• Korean Journal of Adult Nursing
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• v.26 no.3
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• pp.362-371
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• 2014

Purpose: The purpose of this study was to identify Compassion Fatigue (CF), Somatization, and Silencing Response (SR) among nurses and understand intermediate effects between the variables. Methods: The sample of 240 nurses who were working three shifts in medical and surgical wards, and emergency room were recruited in three hospitals with over 700 beds. A structured questionnaire was used which included CF, Somatization and SR scales. The data were analyzed using descriptive statistics, ANOVA, Pearson's correlation coefficients and stepwise multiple regression. Results: There were statistically significant differences in CF, Somatization and SR depending on perceived personal health condition, experience of turnover, co-worker support. There were significant correlations between those study variables. The result also indicated that burnout (${\beta}$=.81, p<.001) which is a part of Secondary Traumatic Stress and Somatization (${\beta}$=.79, p<.001) have the role of partial mediator in the relationship between Secondary Traumatic Stress and Silencing response. Conclusion: The results of study show that an intermediary role by Burnout and Somatization in Silencing response of nurses is important for effective human resource management in hospital nursing staffs. Effective human resource management which includes mentoring and social support system can enhance the professional quality of life of nurses, which will eventually contribute to the quality of care by those care providers and counselors.

• BMB Reports
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• v.41 no.5
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• pp.376-381
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• 2008

The discovery of RNA silencing inhibition by virus encoded suppressors or low temperature leads to concerns about the stability of transgenic resistance. RNA-dependent RNA polymerase (RdRp) has been previously characterized to be essential for transgene-mediated RNA silencing. Here we showed that low temperature led to the inhibition of RNA silencing, the loss of viral resistance and the reduced expression of host RdRp homolog (NtRdRP1) in transgenic T4 progeny with untranslatable potato virus Y coat protein (PVY-CP) gene. Moreover, RNA silencing and the associated resistance were differently inhibited by potato virus X (PVX) and tobacco mosaic virus (TMV) infections. The increased expression of NtRdRP1 in both PVX and TMV infected plants indicated its general role in response to viral pathogens. Collectively, we propose that biotic and abiotic stress factors affect RNA silencing-mediated resistance in transgenic tobacco plants and that their effects target different steps of RNA silencing.

• Plant Biotechnology Reports
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• v.5 no.3
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• pp.273-281
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• 2011

Diverse epigenetic phenotypes are frequently found during research on transgenic plants. To understand the factors underlying such diversity, hundreds of independent 35S-GFP transgenic N. benthamiana plants were analyzed. The diverse GFP-expression phenotypes of the transgenic plants were classified into three major types based on the GFP expression patterns and their response to 35S-GFP agroinfiltration: steady-green, silenced and non-uniform phenotype. The non-uniform phenotype was further sub-divided into five minor phenotypes: variegated, red-dropped, on-silencing, partitioned and misty, according to the distribution of GFP expression on the leaves. Many of transgenic plants continuously generated diverse phenotypes over several generations despite the transgene identity. Such epigenetic GFP phenotyping was found to be the result of spontaneous transgene silencing mediated by either or both of post-transcriptional gene silencing (PTGS) and transcriptional gene silencing (TGS). This finding was verified by the detection of 21- and 24-nt small interfering RNA (siRNA) molecules, and DNA methylation in the transgenic plants that showed repeated epigenetic variation. Agroinfiltration demonstrated that irregular distribution of GFP on a leaf was the result of erratic transgene silencing, and the technique also proved to be a rapid and effective method for selecting fully silenced plants within 3 days. Furthermore, two novel phenotypes described are potential materials for in-depth investigations into the genes and mechanisms responsible for spontaneous transgene silencing.

• Molecules and Cells
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• v.27 no.6
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• pp.689-695
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• 2009

Chemically synthesized small interfering RNAs (siRNAs) can specifically knock-down expression of target genes via RNA interference (RNAi) pathway. To date, the length of synthetic siRNA duplex has been strictly maintained less than 30 bp, because an early study suggested that double-stranded RNAs (dsRNAs) longer than 30 bp could not trigger specific gene silencing due to the induction of non-specific antiviral interferon responses. Contrary to the current belief, here we show that synthetic dsRNA as long as 38 bp can result in specific target gene silencing without non-specific antiviral responses. Using this longer duplex structure, we have generated dsRNAs, which can simultaneously knock-down expression of two target genes (termed as dual-target siRNAs or dsiRNAs). Our results thus demonstrate the structural flexibility of gene silencing siRNAs, and provide a starting point to construct multifunctional RNA structures. The dsiRNAs could be utilized to develop a novel therapeutic gene silencing strategy against diseases with multiple gene alternations such as viral infection and cancer.

• Journal of Microbiology and Biotechnology
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• v.32 no.11
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• pp.1406-1415
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• 2022

The formation of macrophage foam cells stimulated by oxidized low-density lipoprotein (ox-LDL) is deemed an important cause of atherosclerosis. Transcription factor Yin Yang 1 (YY1), which is a universally expressed multifunctional protein, is closely related to cell metabolism disorders such as lipid metabolism, sugar metabolism, and bile acid metabolism. However, whether YY1 is involved in macrophage inflammation and lipid accumulation still remains unknown. After mouse macrophage cell line RAW264.7 cells were induced by ox-LDL, YY1 and proprotein convertase subtilisin/kexin type 9 (PCSK9) expressions were found to be increased while low-density lipoprotein receptor (LDLR) expression was lowly expressed. Subsequently, through reverse transcription-quantitative polymerase chain reaction (RT-qPCR), Western blot analysis, Oil Red O staining and cholesterol quantification, it turned out that silencing of YY1 attenuated the inflammatory response and lipid accumulation in RAW264.7 cells caused by ox-LDL. Moreover, results from the JASPAR database, chromatin immunoprecipitation (ChIP) assay, luciferase reporter assay and Western blot analysis suggested that YY1 activated PCSK9 by binding to PCSK9 promoter and modulated the expression of LDLR in the downstream of PCSK9. In addition, the results of functional experiments demonstrated that the inhibitory effects of YY1 interference on ox-LDL-mediated macrophage inflammation and lipid accumulation were reversed by PCSK9 overexpression. To sum up, YY1 depletion inhibited its activation of PCSK9, thereby reducing cellular inflammatory response, cholesterol homeostasis imbalance, and lipid accumulation caused by ox-LDL.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.4
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• pp.2295-2299
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• 2013

Background: To explore the role of caveolin-1(CAV-1) gene silencing on MAPK activation in lipopolysaccharide (LPS)-challenged human mammary epithelial cells. Methods: We established a MCF-10ACE of CAV-1 gene silencing from human mammary epithelial cell line MCF-10A by RNAi technology. DNA Microarray were used to detect the expression of inflammation-associated genes in MCF10ACE. Western blotting was used to examine the activation of MAPK in lipopolysaccharide(LPS)-challenged MCF-10A and MCF-10ACE. Moreover, immunofluorescence and Western bloting were performed to detect the co-localization of CAV-1 and toll-like receptor 4 (TLR4) in human mammary epithelial cells. Results: MCF-10ACE exhibited significant increases in inflammation-associated gene expression, especially IL-6 (~7-fold) and IL6R (~17-fold). In addition, LPS-induced p38 MAPK and JNK MAPK activation was significantly increased in MCF-10ACE. Furthermore, CAV-1 co-localized with TLR4 and appeared a negative correlation trend. Conclusion: CAV-1 gene silencing promotes MAPK activation via TLR4 signaling in human mammary epithelial cells response to LPS.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.1
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• pp.43-51
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• 2018

Although cisplatin is one of the most effective antitumor drugs for ovarian cancer, the emergence of chemoresistance to cisplatin in over 80% of initially responsive patients is a major barrier to successful therapy. The precise mechanisms underlying the development of cisplatin resistance are not fully understood, but alteration of DNA methylation associated with aberrant gene silencing may play a role. To identify epigenetically regulated genes directly associated with ovarian cancer cisplatin resistance, we compared the expression and methylation profiles of cisplatin-sensitive and -resistant human ovarian cancer cell lines. We identified ${\alpha}$-N-acetylgalactosaminidase (NAGA) as one of the key candidate genes for cisplatin drug response. Interestingly, in cisplatin-resistant cell lines, NAGA was significantly down-regulated and hypermethylated at a promoter CpG site at position +251 relative to the transcriptional start site. Low NAGA expression in cisplatin-resistant cell lines was restored by treatment with a DNA demethylation agent, indicating transcriptional silencing by hyper-DNA methylation. Furthermore, overexpression of NAGA in cisplatin-resistant lines induced cytotoxicity in response to cisplatin, whereas depletion of NAGA expression increased cisplatin chemoresistance, suggesting an essential role of NAGA in sensitizing ovarian cells to cisplatin. These findings indicate that NAGA acts as a cisplatin sensitizer and its gene silencing by hypermethylation confers resistance to cisplatin in ovarian cancer. Therefore, we suggest NAGA may be a promising potential therapeutic target for improvement of sensitivity to cisplatin in ovarian cancer.

• Proceedings of the Korean Society of Plant Pathology Conference
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• 2003.10a
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• pp.76.1-76
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• 2003

The coat protein (CP) of Turnip crinkle virus (TCV) is organized into 3 distinct domains, R domain (RNA-binding) connected by an arm, 5 domain and P domain. We have previously shown that the CP of TCV strongly suppresses RNA silencing, and have mapped N-terminal R domain of which is also the elicitor of resistance response in the Arabidopsis ecotype Di-17 carrying the HRT resistance gene. In order to map the region in the TCV CP that is responsible for silencing suppression, a series of CP mutants were constructed, transformed into Agrobacterium, coinfiltrated either with HC-Pro (the helper component proteinase of tobacco etch potyvirus) known as a suppressor of PTGS or GFP constructs into leaves of Nicotiana benthmiana expressing GFP transgenically. In the presence of HC-Pro, all CP mutants were well protected, accumulating mutant CP mRNAs and their proteins even 5 days post-infiltration (DPI). In the presence of GFP, some mutant constructs which showed the accumulation of CP mutants and GFP mRNAs at early stage but eventually degraded at 5 DPI. Only a mutant which carrying 4 amino acid deletion of R domain was tolerable to maintain suppressing activity, suggesting that the suppressing activity is not directly related with the eliciting activity. A transient assay also revealed that the mutants synthesized their proteins, suggesting that a full length of CP sequences and its intact structure are required to stabilize CP, which suppresses the RNA silencing.

• Journal of Plant Biotechnology
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• v.45 no.3
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• pp.183-189
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• 2018

The plant hormone auxin regulates the overall metabolic processes essential for plant growth and development. Auxin signaling is mediated by early auxin response genes, which are classified into three major families: AUXIN/INDOLE ACETIC ACID (AUX/IAA), GRETCHEN HAGEN3 (GH3) and SMALL AUIN UP RNA (SAUR). The SAUR gene family is the largest family among early auxin response genes and encodes the small and highly unstable gene products. The functional roles of SAUR genes have remained unclear for many years. The traditional genetic and molecular studies on the SAUR functions have been hampered by their likely genetic redundancy and tandem arrays of highly related genes in the plant genome, together with the molecular characteristics of SAUR. However, recent studies have suggested possible roles of SAUR in a variety of tissues and developmental stages in accordance with the novel approaches such as gain-of-function and RNA silencing techniques. In this review, the recent research progress on the functional roles and regulatory mechanisms of SAUR and a set of possible future works are discussed.