• 식물병연구
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• 제23권3호
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• pp.249-255
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• 2017

벼 도열병은 벼를 재배하는 지역에서는 가장 중요한 병 중 하나이다. 특히, 벼 도열병균은 기주인 벼와 Gene-for-Gene 상호작용이 적용 가능한 대표적인 모델 식물병원성 곰팡이다. 우리나라는 1980년 이래로 벼 도열병균의 레이스를 분석하기 위해 8개의 판별 품종을 이용한 시스템을 구축하여 분류하였다. 그러나 이 판별 품종이 어떤 저항성 유전자를 가지고 있는지에 관해 명확한 정보가 없어 새로운 레이스의 출현이나 병 저항성 붕괴 등에 대하여 과학적인 분석이 어려웠다. 최근 병원균의 레이스와 벼의 저항성 유전자의 상호작용 이해를 돕기 위해 LTH 품종에 단인자 저항성 계통을 각각 다르게 도입한 판별시스템이 개발되었다. 본 연구에서는 우리나라의 1995년부터 2015년까지 분리된 4개의 다른 레이스 KI101, KI201, KI401 및 KJ101로부터 총 50개 균주를 선발하여 LTH 품종에 기반한 단인자 저항성 계통에 접종하여 그 결과를 이전 레이스와 비교 분석해 보았다. 그 결과 한국형 판별시스템으로 분류된 동일 레이스내의 균주들이 단인자 계통에서 서로 다른 반응을 보였다. 이 결과 동일 레이스에 속하는 균주들이 서로 다른 비병원성 유전자를 지닌 것을 의미하며, 더 나아가 새로운 저항성 벼 품종 육종에 유용한 정보를 제공하기 어려울 것으로 추정되었다. 이 연구 결과 현재의 판별시스템과 더불어 단인자 저항성 품종을 통한 판별시스템 도입이 요구되었다. 이 연구 결과는 향후 한국의 판별시스템 개발에 기초 자료로 활용 될 수 있을 것이다.

• 한국생물정보학회:학술대회논문집
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• 한국생물정보시스템생물학회 2003년도 제2차 연례학술대회 발표논문집
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• pp.1-1
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• 2003

It is clear that computers will play a key role in the biology of the future. Even now, it is virtually impossible to keep track of the key proteins, their names and associated gene names, physical constants(e.g. binding constants, reaction constants, etc.), and hewn physical and genetic interactions without computational assistance. In this sense, computers act as an auxiliary brain, allowing one to keep track of thousands of complex molecules and their interactions. With the advent of gene expression array technology, many experiments are simply impossible without this computer assistance. In the future, as we seek to integrate the reductionist description of life provided by genomic sequencing into complex and sophisticated models of living systems, computers will play an increasingly important role in both analyzing data and generating experimentally testable hypotheses. The future of bioinformatics is thus being driven by potent technological and scientific forces. On the technological side, new experimental technologies such as microarrays, protein arrays, high-throughput expression and three-dimensional structure determination prove rapidly increasing amounts of detailed experimental information on a genomic scale. On the computational side, faster computers, ubiquitous computing systems, high-speed networks provide a powerful but rapidly changing environment of potentially immense power. The challenges we face are enormous: How do we create stable data resources when both the science and computational technology change rapidly? How do integrate and synthesize information from many disparate subdisciplines, each with their own vocabulary and viewpoint? How do we 'liberate' the scientific literature so that it can be incorporated into electronic resources? How do we take advantage of advances in computing and networking to build the international infrastructure needed to support a complete understanding of biological systems. The seeds to the solutions of these problems exist, at least partially, today. These solutions emphasize ubiquitous high-speed computation, database interoperation, federation, and integration, and the development of research networks that capture scientific knowledge rather than just the ABCs of genomic sequence. 1 will discuss a number of these solutions, with examples from existing resources, as well as area where solutions do not currently exist with a view to defining what bioinformatics and biology will look like in the future.

• Journal of Ginseng Research
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• 제44권5호
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• pp.690-696
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• 2020

Background: As the main metabolites of ginsenosides, 20(S, R)-protopanaxadiol [PPD(S, R)] and 20(S, R)-protopanaxatriol [PPT(S, R)] are the structural basis response to a series of pharmacological effects of their parent components. Although the estrogenicity of several ginsenosides has been confirmed, however, the underlying mechanisms of their estrogenic effects are still largely unclear. In this work, PPD(S, R) and PPT(S, R) were assessed for their ability to bind and activate human estrogen receptor α (hERα) by a combination of in vitro and in silico analysis. Methods: The recombinant hERα ligand-binding domain (hERα-LBD) was expressed in E. coli strain. The direct binding interactions of ginsenosides with hERα-LBD and their ERα agonistic potency were investigated by fluorescence polarization and reporter gene assays, respectively. Then, molecular dynamics simulations were carried out to simulate the binding modes between ginsenosides and hERα-LBD to reveal the structural basis for their agonist activities toward receptor. Results: Fluorescence polarization assay revealed that PPD(S, R) and PPT(S, R) could bind to hERα-LBD with moderate affinities. In the dual luciferase reporter assay using transiently transfected MCF-7 cells, PPD(S, R) and PPT(S, R) acted as agonists of hERα. Molecular docking results showed that these ginsenosides adopted an agonist conformation in the flexible hydrophobic ligand-binding pocket. The stereostructure of C-20 hydroxyl group and the presence of C-6 hydroxyl group exerted significant influence on the hydrogen bond network and steric hindrance, respectively. Conclusion: This work may provide insight into the chemical and pharmacological screening of novel therapeutic agents from ginsenosides.

• Clinical and Experimental Pediatrics
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• 제59권8호
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• pp.319-327
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• 2016

Allergic diseases such as asthma, allergic rhinitis, atopic dermatitis, and food allergy, are most common chronic, noncommunicable diseases in childhood. In the past few decades, the prevalence has increased abruptly worldwide. There are 2 possible explanations for the rising prevalence of allergic diseases worldwide, that an increased disease-awareness of physician, patient, or caregivers, and an abrupt exposure to unknown hazards. Unfortunately, the underlying mechanisms remain largely unknown. Despite the continuing efforts worldwide, the etiologies and rising prevalence remain unclear. Thus, it is important to identify and control risk factors in the susceptible individual for the best prevention and management. Genetic susceptibility or environments may be a potential background for the development of allergic disease, however they alone cannot explain the rising prevalence worldwide. There is growing evidence that epigenetic change depends on the gene, environment, and their interactions, may induce a long-lasting altered gene expression and the consequent development of allergic diseases. In epigenetic mechanisms, environmental tobacco smoke (ETS) exposure during critical period (i.e., during pregnancy and early life) are considered as a potential cause of the development of childhood allergic diseases. However, the causal relationship is still unclear. This review aimed to highlight the impact of ETS exposure during the perinatal period on the development of childhood allergic diseases and to propose a future research direction.

• Asian Pacific Journal of Cancer Prevention
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• 제15권16호
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• pp.6613-6618
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• 2014

Background: The X-ray repair cross-complementing group 3 (XRCC3) is a highly suspected candidate gene for cancer susceptibility. Attention has been drawn upon associations of the XRCC3 Thr241Met polymorphism with breast cancer risk. However, the previous published findings remain controversial. Hence, we performed a meta-analysis to accurately evaluate any association between breast cancer and XRCC3 T241M (23, 812 cases and 25, 349 controls) in different inheritance models. Materials and Methods: PubMed and Web of Science databases were searched systematically until December 31, 2013 to obtain all the records evaluating the association between the XRCC3 Thr241Met polymorphism and breast cancer risk. Crude odds ratios (ORs) together with 95% confidence intervals (CIs) were used to assess the strength of associations. Results: When all eligible studies were pooled into the meta analysis of XRCC3 T241M polymorphism, a significantly increased breast cancer risk was observed in heterozygote comparison (OR=1.06, 95%CI=1.01-1.12). No significant associations were found in other models. In subgroup analysis, this polymorphism seemed to be associated with elevated breast risk in Asians. No publication bias was detected. Conclusions: This meta-analysis suggests that the T241M polymorphism confers a weakly increased breast cancer risk. A study with the larger sample size is needed to further evaluate gene-gene and gene-environment interactions of the XRCC3 T241M polymorphism with breast cancer risk.

• Asian Pacific Journal of Cancer Prevention
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• 제13권3호
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• pp.815-819
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• 2012

Aim: We conducted a meta-analysis to analyze the influence of GSTM1 and GSTT1 gene polymorphisms on cervical cancer risk, and explore gene-environment interactions. Methods: Identification of relevant studies was carried out through a search of Medline and the EMbase up to Oct. 2011. All case-control studies that investigated the association between GSTM1 and GSTT1 gene polymorphisms and risk of cervical cancer were included. The pooled odds ratio (OR) was used for analyses of results and the corresponding 95% confidence intervals (CI) were estimated. Results: A total of 21 case-control studies were included in the meta-analysis of GSTM1 (2,378 cases and 2,639 controls) and GSTT1 (1,229 cases and 1,223 controls) genotypes. The overall results showed that the GSTM1 null was related to an increased risk of cervical cancer (OR=1.50, 95% CI=1.21-1.85). Subgroup analysis were performed based on smoking and ethnicity. Our results showed that smokers with null GSTM1 genotype had a moderate increased risk of cervical cancer (OR=1.85, 95% CI=1.07-3.20). For the ethnicity stratification, moderate significantly increased risk of null GSTM1 genotype was found in Chinese (OR=2.12, 95% CI=1.43-3.15) and Indian populations (OR=2.07, 95% CI=1.49-2.88), but no increased risk was noted in others. Conclusion: This meta-analysis provided strong evidence that the GSTM1 genotype is associated with the development of cervical cancer, especially in smokers, and Chinese and Indian populations. However, no association was found for GSTT1 null genotype carriers.

• Molecules and Cells
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• 제38권5호
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• pp.452-456
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• 2015

Obesity is the fifth leading risk for death globally, and a significant challenge to global health. It is a common, complex, non-malignant disease and develops due to interactions between the genes and the environment. DNA methylation can act as a downstream effector of environmental signals; analysis of this process therefore holds substantial promise for identifying mechanisms through which genetic and environmental factors jointly contribute to disease risk. To assess the effects of excessive weight and obesity on gene-specific methylation levels of promoter regions, we determined the methylation status of four genes involved in inflammation and oxidative stress [interleukin 6 (IL6), tumor necrosis factor ${\alpha}$ ($TNF{\alpha}$), mitochondrial transcription factor A (TFAM), and glucose transport 4 (GLUT4)] in blood cell-derived DNA from healthy women volunteers with a range of body mass indices (BMIs) by methylation-specific PCR. Interestingly, the samples from obese individuals ($BMI{\geq}30kg/m^2$) showed significantly increased hypermethylation for IL6 gene compared to normal weight ($BMI<23kg/m^2$) and overweight sample ($23kg/m^2{\leq}BMI<30kg/m^2$) (P = 0.034 and P = 0.026). However there was no statistically significant difference in promoter methylation of the other 3 genes between each group. These findings suggest that aberrant DNA methylation of IL6 gene promoter may play an important role in the etiology and pathogenesis of obesity and IL6 methylation could be used as molecular biomarker for obesity risk assessment. Further studies are required to elucidate the potential mechanisms underlying this relationship.

• Asian Pacific Journal of Cancer Prevention
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• 제13권5호
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• pp.2139-2144
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• 2012

Objective: Gastric cancer remains a major health problem in China. We hypothesized that XRCC1 Arg194Trp and ADPRT Val762Ala may be associated with risk. Methods: We designed a multicenter 1:1 matched case-control study of 307 pairs of gastric cancers and controls between October 2010 and August 2011. XRCC1 Arg194Trp and ADPRT Val762Ala were sequenced, and demographic data as well as lifestyle factors were collected using a self-designed questionnaire. Results: Individuals carrying XRCC1 Trp/Trp or Arg/Trp variant genotype had a significantly increased risk of gastric cancer (OR, 1.718; 95% CI, 1.190-2.479), while the OR for ADPRT Val762Ala variant genotype (Ala/Ala or Val/Ala) was 1.175 (95% CI, 0.796-1.737). No gene-gene or gene-environment interactions were found. In addition, family history of cancer and drinkers proportion were higher among cases than among controls (P<0.05). Conclusions: XRCC1 194 Arg/Trp or Trp/Trp genotype, family history of cancer, and drinking are suspected risk factors of gastric cancer from our study. Our findings may offer insight into further similar large gene-environment and gene-gene studies in this region.

• 한국생물정보학회:학술대회논문집
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• 한국생물정보시스템생물학회 2004년도 The 3rd Annual Conference for The Korean Society for Bioinformatics Association of Asian Societies for Bioinformatics 2004 Symposium
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• pp.39-49
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• 2004

When there is a lack of detailed kinetic information, dFBA(dynamic flux balance analysis) has correctly predicted cellular behavior under given environmental conditions with FBA and different ial equations. However, until now, dFBA has centered on substrate concentration, cell growth, and gene on/off, but a detailed hierarchical structure of a regulatory network has not been taken into account. For this reason, the dFBA has limited the represen tation of interactions between specific regulatory proteins and genes and the whole transcriptional regulation mechanism with environmental change. Moreover, to calculate optimal metabolic flux distribution which maximizes the growth flux and predict the b ehavior of cell system, linear programming package(LINDO) and spreadsheet package(EXCEL) have been used simultaneously. thses two software package have limited in the visual representation of simulation results and it can be difficult for a user to look at the effects of changing inputs to the models. Here, we descirbes the construction of hierarchical regulatory network with defined symbolsand the development of an integrated system that can predict the total control mechanism of regulatory elements (opero ns, genes, effectors, etc.), substrate concentration, growth rate, and optimal flux distribution with time. All programming procedures were accoplished in a visual programming environment (LabVIEW).

• Toxicological Research
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• 제20권3호
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• pp.205-211
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• 2004

Concern that some chemicals in our environment may affect human health by disrupt-ing normal endocrine function has prompted a research on interactions of environmental contaminants with steroid hormone receptor. Toxaphene and chlordane are among the 12 persistent organic pollutants identified by the United Nations Environment Programme as requiring urgent attention. We compared the estrogenic activity of two organochlorine pesticides, toxaphene and chlordane, at estrogen receptor a (ER$\alpha$) and estrogen receptor $\beta$ (ER$\beta$). Human hepatoma cells (HepG2) were transiently transfected with rat ER$\alpha$ or ER$\beta$ plus an estrogen-responsive complement C3-luciferase (C3-Luc) reporter gene. After transfection, cells were treated with various concentrations of toxaphene and chlordane to investigate agonism or antagonism of these chemicals. Both toxaphene and chlordane were potent agonists in HepG2 cells for ER$\alpha$. In contrast, these chemicals had a minimal agonist activity with ER$\beta$ and almost abolished 17$\beta$-estradiol-induced ER$\beta$-mediated activity. Therefore, toxaphene and chlordane behaved as an ER$\alpha$ agonist and an ER$\beta$ antagonist with estrogen-responsive reporter plasmid C3-Luc, and exposure to these organochlorine pesticides could have a crictical effect on normal endocrine function.