of <I>EGFR</I> is associated with <I>GBAS</I> expression and survival outcomes of patients with surgically resected early‐stage NSCLC.</P>
Choi, Jix2010,Hye,Gwak, Mi‐,Jin,Chung, Seox2010,Jin,Kim, Kwangx2010,Ok,O'Mahony, Michael,Ishii, Rie,Bae, Yex2010,Won John Wiley Sons, Ltd 2015 Journal of the Science of Food and Agriculture Vol.95 No.8
<P><B>Abstract</B></P><P><B>BACKGROUND</B></P><P>The present study cross‐culturally investigated the drivers of liking for traditional and ethnic chicken marinades using descriptive analysis and consumer taste tests incorporating the check‐all‐that‐apply (CATA) method. Seventy‐three Koreans and 86 US consumers participated. The tested sauces comprised three tomato‐based sauces, a teriyaki‐based sauce and a Korean spicy seasoning‐based sauce. Chicken breasts were marinated with each of the five barbecue sauces, grilled and served for evaluation. Descriptive analysis and consumer taste tests were conducted. Consumers rated the acceptance on a hedonic scale and checked the reasons for (dis)liking by the CATA method for each sauce. A general linear model, multiple factor analysis and chi‐square analysis were conducted using the data.</P><P><B>RESULTS</B></P><P>The results showed that the preference orders of the samples between Koreans and US consumers were strikingly similar to each other. However, the reasons for (dis)liking the samples differed cross‐culturally. The drivers of liking of two sauces sharing relatively similar sensory profiles but differing significantly in hedonic ratings were effectively delineated by reasons of (dis)liking CATA results.</P><P><B>CONCLUSION</B></P><P>Reasons for (dis)liking CATA proved to be a powerful supporting method to understand the internal drivers of liking which can be overlooked by generic descriptive analysis. © 2014 Society of Chemical Industry</P>
Kim, Taex2010,Jin,Kim, Nayoung,Kim, Eunx2010,Ok,Choi, Jongx2010,Rip,Bluestone, Jeffrey A.,Lee, Kyungx2010,Mi Blackwell Publishing Ltd 2010 Immunology Vol.130 No.4
<P><B>Summary</B></P><P>Natural killer (NK) cells can destroy xenogeneic tissues by antibody‐dependent cell cytotoxicity (ADCC) and direct lysis. Unlike ADCC, activating interactions between human NK receptors and their cognate ligands in pigs are not fully elucidated. We set up this study to identify human NK activating receptors recognizing porcine cells isolated from distinct organs, e.g., aorta, cornea and liver, and to provide a molecular basis for effective immunosuppressive regimens. Among the array of NK receptors tested, NKp46, 2B4, CD49d, CD48, CD2 and NKG2D, only CD2 and NKG2D were shown to be involved in both cytotoxicity and cytokine (interferon‐γ and tumour necrosis factor‐α) production against porcine targets. Simultaneous blocking of CD2 and NKG2D by combining its monoclonal antibodies further suppressed xenogeneic NK responses. Moreover, addition of a suboptimal dose of PD98059, an extracellular signal‐regulated kinase (ERK) kinase inhibitor, to those cells maximally reduced NK cytotoxicity, suggesting that ERK plays an important role in NK‐mediated xenoreactivity. These impairments in NK cells were tightly associated with defective intracellular calcium mobilization and the subsequent degranulation process. Therefore, our data demonstrate a distinct role of CD2 and NKG2D on human NK cells in recognizing porcine grafts and further provide a potentially efficacious combinational regimen using anti‐CD2 and anti‐NKG2D monoclonal antibodies with PD98059</accessionId> in a pig‐to‐human transplantation model.</P>