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Lee, Siyoung,Kim, Eunsom,Jhun, Hyunjhung,Hong, Jaewoo,Kwak, Areum,Jo, Seunghyun,Bae, Suyoung,Lee, Jongho,Kim, Busun,Lee, Jungmin,Youn, Sulah,Kim, Somi,Kim, Miyeon,Kim, Hyunwoo,Lee, Youngmin,Choi, Dong American Society for Biochemistry and Molecular Bi 2016 The Journal of biological chemistry Vol.291 No.28
<P>Although it has been established that diabetes increases susceptibility to infections, the role of insulin (INS) in the immune response is unknown. Here, we investigated the immunological function of INS. Proinsulin dimer (pINSd) was a potent immune stimulus that induced inflammatory cytokines, but mature INS was unable to induce an immune response. An affinity-purified rabbit polyclonal antibody raised against mature IL-1α recognized IL-1α and pINS but failed to detect mature INS and IL-1β. Analysis of the pINS sequence revealed the existence of an INS/IL-1α motif in the C-peptide of pINS. Surprisingly, the INS/IL-1α motif was recognized by monoclonal antibody raised against IL-1α. Deleting the INS/IL-1α motif in pINSd and IL-1α changed their activities. To investigate the pINSd receptor, the reconstitution of IL-1 receptor 1 (IL-1R1) in Wish cells restored pINSd activity that was reversed by an IL-1R antagonist. These data suggested that pINSd needs IL-1R1 for inflammatory cytokine induction. Mouse embryo fibroblast cells of IL-1R1-deficient mice further confirmed that pINSd promotes immune responses through IL-1R1.</P>
SDL-92에서 객체지향 언어의 코드 생성을 위한 개념 변환
이시영(Siyoung Lee),이동길(DongGill Lee),이준경(Joon-Kyung Lee),김승호(Sung-Ho Kim) 한국정보과학회 2000 정보과학회논문지 : 소프트웨어 및 응용 Vol.27 No.5
시스템의 명세 및 기술 언어인 SDL-92는 객체지향 개념의 도입에서 기존의 시스템 명세 및 설계 문서들과 사용자들을 포용하기 위해 프로세스와 시그널에 기반한 통신 방법을 고수하였다. 이러한 객체지향 개념의 도입은 메소드와 객체 기반의 객체지향 언어 프로그램의 자동 생성에 있어 대응 개념의 부재라는 문제점뿐만 아니라 이에 따르는 가시성 및 통신 방법과 같은 부수적인 문제점들까지 유발하고 있다. 따라서 본 논문에서는 메소드와 객체에 기반한 일반적인 객체지향 언어 모델을 제시한 후, SDL-92에서 제시된 모델로의 변환에서 발생하는 문제점들을 고찰하고 이를 해결할 수 있는 개념 변환 방법들을 제시한다. 제시된 변환 방법은 목적 언어의 구문으로의 사상 방법을 제공함으로써 객체들에 내장된 병렬성을 활용할 수 있고 변환된 프로그램에 대해 컴파일러 수준의 이식성을 보장할 수 있다. SDL-92, the language for specification and description of system, has held on to the communication method that based on processes and signals in the adoption of object-oriented concept to embrace the previous documents of system specification and description and users. It has caused problems, not only the absence of corresponding concepts in automatic generation to object-oriented language program based on method and object, but also some side effects accompanied by them like visibility and communication method. So, in this paper, we present a general object-oriented language model which based on method and object, make a study of problems in the transformation from SDL-92 to proposed model, and then propose conceptual transformation methods to solve them. The proposed transformation method can utilize the built-in parallelism in objects and guarantee the compiler level portability in translated program by providing translation into the syntax of target language.
Lee Jaewon,Ha Jihoon,Kim Jun-Hyeong,Seo Dongyeob,Kim Minbeom,Lee Yerin,Park Seong Shil,Choi Dahee,Park Jin Seok,Lee Young Jae,Yang Siyoung,Yang Kyung-Min,Jung Su Myung,Hong Suntaek,Koo Seung-Hoi,Bae Y 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
The signaling pathways governing acetaminophen (APAP)-induced liver injury have been extensively studied. However, little is known about the ubiquitin-modifying enzymes needed for the regulation of APAP-induced liver injury. Here, we examined whether the Pellino3 protein, which has E3 ligase activity, is needed for APAP-induced liver injury and subsequently explored its molecular mechanism. Whole-body Peli3−/− knockout (KO) and adenovirus-mediated Peli3 knockdown (KD) mice showed reduced levels of centrilobular cell death, infiltration of immune cells, and biomarkers of liver injury, such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), upon APAP treatment compared to wild-type (WT) mice. Peli3 deficiency in primary hepatocytes decreased mitochondrial and lysosomal damage and reduced the mitochondrial reactive oxygen species (ROS) levels. In addition, the levels of phosphorylation at serine 9 in the cytoplasm and mitochondrial translocation of GSK3β were decreased in primary hepatocytes obtained from Peli3−/− KO mice, and these reductions were accompanied by decreases in JNK phosphorylation and mitochondrial translocation. Pellino3 bound more strongly to GSK3β compared with JNK1 and JNK2 and induced the lysine 63 (K63)-mediated polyubiquitination of GSK3β. In rescue experiments, the ectopic expression of wild-type Pellino3 in Peli3−/− KO hepatocytes restored the mitochondrial translocation of GSK3β, but this restoration was not obtained with expression of a catalytically inactive mutant of Pellino3. These findings are the first to suggest a mechanistic link between Pellino3 and APAP-induced liver injury through the modulation of GSK3β polyubiquitination.
Lee, Siyoung,Choi, Dong-Ki,Kwak, Areum,Kim, Sinae,Nguyen, Tam Thanh,Gil, Gaae,Kim, Eunhye,Yoo, Kwang Ha,Kim, In Ae,Lee, Youngmin,Jhun, Hyunjhung,Chan, Edward D.,Bai, Xiyuan,Kim, Hyunwoo,Kim, Yong-Sung 한국조명·전기설비학회 2017 한국조명·전기설비학회 학술대회논문집 Vol. No.
<P>The induction of interleukin (IL)-32 in bone marrow (BM) inflammation is crucial in graft versus host disease (GvHD) that is a common side effect of allogeneic BM transplantation. Clinical trials on α-1 antitrypsin (AAT) in patients with GvHD are based on the preliminary human and mouse studies on AAT reducing the severity of GvHD. Proteinase 3 (PR3) is an IL-32-binding protein that was isolated from human urine. IL-32 primarily induces inflammatory cytokines in myeloid cells, probably due to PR3 expression on the membrane of the myeloid lineage cells. The inhibitory activity of AAT on serine proteinases may explain the anti-inflammatory effect of AAT on GvHD. However, the anti-inflammatory activity of AAT on BM cells remains unclear. Mouse BM cells were treated with IL-32γ and different inflammatory stimuli to investigate the anti-inflammatory activity of AAT. Recombinant AAT-Fc fusion protein inhibited IL-32γ-induced IL-6 expression in BM cells, but failed to suppress that induced by other stimuli. In addition, the binding of IL-32γ to PR3 was abrogated by AAT-Fc. The data suggest that the specific anti-inflammatory effect of AAT in mouse BM cells is due to the blocking of IL-32 binding to membrane PR3.</P>