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Lee, Hyung Chul,Jung, Seung Hee,Hwang, Hyun Jung,Kang, Donghee,De, Supriyo,Dudekula, Dawood B.,Martindale, Jennifer L.,Park, Byungkyu,Park, Seung Kuk,Lee, Eun Kyung,Lee, Jeong-Hwa,Jeong, Sunjoo,Han, K Oxford University Press 2017 Nucleic acids research Vol.45 No.11
<P><B>Abstract</B></P><P>RNA-binding proteins (RBPs) are involved in mRNA splicing, maturation, transport, translation, storage and turnover. Here, we identified <I>ACOT7</I> mRNA as a novel target of human WIG1. <I>ACOT7</I> mRNA decay was triggered by the microRNA miR-9 in a WIG1-dependent manner via classic recruitment of Argonaute 2 (AGO2). Interestingly, AGO2 was also recruited to <I>ACOT7</I> mRNA in a WIG1-dependent manner in the absence of miR-9, which indicates an alternative model whereby WIG1 controls AGO2-mediated gene silencing. The WIG1–AGO2 complex attenuated translation initiation via an interaction with translation initiation factor 5B (eIF5B). These results were confirmed using a WIG1 tethering system based on the MS2 bacteriophage coat protein and a reporter construct containing an MS2-binding site, and by immunoprecipitation of WIG1 and detection of WIG1-associated proteins using liquid chromatography-tandem mass spectrometry. We also identified WIG1-binding motifs using photoactivatable ribonucleoside-enhanced crosslinking and immunoprecipitation analyses. Altogether, our data indicate that WIG1 governs the miRNA-dependent and the miRNA-independent recruitment of AGO2 to lower the stability of and suppress the translation of <I>ACOT7</I> mRNA.</P>
Improvement Characteristics of Bio-active Materials Coated Fabric on Rat Muscular Mitochondria
Lee, Donghee,Kim, Young-Won,Kim, Jung-Ha,Yang, Misuk,Bae, Hyemi,Lim, Inja,Bang, Hyoweon,Go, Kyung-Chan,Yang, Gwang-Wung,Rho, Yong-Hwan,Park, Hyo-Suk,Park, Eun-Ho,Ko, Jae-Hong The Korean Society of Pharmacology 2015 The Korean Journal of Physiology & Pharmacology Vol.19 No.3
This study surveys the improvement characteristics in old-aged muscular mitochondria by bio-active materials coated fabric (BMCF). To observe the effects, the fabric (10 and 30%) was worn to old-aged rat then the oxygen consumption efficiency and copy numbers of mitochondria, and mRNA expression of apoptosis- and mitophagy-related genes were verified. By wearing the BMCF, the oxidative respiration significantly increased when using the 30% materials coated fabric. The mitochondrial DNA copy number significantly decreased and subsequently recovered in a dose-dependent manner. The respiratory control ratio to mitochondrial DNA copy number showed a dose-dependent increment. As times passed, Bax, caspase 9, PGC-$1{\alpha}$ and ${\beta}$-actin increased, and Bcl-2 decreased in a dose-dependent manner. However, the BMCF can be seen to have had no effect on Fas receptor. PINK1 expression did not change considerably and was inclined to decrease in control group, but the expression was down-regulated then subsequently increased with the use of the BMCF in a dose-dependent manner. Caspase 3 increased and subsequently decreased in a dose-dependent manner. These results suggest that the BMCF invigorates mitophagy and improves mitochondrial oxidative respiration in skeletal muscle, and in early stage of apoptosis induced by the BMCF is not related to extrinsic death-receptor mediated but mitochondria-mediated signaling pathway.
New Division of Work in IT Service Project : Defining Emerging New Roles and Explicating Conflicts
Donghee Lee 한국경영정보학회 2018 한국경영정보학회 학술대회논문집 Vol.2018 No.11
2010년 이후의 IT는 그 이전에 개발되어 오던 IT에 비하면 아주 성숙된 기술들로 사용자들에게 다가왔다. 예를 들어 클라우드, 빅데이터, 소셜미디어, 모바일컴퓨팅, 사물인터넷 등의 기술들은 이전의 기술들과는 다른 형태의 특성들을 타나내고 있다 [1]. 스마트폰들이 일상화되어 가면서 켬퓨팅 디바이스들이 태블릿과 여타 임베디드 내지는 웨어러블 컴퓨팅으로 진화하고 있는 것이다. 이러한 미래형 변화의 시초는 사용자인터페이스(UI)나 사용자 경험(UX)을 중요시하는 트렌드와 그 궤를 같이 한다 [2]. 이렇게 UX와 UI가 정보시스템개발을 개발하는 데 있어서 아주 중요한 활동, 특히 프론트엔드의 활동으로 등장하게 된 것이다. 모바일이나 웹개발에서만 중요하게 등장한 것이 아니라 소프트웨어엔지니어링에 초점이 맞추어져 있던 기존의 IT서비스 프로젝트들에 있어서도 중요한 활동으로 등장하게 된다[3, 4]. 이러한 맥락에서 웹과 모바일 서비스 프로젝트들에서 일반화되었던 서비스의 “기획, 디자인, 개발, 퍼블리싱, 운영[5]” 등의 세부 업무 분화가 일반적인 IT서비스 프로젝트들에게도 전이가 되고 있는 것이다[6, 7]. 이러한 업무 세분화는 실제 직군의 변화로 이어지고 있다. 세분화된 특정분야의 전문가 직군이 새롭게 생겨난 것이다. 또한 이런 직군의 세분화와 더불어 동일 프로젝트안에서 참여자들간의 협업과 협력 작업에 있어서 그 전에 볼 수 없었던 새로운 양상이 나타나기 시작한다. 이에 따른 갈등의 양상도 기존의 모습과는 다른 형태로 나타나기 시작한 것으로 파악된다. 새로운 업무관계와 이로 인한 갈등은 협력작업이 중요한 IT서비스 프로젝트 진행 중에 업무 이해 차이에서 오는 커뮤니케이션 문제를 발생시키고, 결국 추가비용 발생, 일정 지연, 품질 저하 등의 프로젝트 성과 저하로 이어지는 것이다. 이러한 맥락에서 본 연구에서는 IT 서비스 구축 업무 프로세스의 변화의 사례들을 조사하고 업무 프로세스를 심층 상세 분석하고 비교한다. 실제 프로젝트 참여자들을 인터뷰하고 관련 문서들을 수집, 내용 분석을 하여 각 직군 업무의 내용과 프로세스를 파악한다. 업무 프로세스 요소간 상호연관성을 분석하여 업무의 패턴을 찾아내고 각각의 역할 모델을 분석하여 새로이 나타나고 있는 업무 패턴을 조망해보고자 한다.
Lee, Donghee,Yang, Sung American Chemical Society 2013 ACS APPLIED MATERIALS & INTERFACES Vol.5 No.7
<P>Polydimethylsiloxane (PDMS) is widely used as a substrate in miniaturized devices, given its suitability for execution of biological and chemical assays. Here, we present a patterning approach for PDMS, which uses an on-chip Parylene-C microstencil to pattern proteins and cells. To implement the on-chip Parylene-C microstencil, we applied SiO<I>x</I>-like nanoparticle layers using atmospheric-pressure plasma-enhanced chemical vapor deposition (AP-PECVD) of tetraethyl orthosilicate (TEOS) mixed with oxygen. The complete removal of Parylene-C from PDMS following application of SiO<I>x</I>-like nanoparticle layers was demonstrated by various surface characterization analysis, including optical transparency, surface morphology, chemical composition, and peel-off force. Furthermore, the effects of the number of AP-PECVD treatments were investigated. Our approach overcomes the tendency of Parylene-C to peel off incompletely from PDMS, which has limited its use with PDMS to date. The on-chip Parylene-C microstencil approach that is based on this Parylene-C peel-off process on PDMS can pattern proteins with 2-μm resolution and cells at single-cell resolution with a vacancy ratio as small as 10%. This provides superior user-friendliness and a greater degree of geometrical freedom than previously described approaches that require meticulous care in handling of stencil. Thus, this patterning method could be applied in various research fields to pattern proteins or cells on the flexible PDMS substrate.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/aamick/2013/aamick.2013.5.issue-7/am4001166/production/images/medium/am-2013-001166_0012.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/am4001166'>ACS Electronic Supporting Info</A></P>
Lee, Donghee,Ryu, Kwon-Yul Elsevier 2017 Biochemical and biophysical research communication Vol. No.
<P><B>Abstract</B></P> <P>The polyubiquitin genes <I>Ubb</I> and <I>Ubc</I> are upregulated under oxidative stress induced by arsenite [As(III)]. However, the role of ubiquitin (Ub) under As(III) exposure is not known in detail. In a previous study, we showed that the reduced viability observed in <I>Ubc</I> <SUP>−/−</SUP> mouse embryonic fibroblasts under As(III) exposure was not due to dysregulation of the Nrf2–Keap1 pathway, which prompted us to investigate another NFE2 family protein, nuclear factor erythroid 2-related factor 1 (Nrf1). In this study, we found that Ub deficiency due to <I>Ubc</I> knockdown in N2a cells reduced cell viability and proteasome activity under As(III) exposure. Furthermore, mRNA levels of the proteasome subunit <I>Psma1</I> were also reduced. In addition, Ub deficiency led to the nuclear accumulation of the p65 isoform of Nrf1 under As(III) exposure. Interestingly, the overexpression of p65-Nrf1 recapitulated the phenotypes of Ub-deficient N2a cells under As(III) exposure. On the other hand, <I>Nrf1</I> knockdown suppressed the death of Ub-deficient N2a cells upon exposure to As(III). Therefore, the levels of p65-Nrf1 may play an important role in the maintenance of cell viability under oxidative stress induced by As(III).</P> <P><B>Highlights</B></P> <P> <UL> <LI> N2a cells exhibit reduced viability upon exposure to As(III) via <I>Ubc</I> knockdown. </LI> <LI> As(III)-induced proteasomal regulation is impaired in Ub-deficient N2a cells. </LI> <LI> Ub deficiency leads to the nuclear accumulation of p65-Nrf1 under As(III) exposure. </LI> <LI> p65 expression recapitulates As(III)-induced phenotypes of Ub-deficient N2a cells. </LI> <LI> <I>Nrf1</I> knockdown suppressed As(III)-induced death of Ub-deficient N2a cells. </LI> </UL> </P>
Lee, Donghee,Seo, Yelim,Kim, Young-Won,Kim, Seongtae,Bae, Hyemi,Choi, Jeongyoon,Lim, Inja,Bang, Hyoweon,Kim, Jung-Ha,Ko, Jae-Hong The Korean Society of Pharmacology 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.2
Despite increased evidence of bio-activity following far-infrared (FIR) radiation, susceptibility of cell signaling to FIR radiation-induced homeostasis is poorly understood. To observe the effects of FIR radiation, FIR-radiated materials-coated fabric was put on experimental rats or applied to L6 cells, and microarray analysis, quantitative real-time polymerase chain reaction, and wound healing assays were performed. Microarray analysis revealed that messenger RNA expressions of rat muscle were stimulated by FIR radiation in a dose-dependent manner in amount of 10% and 30% materials-coated. In 30% group, 1,473 differentially expressed genes were identified (fold change [FC] > 1.5), and 218 genes were significantly regulated (FC > 1.5 and p < 0.05). Microarray analysis showed that extracellular matrix (ECM)-receptor interaction, focal adhesion, and cell migration-related pathways were significantly stimulated in rat muscle. ECM and platelet-derived growth factor (PDGF)-mediated cell migration-related genes were increased. And, results showed that the relative gene expression of actin beta was increased. FIR radiation also stimulated actin subunit and actin-related genes. We observed that wound healing was certainly promoted by FIR radiation over 48 h in L6 cells. Therefore, we suggest that FIR radiation can penetrate the body and stimulate PDGF-mediated cell migration through ECM-integrin signaling in rats.