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C-terminally mutated tubby protein accumulates in aggresomes
( Sunshin Kim ),( Ho Jin Sung ),( Ji Won Lee ),( Yun Hee Kim ),( Yong-seok Oh ),( Kyong-ah Yoon ),( Kyun Heo ),( Pann-ghill Suh ) 생화학분자생물학회(구 한국생화학분자생물학회) 2017 BMB Reports Vol.50 No.1
The tubby protein (Tub), a putative transcription factor, plays important roles in the maintenance and function of neuronal cells. A splicing defect-causing mutation in the 3`-end of the tubby gene, which is predicted to disrupt the carboxy-terminal region of the Tub protein, causes maturity-onset obesity, blindness, and deafness in mice. Although this pathological Tub mutation leads to a loss of function, the precise mechanism has not yet been investigated. Here, we found that the mutant Tub proteins were mostly localized to puncta found in the perinuclear region and that the C-terminus was important for its solubility. Immunocytochemical analysis revealed that puncta of mutant Tub co-localized with the aggresome. Moreover, whereas wild-type Tub was translocated to the nucleus by extracellular signaling, the mutant forms failed to undergo such translocation. Taken together, our results suggest that the malfunctions of the Tub mutant are caused by its misfolding and subsequent localization to aggresomes. [BMB Reports 2017; 50(1): 37-42]
NF-kappa B prevents beta cell death and autoimmune diabetes in NOD mice.
Kim, Sunshin,Millet, Isabelle,Kim, Hun Sik,Kim, Ja Young,Han, Myoung Sook,Lee, Moon-Kyu,Kim, Kwang-Won,Sherwin, Robert S,Karin, Michael,Lee, Myung-Shik National Academy of Sciences 2007 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.104 No.6
<P>Whereas NF-kappaB has potent antiapoptotic function in most cell types, it was reported that in pancreatic beta cells it serves a proapoptotic function and may contribute to the pathogenesis of autoimmune type 1 diabetes. To investigate the role of beta cell NF-kappaB in autoimmune diabetes, we produced transgenic mice expressing a nondegradable form of IkappaBalpha in pancreatic beta cells (RIP-mIkappaBalpha mice). beta cells of these mice were more susceptible to killing by TNF-alpha plus IFN-gamma but more resistant to IL-1beta plus IFN-gamma than normal beta cells. Similar results were obtained with beta cells lacking IkappaB kinase beta, a protein kinase required for NF-kappaB activation. Inhibition of beta cell NF-kappaB accelerated the development of autoimmune diabetes in nonobese diabetic mice but had no effect on glucose tolerance or serum insulin in C57BL/6 mice, precluding a nonphysiological effect of transgene expression. Development of diabetes after transfer of diabetogenic CD4(+) T cells was accelerated in RIP-mIkappaBalpha/nonobese diabetic mice and was abrogated by anti-TNF therapy. These results suggest that under conditions that resemble autoimmune type 1 diabetes, the dominant effect of NF-kappaB is prevention of TNF-induced apoptosis. This differs from the proapoptotic function of NF-kappaB in IL-1beta-stimulated beta cells.</P>
Rapid Cellulose-Mediated Microwave Sintering for High-Conductivity Ag Patterns on Paper
Jung, Sunshin,Chun, Su Jin,Shon, Chae-Hwa American Chemical Society 2016 ACS APPLIED MATERIALS & INTERFACES Vol.8 No.31
<P>Cellulose-based paper is essential in everyday life, but it also has further potentials for use in low-cost, printable, disposable, and eco-friendly electronics. Here, a method is developed for the cellulose-mediated microwave sintering of Ag patterns on conventional paper, in which the paper plays a significant role both as a flexible insulating substrate for the conductive Ag pattern and as a lossy dielectric media for rapid microwave heating. The anisotropic dielectric properties of the cellulose fibers mean that a microwave electric field applied parallel to the paper substrate provides sufficient heating to produce Ag patterns with a conductivity 29-38% that of bulk Ag in a short period of time (similar to 1 s) at 250-300 degrees C. Significantly, there is little thermal degradation of the substrate during this process. The microwave-sintered Ag patterns exhibit good mechanical stability against 10 000 bending cycles and can be easily soldered with lead-free solder. Therefore, cellulose-mediated microwave sintering presents a promising means of achieving short processing times and high electrical performance in flexible paper electronics.</P>
안순신(Sunshin An) 한국정보과학회 1992 정보과학회논문지 Vol.19 No.6
본 연구에서는 새로운 분산 객체 모델을 제시한다. 기존의 분산 시스템들은 중앙집중 모델의 분산 버젼들이지만, 본 모델은 분산 실세계를 고려한 분산 시스템 모델이다. 본 모델에서의 주요 특성은 객체 독립성, 객체 동질성, 객체간 동일한 통신 방식, 객체와 튜플에 대한 접근 제어, 객체 스키마 변경, 복합 속성과 뷰 특성이 있다. 또한 3절에서 본 모델의 장점을 다른 모델과 비교하였다. In this paper, we introduce a new distributed object model. The existing distributed systems are the distributed versions of a centralized model. But, our model is a distributed model which considers the distributed real world. The main features are object independence, object homogeneity, object uniform communications, object and tuple access control, object schema change, complex attribute and view feature. Also, advantages compared with other models are shown in Sec. 3.
Kyung-SunShin,Eun-YoungShin,Chan-SooLee,Song-HuaQuan,Kyung-NamWoo,Nak-KyunSoung,Sahng-JuneKwak,SeungRyulKim,Eung-GookKim 생화학분자생물학회 2002 Experimental and molecular medicine Vol.34 No.2
p21-activated kinase (PAK) targeting to the plasmamembrane is essential for PC12 cell neurite out-growth. Phospholipase C- g1 (PLC-g1) can mediatethe PAK translocation in response to growth factors,since PLC-g1 binds to both tyrosine-phosphorylatedreceptor tyrosine kinases and PAK through its SH2and SH3 domain, respectively. In the present study,we examined a potential role for PLC- g1 in the basicfibroblast growth factor (bFGF)-induced PAK trans-location using stable PC12 cell lines that over-expres in a tetracycline-inducible manner either thewild-type FGFR-1 or the Y766F FGFR-1 mutant.Phosphatidylinositol hydrolysis was increased 6.5-fold in response to bFGF in the wild type cels butnegligible in the mutant cells. The recombinant GST-PLC-g1 SH3 was able to bind to PAK1 but not GSTalone. However, examination of PLC- g1 as an adap-tor for translocation of PAK1 in cells showed thatboth cells transfected with pEGFP-PAK1 was able todifferentiate for 24 h, as visualized by laser confocalmicroscopy. Translocation of PAK1 to growth conesoccurs at similar levels in both wild and mutant cells.These results suggest that a protein(s) other thanPLC-g1 is functionally relevant for PAK targeting.
Kim, Sunshin,Kim, Hun Sik,Chung, Kun Wook,Oh, Seung Hoon,Yun, Jong Won,Im, Sin-Hyeog,Lee, Moon-Kyu,Kim, Kwang-Won,Lee, Myung-Shik American Diabetes Association] 2007 Diabetes Vol.56 No.10
<P>OBJECTIVE: We have reported important roles for signal transducer and activator of transcription-1 (STAT1) in pancreatic beta-cell death by cytokines in vitro. However, in vivo evidence supporting the role for STAT1 in natural type 1 diabetes has not been reported. We studied whether STAT1 plays an important role in the development of natural type 1 diabetes. RESEARCH DESIGN AND METHODS: We produced nonobese diabetic (NOD)/STAT1(-/-) mice by backcrossing and studied the in vivo role of STAT1 in beta-cell death and type 1 diabetes. RESULTS: STAT1(-/-) islet cells were resistant to death by interferon (IFN)-gamma/tumor necrosis factor (TNF)-alpha or IFN-gamma/interleukin (IL)-1 beta combination. Cytochrome c translocation by IFN-gamma/TNF-alpha was abrogated in STAT1(-/-) islet cells. The induction of X-linked inhibitor of apoptosis protein by TNF-alpha was inhibited by IFN-gamma in STAT1(+/-) islet cells but not in STAT1(-/-) islet cells. Inducible nitric oxide (NO) synthase induction and NO production by IFN-gamma/IL-1 beta were impaired in STAT1(-/-) islet cells. Strikingly, diabetes and insulitis were completely abrogated in NOD/STAT1(-/-) mice. Development of diabetes after CD4(+) diabetogenic T-cell transfer was inhibited in those mice. STAT1(-/-) neonatal pancreata were not destroyed when grafted into diabetic NOD/BDC2.5 mice that developed CD4(+) T-cell-dependent islet cell death. In NOD/STAT1(-/-) mice, autoreactive T-cell priming was not impaired, but Th1 differentiation was impaired. A janus kinase (JAK) 2 inhibitor upstream of STAT1 attenuated islet cell death by IFN-gamma/TNF-alpha or IFN-gamma/IL-1 beta and delayed diabetes onset in NOD/BDC2.5-SCID mice. CONCLUSIONS: These data demonstrate a critical role for STAT1 in beta-cell death, T-cell immunoregulation, and type 1 diabetes in vivo and suggest potential therapeutic values of STAT1 or JAK inhibitors in the treatment/prevention of type 1 diabetes.</P>
김선신 ( Sunshin Kim ),정광수 ( Kwang Su Jung ),류근호 ( Keun Ho Ryu ) 한국정보처리학회 2005 한국정보처리학회 학술대회논문집 Vol.12 No.2
단백질 구조로부터 단백질사이의 기능관계를 유추하는 일은 생명정보학에 있어서 중요한 연구과제이다. 여기서, 단백질 1차 구조로부터 단백질 기능관계의 예측이 용이한 진화적으로 가까운 종간에는, 아미노산 서열을 비교하여 결과를 획득하고, 진화적으로 먼 종간에는 단백질 3차 구조 및 표면구조를 종합적으로 활용함으로써, 단백질간의 기능관계를 보다 효율적이고 정확하게 예측할 수 있음을 보인다.