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Methyltransferase of a cell culture-adapted hepatitis E inhibits the MDA5 receptor signaling pathway
Jinjong Myoung,Jeong Yoon Lee,Kang Sang Min 한국미생물학회 2019 The journal of microbiology Vol.57 No.12
Hepatitis E virus (HEV) is a causative agent of acute hepatitis and jaundice. The number of human infections is approximated to be over 20 million cases per year. The transmission is mainly via the fecal-oral route and contaminated water and food are considered to be a major source of infection. As a mouse model is not available, a recent development of a cell culture-adapted HEV strain (47832c) is considered as a very important tools for molecular analysis of HEV pathogenesis in cells. Previously, we demonstrated that HEV-encoded methyltransferase (MeT) encoded by the 47832c strain inhibits MDA5- and RIG-I-mediated activation of interferon β (IFN-β) promoter. Here, we report that MeT impairs the phosphorylation and activation of interferon regulatory factor 3 and the p65 subunit of NF-κB in a dose-dependent manner. In addition, the MeT encoded by the 47832c, but not that of HEV clinical or field isolates (SAR-55, Mex-14, KC-1, and ZJ-1), displays the inhibitory effect. A deeper understanding of MeTmediated suppression of IFN-β expression would provide basis of the cell culture adaptation of HEV.
( Jinjong Myoung ),( Kang Sang Min ) 한국미생물·생명공학회 2019 Journal of microbiology and biotechnology Vol.29 No.7
Hepatitis E virus (HEV) accounts for 20 million infections in humans worldwide. In most cases, the infections are self-limiting while HEV genotype 1 infection cases may lead to lethal infections in pregnant women (~ 20% fatality). The lack of small animal models has hampered detailed analysis of virus-host interactions and HEV-induced pathology. Here, by employing a recently developed culture-adapted HEV, we demonstrated that methyltransferase, a nonstructural protein, strongly inhibits melanoma differentiation-associated gene 5 (MDA5)-mediated activation of type I interferon responses. Compared to uninfected controls, HEV-infected cells display significantly lower levels of IFN-β promoter activation when assessed by luciferase assay and RT-PCR. HEV genome-wide screening showed that HEV-encoded methyltransferase (MeT) strongly inhibits MDA5-mediated transcriptional activation of IFN-β and NF-κB in a dose-responsive manner whether or not it is expressed in the presence/absence of a tag fused to it. Taken together, current studies clearly demonstrated that HEV MeT is a novel antagonist of MDA5-mediated induction of IFN-β signaling.
Beyond Viral Interferon Regulatory Factors: Immune Evasion Strategies
( Jinjong Myoung ),( Shin-ae Lee ),( Hye-ra Lee ) 한국미생물 · 생명공학회 2019 Journal of microbiology and biotechnology Vol.29 No.12
The innate immune response serves as a first-line-of-defense mechanism for a host against viral infection. Viruses must therefore subvert this anti-viral response in order to establish an efficient life cycle. In line with this fact, Kaposi’s sarcoma-associated herpesvirus (KSHV) encodes numerous genes that function as immunomodulatory proteins to antagonize the host immune system. One such mechanism through which KSHV evades the host immunity is by encoding a viral homolog of cellular interferon (IFN) regulatory factors (IRFs), known as vIRFs. Herein, we summarize recent advances in the study of the immunomodulatory strategies of KSHV vIRFs and their effects on KSHV-associated pathogenesis.
Fault Insertion Test를 이용한 Column Type MDPS 고장진단 로직 검증 시뮬레이터 개발
이진종(Jinjong Lee),김하연(Hayeun Kim),유은영(Eunyoung Yoo),전승훈(Seunghoon Jeon),박정인(Jungin Park) 한국자동차공학회 2011 한국자동차공학회 학술대회 및 전시회 Vol.2011 No.11
This paper describes developing a fault diagnosis logic simulator of column type MDPS can be tested manually and automatically, using Fault Insertion Test. Tester can input the fault condition such as open/short test to ECU I/O. Through this developing simulator project, verification, validation and regression test before in vehicle will be strengthened; it also can reduce cost and time.
핵융합로 구조용 저방사화강의 용접열영향부 후열처리 균열 감수성
이진종(Jinjong Lee),문준오(Joonoh Moon),이창훈(Chang-Hoon Lee),박준영(Jun-Young Park),이태호(Tae-Ho LEE),홍현욱(Hyun-Uk Hong),조경목(Kyung-Mox Cho) 대한용접·접합학회 2016 대한용접·접합학회지 Vol.34 No.6
Post-Weld Heat Treatment (PWHT) cracking susceptibility in the weld heat-affected zone (HAZ) of reduced activation ferritic-martensitic (RAFM) steels was evaluated through stress-rupture tests. 9Cr-1W based alloys including different C, Ta and Ti content were prepared. The coarse grained heat-affected zone (CGHAZ) samples were simulated with welding condition of 30 kJ/cm heat input. CGHAZ samples consisted of martensite matrix. Stress rupture experiments were carried out using a Gleeble simulator at temperatures of 650-750℃ and at stress levels of 125-550 MPa, corresponding to PWHT condition. The results revealed that PWHT cracking resistance was improved by Ti addition, i.e., Ti contributed to the formation of fine and stable MX precipitates and suppression of coarse M23C6 carbides, resulting in improvement of stress rupture ductility. Meanwhile, rupture strength increased with increasing solute C content.
( Eunha Kim ),( Jinjong Myoung ) 한국미생물생명공학회(구 한국산업미생물학회) 2018 Journal of microbiology and biotechnology Vol.28 No.11
Upon viral infection, the host cell recognizes the invasion through a number of pattern recognition receptors. Melanoma differentiation associated gene 5 (MDA5) and retinoic acidinducible gene-I (RIG-I) recognize RNA molecules derived from invading viruses, activating down-stream signaling cascades, culminating in the induction of the type I interferon. On the other hand, viruses have evolved to evade type I interferon-mediated inhibition. Hepatitis E virus has been shown to encode a few antagonists of type I interferon and it is not surprising that viruses encode multiple mechanisms of viral evasion. In the present study, we demonstrated that HEV PCP strongly down-regulates MDA5-mediated activation of interferon β induction in a dose-dependent manner. Interestingly, MDA5 protein expression was almost completely abolished. In addition, polyinosinic polycytidylic acid (poly(I:C))- and Sendai virus-mediated activation of type I interferon responses were similarly abrogated in the presence of HEV PCP. Furthermore, HEV PCP down-regulates several molecules that play critical roles in the induction of type I IFN expression. Taken together, these data collectively suggest that HEV-encoded PCP is a strong antagonist of type I interferon.