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Lee, Ji Hee,Bae, Jeong A,Lee, Jae Hyuk,Seo, Young-Woo,Kho, Dhong Hyo,Sun, Eun Gene,Lee, Song Eun,Cho, Sang Hee,Joo, Young Eun,Ahn, Kyu Youn,Chung, Ik Joo,Kim, Kyung Keun British Medical Association 2010 Gut Vol.59 No.7
<P>BACKGROUND AND AIMS: 90K, a tumour-associated glycoprotein, interacts with galectins and has roles in host defence by augmenting the immune response, but the serum 90K level was suggested to indicate poor prognosis in several cancers. The cellular mechanisms of 90K action on colorectal cancer (CRC) cell motility and its effect on CRC progression were investigated. METHODS: The impact of 90K was analysed by combining cell cultures, in vitro assays, and immunohistochemistry. RESULTS: Secreted 90K suppresses CRC cell invasion, but this action of 90K is masked through binding with extracellular galectins. A novel pathway is identified comprising a secretory 90K and a CD9/CD82 tetraspanin web; in this pathway, 90K interacts with CD9/CD82, suppresses the Wnt/beta-catenin signal via a novel proteasomal-ubiquitination mechanism of beta-catenin that is dependent on ISG15 (interferon-stimulated gene-15) modification (ISGylation) but not on glycogen synthase kinase 3beta (GSK-3beta) and Siah/Adenomatous polyposis coli (APC). In a syngeneic mouse colon tumour model, tumour growth and lung metastasis were increased with 90K knockdown. In colon tissues from stage IV human CRC and invading cancer cells of corresponding metastatic liver tissues, in which beta-catenin and galectin expression was higher, immunostained 90K and CD9/CD82 were lower than in adjacent hepatic tissues or colon tissues from stage I. CONCLUSIONS: 90K itself has antitumour activity in CRC cells via suppression of Wnt signalling with a novel mechanism of ISGylation-dependent ubiquitination of beta-catenin when it interacts with CD9/CD82, but is downregulated in advanced CRC tissues. The data suggest a strategy of strengthening this novel pathway with concomitant knockdown of galectins as a potential therapeutic approach to CRC progression.</P>
Joo, Eun Hye,Kuila, Tapas,Kim, Nam Hoon,Lee, Joong Hee,Kim, Seon A.,Park, Eu Gene,Lee, Un Hyeung Trans Tech Publications, Ltd. 2013 Advanced materials research Vol.747 No.-
<P>Preparation of functionalized graphene by electrochemical exfoliation of graphite rod using sodium dodecyl benzene sulfonate (SDBS) is reported. SDBS solution has been used as the electrolyte as well as functional groups. SDBD is an anionic surfactant which helps to provide uniform dispersion in water and prevents the π-π π-π stacking as well. XRD result indicates the formation of graphene whereas; the functionalization of graphene was confirmed through the FT-IR spectrum, which shows presence of peaks corresponding to SO3<SUP>-</SUP>. UV-vis spectroscopy demonstrates the dispersibility of SDBS-functionalized graphene, and peaks of SDBS and graphene appeared at 225 nm and 260nm, respectively. Raman spectroscopy show ID/IGIDIG ratio is < 1. It means that defects of SDBS-functionalized graphene are reduced.</P>
분산 PKI 메커니즘을 고려한 안전한 클러스터 기반 라우팅 프로토콜에 관한 연구
한진백 ( Gene-beck Hahn ),양대헌 ( Dae-hun Nyang ),김신규 ( Sin-kyu Kim ),서성훈 ( Sung-hoon Seo ),송주석 ( Joo-seok Song ) 한국정보처리학회 2004 한국정보처리학회 학술대회논문집 Vol.11 No.1
본 연구에서는 MANET(Mobile Ad Hoc Network)에서 분산 PKI(Public Key Infrastructure) 메커니즘을 라우팅 프로토콜에 적용하기 위한 방법을 제안한다. 이를 위해 MANET 이 사용하는 라우팅 프로토콜로 CBRP(Cluster Based Routing Protocol)를 고려한다. 제안하는 프로토콜은 CBRP 의 기능과 분산 PKI 메커니즘을 활용하여 효율적으로 인증서 체인을 찾을 수 있고, 이를 통해 통신노드 상호간의 세션키 설정과 송수신하고자 하는 데이터에 대한 암호화를 지원한다. 또한, 라우팅 프로토콜의 안전한 동작을 위해 제안하는 프로토콜은 전자서명된 HELLO 메시지를 교환하여 악의적인 공격자들에 대해 신뢰성을 제공하고, 안전한 라우팅을 가능하게 한다.
Upregulation of GM-CSF by TGF-β1 in epithelial mesenchymal transition of human HERS/ERM cells.
Lee, Joo-Hee,Nam, Hyun,Um, Soyoun,Lee, Juhwan,Lee, Gene,Seo, Byoung Moo Springer 2014 In vitro cellular & developmental biology Animal Vol.50 No.5
<P>Hertwig's epithelial root sheath/epithelial rests of Malassez (HERS/ERM) have been suggested to play an important role in tooth root formation, particularly in periodontal development. Epithelial mesenchymal transition (EMT) has been suggested to contribute to root development in tooth. However, the mechanism of interaction between HERS/ERM cells and dental mesenchymal cells has not been fully understood. In this study, we investigated the effect of exogenous transforming growth factor beta 1 (TGF-beta 1) in human HERS/ERM cells in order to verify the role of granulocyte macrophage colony-stimulating factor (GM-CSF) in EMT process. Antibody array was used to screen secretion factors by exogenous TGF-beta 1. Secretion of GM-CSF was increased by exogenous TGF-beta 1. Expression levels of EMT markers, vimentin, ZEB1 (zinc finger E-box binding homeobox 1), and E-cadherin, were confirmed using reverse transcription polymerase chain reaction and immunocytochemistry. Treatment with GM-CSF increased the expression of vimentin and ZEB1, similar to TGF-beta 1 treatment, and decreased the expression of E-cadherin. Our results suggest that GM-CSF could induce EMT in human HERS/ERM cells.</P>