• Title/Summary/Keyword: Kim Il Sung

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Intracellular Signaling Pathways for Type II IgE Receptor (CD23) Induction by Interleukin - 4 and Anti - CD40 Antibody

  • Kim, Hyun-Il;Park, Hee-Jeoung;Lee, Choong-Eun
    • BMB Reports
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    • v.30 no.6
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    • pp.431-437
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    • 1997
  • Since the role of CD40 on the interleukin-4(IL-4) -induced B cell activation has been strongly implicated in the agumentation of IgE production and response, we have investigated the intracelluar signaling pathways utilized by IL-4 and CD40 for type II IgE receptor (CD23) expression. IL-4 and anti-CD40 antibody treatment of human B cells, independently caused a rapid induction of CD23 gene activation within 2 h. There was a noticeable synergism between the action of the two agents inducing CD23 expression: the addition of anti-CD40 to the IL-4-treated culture significantly agumented the IL-4-induced CD23 on both mRNA and surface protein levels, and the inclusion of IL-4 in the anti-CD40-treated cells caused a further increase of CD23 expression far above the maximal level induced by anti-CD40. Protein tyrosine kinase (PTK) inhibitors effectively suppressed the both IL-4- and anti -CD40-induced CD23 expression. whereas protein kinase C (PKC) inhibitors had no effects. Electrophoretic mobility shift assays (EMSA) have shown that IL-4 and anti-CD40 induce the activation of NF-IL-4 and $NF-_{K}B$, respectively, binding to the CD23 promoter, both in a PKC-independent and PTK-dependent manner. These data suggest that the synergistic activation of CD23 gene expression by IL-4 and anti-CD40 is mediated by co-operative action of distinct nuclear factors. each of which is rapidly activated via PKC-independent and PTK-dependent process.

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Expression Profile of Inflammatory Genes in Human Airway Epithelial A549 Cells

  • Sohn, Sung-Hwa;Ko, Eun-Jung;Kim, Sung-Hoon;Kim, Yang-Seok;Shin, Min-Kyu;Hong, Moo-Chang;Bae, Hyun-Su
    • Molecular & Cellular Toxicology
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    • v.5 no.1
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    • pp.44-50
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    • 2009
  • This study was conducted to evaluate the inflammation mechanisms of tumor necrosis factor-$\alpha$ (TNF-$\alpha$), interleukin-4 (IL-4), and IL-$1{\beta}$-induced stimulation of A549 human epithelial cells. In the present study, A549 cells were stimulated with TNF-$\alpha$, IL-4 and IL-$1{\beta}$ to induce expression of chemokines and adhesion molecules involved in eosinophil chemotaxis. The effects of TNF-$\alpha$, IL-4 and IL-$1{\beta}$ on gene expression profiles in A549 cells were evaluated by oligonucleotide microarray and Real time RT-PCR. The gene expression profiles for the A549 cells varied depending on the cytokines. Also, the results of the microarray and Real time RT-PCR revealed that inflammatory-related genes were up-regulated in cytokine stimulated A549 cells. Cytokines can affect inflammation in A549 cells. A microarray-based genomic survey is a high-throughput approach that enables evaluation of gene expression in cytokine stimulated cell lines.

Reaction of 2-Mercaptobenzothiazole (2-Mercaptobenzothiazole의 반응)

  • In Kyu Kim;Sun Il Kim;Chan Mo Yu;Il-Gook Chung;Joon Won Park;Sang Chul Shim
    • Journal of the Korean Chemical Society
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    • v.28 no.6
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    • pp.412-417
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    • 1984
  • A highly efficient and general route to obtain the alkyl derivatives of 2-mercaptobenzothiazole is described. Depending on the reaction conditions 2-methylmercaptobenzothiazole gave various products with chlorinating agents probably due to the lability of the probable chlorosulfonium ion intermediate.

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